FINAL EXAM

Dysautonomia

no taste bud or pain

20. General somatic afferents of cranial nerve 7,9,10 connects to second order neurons in

spinal trigeminal nucleus

21. Lower motor neurons are found in

ventral horn of the spinal cord trigeminal motor nucleus nucleus ambiguus hypoglosal nucleus

What happens when Gaba binds to a Chlorine Channel?

• Cl can go into cell and hyperpolarizes • GABA is inhibitory AA• GABA main inhibitory in CNS• Glycine is more at the spinal cord level inhibitory NT

What are other characteristics regarding glutamate?

• It also has G-protein coupled receptors• That's is why glutamate can do so many diff functions • You also have metabotropic glutamate receptors (11 different subtypes)• Pretty much glutamate does a lot of work

Explain jaw protrusion

*exception to contralateral muscle control*In order to get smooth jaw protrusion, we need our lateral pterygoid muscles to work together1) One motor neuron fires and it splits to synapse at BOTH trigeminal motor nucleu at the same time 2) 2nd order efferent neurons stimulate the lateral pterygoids and the jaw is pulled forwardNote: For protrusion it is bilateral innervationFor lateral only one side is stimulated at a time

Lesions

- Lesion of medial lemniscus, VPL thalamus, PLIC and medial and upper lateral postcentral gyrus (above internal arcuate fibers) produce CONTRALATERAL loss of discriminative touch and conscious proprioception from limbs and trunk- Lesion of dorsal column or gracile cuneate nuclei (below internal arcuate fibers) produce ipsilateral loss of discriminative touch and conscious proprioception from the limbs and trunk

Naloxone is an opioid antagonist. How is it taken? Explain why Naltrexone side-effects are worse.

- Naloxone is given nasally or by IV but cannot be taken orally- Naltrexone has potentially more cardiovascular side-effects --↑ HR, BP, arrhythmias than the other antagonists.Extra Notes: Naloxone versus Naltrexone Both of these medications are opiate antagonist drugs, meaning that they prevent or block opiate drugs from reaching the brain at a cellular level.Naloxone is most often used as a short-term opiate blocker, even though it is similar to naltrexone in its chemical structure. It is not designed to be used for long-term treatment of the abuse of opiate drugs; instead, it is more often used as an emergency treatment for people who overdose on opiate drugs.Naloxone acts quickly, immediately knocking opiate drugs off the receptors in the brain and reversing the effects of opiate overdose, particularly serious issues with decreased heart rate and breathing rate. Once naloxone is administered to an individual who has overdosed, the person begins to breathe regularly, and their system normalizes. Use of this drug can prevent brain damage as a result of an overdose on opiate drugs such as heroin and even powerful opiate drugs like fentanyl, which are extremely dangerous. The faster the drug can be administered, the better the chance that it can save the person's life, as the effects typically occur within five minutes of administration. Naloxone can be administered via an injection or nasal spray.Naltrexone is used differently than naloxone. It is a slower-acting drug. Naltrexone is more often used for people who are recovering from opiate abuse or alcohol abuse. It is most effective after the person has been abstinent from alcohol or drugs for a week to two weeks. Its effectiveness is designed to prevent relapse by attaching to the opiate receptors in the brain and preventing cravings for these drugs. It is not effective at controlling withdrawal symptoms. It does not produce a "high" (neither does naloxone), and the use of naltrexone also reduces the high from drugs and alcohol if they are taken.

We have reviewed the S and PS NS in this section. As a review, compare the efferent pathways of the motor and autonomic NS

- Somatic Motor PathwayCNS --> release ACh to Nicotinic Receptor located on Skeletal Muscle- Autonomic Pathways (The autonomic nervous system is divided into three parts: the sympathetic nervous system, the parasympathetic nervous system and the enteric nervous system. The autonomic nervous system controls smooth muscle of the viscera (internal organs) and glands.)1) Parasympathetic Pathway- CNS --> Ganglion (Release ACh to Nicotinic Receptors) --> Autonomic Effectors that have Muscarinic Receptors (ACh released to these receptors)2) Sympathetic Pathway- Note: Adrenergic receptors have 2 main types - Alpha and Beta- CNS --> Ganglion (Release ACh to Nicotinic Receptors) --> Autonomic Effectors that have NE receptors (NE released to these receptors) 3) Adrenal Sympathetic Pathway- CNS --> Adrenal Medulla (Release ACh to Nicotinic Receptors at AM)--> Chromaffin Cells which release (Catecholamines) Epinephrine to the blood stream/blood vessel (eventually travels to autonomic effectors)Autonomic Effectors include: Smooth and cardiac muscle, Some endocrine and exocrine glands, Some adipose tissueExtra Notes: - Autonomic pathways, together with somatic motor pathways to skeletal muscle and neuroendocrine pathways, are the means whereby the central nervous system (CNS) sends commands to the rest of the body- Enteric NS: A division of the autonomic nervous system whose component neurons lie within the walls of the digestive organs (esophagus, stomach, intestines, pancreas, gall bladder and pancreato-biliary ducts). The enteric nervous system contains entire nerve circuits for digestive organ control, and can function autonomously.- Adrenergic receptors have two main types, namely, alpha and beta receptors. ... Alpha receptors are mostly involved in the stimulation of effector cells and constriction of blood vessels. On the other hand, beta receptors are mostly involved in the relaxation of effector cells and dilatation of blood vessels.

The neuromuscular junction

1 muscle fiber has one motor plate

What are the clinical uses of Salicylates (aspirin family)?

1) Analgesic -- Mild to moderate pain (e.g., headache, myalgia, arthralgia, and inflammation) alone or w/opioid analgesics --- Peripheral: ↓ PG induced inflammation; Central: dorsal horn/spinal cord2) Antipyretic --- Reset hypothalamic set-point and ↑ heat loss via vasodilation of cutaneous blood vessels and ↑ profuse sweating; MOA: ↓ pyrogen induced PGs & ↓ CNS response to interleukin-13) Anti-inflammatory -- Provide only symptomatic relief (e.g., RA); MOA: ↓ macrophage chemotactic factors, stabilize lysosomes, and reduce migration of leucocytes & macrophages.Meh don't know if you need to know below...4) Anticoagulant --- chronic low doses INHIBIT PLATELET AGGREGATION and prolong bleeding for 10-14 d - - REDUCE risk of transient ischemic attacks (TIA), stroke, non-fatal MI or unstable angina & colon cancerMOA: IRREVERSIBLY inhibits COX-1 & COX-2 to reduce synthesis of thromboxane A2 (vasoconstriction) and the vasodilator PGI; LOW DOSES: selectively reduce TXA2 (thrombic) but NOT PGI (anti-thrombotic effect)

Explain the steps of the pupil reflex (pathways involved in the pupillary light reflex)?

1) CN 2 detects light coming into ONE eye2) Interneuron synapses with CN 3 Parasympathetic Cell bodies in the Edinger-Westphal Nucleus on BOTH sides3) Preganglionic parasympathetic neuron then synapses in the ciliary ganglion4) Postganglionic neuron synapses on Pupillary Constrictor Muscle causing the pupil to constrict5) BOTH pupils will constrict at same time See pic on next tab

Describe the flow of CSF (Know all of this)

1) CSF is secreted by the choroid plexus in the lateral ventricles2) CSF flows through the interventricular foramina (aka Foramen of Monroe) into the 3rd ventricle3) The 3rd ventricle choroid plexus adds more CSF4) CSF flows through the cerebral aqueduct to the 4th ventricle 5) The 4th ventricle choroid plexus adds more CSF6) CSF flows out 2 lateral apertures and 1 median apertureLateral = foramen luschka (LL)Median = foramen of magendie (MM)7) CSF fills the subarachnoid space and bathes the brain and spinal cord8) CSF is reabsorbed into the dural sinuses by arachnoid granulations where it mixes with venous blood*Bloackage of cerebral aqueduct (connection between 3rd and 4th aqueduct) can cause hydrocephaly

What are the autonomic control centers?

1) Hypothalamus - water balance (osmolarity), temperature, hunger2) Pons - respiration, cardiac, vasoconstriction3) Medulla - respirationThe main one is the hypothalamus - he gets info from everywhere

Explain the cellular mechanism for the above question (cellular mechanism underlying analgesia)

1) Increases postsynaptic K+ efflux (hyperpolarizes neurons - less likely to respond to a pain stimulus)2) Inhibition presynaptic Ca2+ influx (reduces glutamate, neuropeptide, norepinephrine, release) --> so 2nd neuron can no longer fire an APNote: potassium most abundant cation inside cell, sodium most abundant outside

Explain the Sympathetic pathway

1) Release Acetylcholine (ACh) from the Preganglionic Neuron2) ACh is received by Nicotinic receptors causing Sodium channels to open and creating a Graded response in the Postganglionic cell body- Nicotinic receptors also respond to Nicotine, which is where the name comes from - These type of receptors that nicotinic receptors are -- Ionotropic receptors which open ion channelsNOTE: The Pre & Postganglionic Neurons Synapse in an autonomic ganglion, which is typically far from the target organ3) The Postganglionic Neuron releases the NT Norepinephrine which is received by Adrenergic Receptors on the Target Organ- Adrenergic Receptors are metabotropic Receptors - G Protein LinkedNOTE: The postganglionic neuron is NOT myelinatedThe Sympathetic System is considered a 2 neuron system: 1) Lateral horn --> Sympathetic ganglia2) Sympathetic ganglia --> Target Organ

What are the classes of Opioid Agonist and Antagonist?- Know groups and drug

1) Strong Agonists - Opium Alkaloids & Derivatives Morphine sulfate 2) Strong Agonists - Synthetic Opioids Meperidine Fentanyl Methadone Oxycodone3) Partial Agonists Codeine Hydrocodone Diphenoxylate4) Weak Agonists Tramadol5) Mixed Agonist - Antagonists Pentazocine Buprenorphine6) Antagonists Naloxone & Naltrexone Methylnaltrexone

What happens during absorption of morphine?

1. Absorption: Oral absorption of morphine is slow and undergoes significant FIRST-PASS METABOLISM in the liver; therefore, IM, SC or IV injections are preferred- Codeine & Oxycodone are well-absorbed orally- Chronic pain: Use new slow-release morphine oral tablets or implanted pumps (PCA)

NSAIDS: Acetic Acid Deritvatives (IDK JUST REMEMBER?)

1. Indomethicin2. 3. Ketorolac- Use: PARENTAL for short-term management of moderate-to-severe pain --> Alternative to opioids4. Diclofenac (non-selective COX inhibitor)- Less GI ulceration than other AA derivatives- Clinical Use: --> RA Osetoarthritis Transdermal Patch (Flector Patch)

When does gestational age occur?

1st day of last normal menstrual cycle

What happens during distribution of morphine?

2. Distribution: Enters ALL body tissues, including the fetus of pregnant women - - Infants born to addicted mothers show physical dependence & withdrawal symptoms- Only small % crosses BBB vs. fentanyl, methadone, heroin --> these are storage (???)

What is Trigeminal Sensory Nucleus?

2nd order sensory cell bodies of CN 5

Unconscious proprioception

4 2nd order tracts originate in dorsal horn (2 proprioceptor-mechanoreceptor combined for each of 2 limbs)- From lower limb: dorsal (posterior) and ventral (anterior) spinocerebellar tracts- From upper limb: cuneo- and rostral spinocerebellar tracts- Cerebellum receives all (and only) signals originating on ipsilateral side

Define Nucleus

A group of neuronal cell bodies inside the CNS

Define a ganglion

A group of neuronal cell bodies outside the CNS

What is the difference between a segmental and peripheral nerve?

A segmental nerve (spinal nerve) is a single segment with a recognizable pattern of distribution - simple on the trunk and modified on the limbs (twisted). The system is numbered compared to peripheral where it is named.Peripheral Nerves is multi-segmental with no apparent pattern without reference to segments - simply named by regionA collection of segmental nerves that have joined together. You would likely see formation of a lot of these in the limbs.Notes from class: Segmental nerves give rise to peripheral nervesSegmental Nerves: based on numbers (C1, C2, etc)One segmentSegments are rotated not in straight bandsSegmental Nerves have a specific pattern or dermatomeSegmental Nerves = Spinal NervesBecause of turning and twisting, many of the segmental nerves may have a mixture of multi-segmental nerves which gives rise to peripheral nerves which have names instead of numbers

9. The corneal blink reflex tests the competence of the following EXCEPT

A. CN VIII

8. the jaw jerk reflex tests the competance of

A. Mandibular nerve B. Trigeminal ganglion C. Mesencephalic trigeminal nucleus

2. Dermatomes are

A. segmental innervation of the skin B. reveptive fields for spinal nerves C. convoluted in limbs

What is the main NT in gustatory system (taste)?

ATP is the main NT in gustatory system

4. C1 spinal nerve exits

Above atlas

What is an action potential? Are their different levels of action potential or how can you tell if it is a strong stimuli or weak stimuli?

Action potential is a rapid, large depolarization followed by hyperpolarization. AP are all or none. They are all uniform in size but if the stimuli is strong then there are more AP that are fired and if it is weak there are less.Even a supra-threshold stimulus will trigger the same AP as a stimulus that just barely reaches the threshold potential.

Where are ependymal cells found?

All ventricles, form choroid plexus, glial cells, neuroepitheliumEpendymal cells have tight junction in choroid plexus that control and filter content of CSFGlucose = source of energy for brain and ependymal cells have many glucose transporters. Choroid plexus allows glucose to ooze out in plasma and incorporates into CSFEpendymal cells of choroid plexus surrounding blood vessels so that blood vessels are never in direct contact with ventricles or CSFCSF can change composition go through ependymal cells to fill ventricles inside brain (lumen)Oozes out into subarachnoid spaceRecirculate through arachnoid granulationsGood circulation throughout brain system

What type of nucleus is the solitary nucleus?

An afferent nuclei

What type of nucleus is the hypoglossal nucleus? CN? Innervation?

An efferent nuclei (Nuclei of the somatic efferent cell column)CN XIIIntrinsic and Extrinsic muscles of the tongue

What is analgesia and how do NSAIDS have an analgesic effect?

Analgesia is synonymous with pain reliefThere are REDUCED PROSTAGLANDIN LEVELS (which normally activates different elements of the inflammatory response like vasodilation, adhesion molecules and inflammatory cells). Given the levels are reduced, there is less sensitization of nociceptive nerve endings by inflammatory mediators (i.e. Bradykinin, 5-HT)Reduced prostaglandin-mediated vasodilation is probably the cause of headache relief

What are the three major actions of NSAIDS?

Analgesic, Anti-Inflammatory, AntipyreticNSAIDS inhibit the synthesis of prostaglandins & in turn activate other inflammatory responses such as vasodilation

What is the antagonist action for nalaxone and naltrexone?

Antagonist Action: --> Both drugs can rapidly and effectively reverse the CNS depression and other side effects (e.g. respiratory depression, analgesia, etc.) of opioids Example: when given to a patient who had pain, they will start to feel the pain again --> Can rapidly precipitate withdrawal symptoms in a person physically dependent on opioids --> To avoid withdrawal, use lower doses, & titrate slowly.

Explain the Anti-Coagulant effect of Thromboxane and Prostacyclin

Anti-Coagulant Effect: Mechanism = Inhibit the synthesis of ThromboxaneNon-selective NSAIDS/ASAProstacyclin: Inhibit COX1 and COX2Thromboxane: Irreversibly inhibit TXA2 production by inhibiting COX. THAT IS WHY ASPIRIN IS ANTI-PLATELET AND MAKES YOU BLEED.COX-2 InhibitorProstacyclin: Will inhibit COX 2Thromboxane: No effectResult: Prostacyclin: Inhibits platelet aggregationThromboxane: Promotes platelet aggregation --> Hemostasis and ThrombosisBalance is maintained but when COX-2 inhibitor binds the it tips the balance. There must be a balance between Thromboxane and Prostacyclin. Selective COX-2 inhibitors are not always good because they selectively inhibit COX 2 stopping inhibition of platelet aggregation, thus, can cause heart attack or stroke.

What is an opioid?

Any naturally occurring OR synthetic compound with morphine-like pharmalogical properties OR antagonists thereof

When does embryonic age occur?

Begins at fertilization

Where do microglial cells come from? What is their role in the NS?

Bone marrow-derived cells, mesoderm cells and mesenchymal cellsThey are the garbage man (phagocytize/phagocytose) neurons and infections to keep the CNS healthy

What is the clinical use of methadone?

CLINICAL USE: Management of chronic pain and for treatment of patients with OPIOID DEPENDENCEMethodone Maintenance Program: Orally active form is used to develop cross-tolerance in heroin addicts by reducing the intense Euphoria and craving ---- decreases reinforcement & criminal activityThis takes longer to get withdrawal symptoms, has longer duration of action (patient does not get the quick high from fast-acting opioid but they also don't experience withdrawal symptoms)*Treatment for opioid dependence*

What is the Edinger-Westphal Nucleus?

CN 3 Preganglionic Parasympathetic Cell Bodies are located hereEventually leads to muscles of pupil constrictionLies in the midbrain periaqueductal grey matter. Its axons leave in the oculomotor nerve and pass to the ciliary ganglion in the orbit, from which postganglionic fibers innervate the sphincter pupillae and ciliary muscles within the eye

What includes gray matter, nucleus and cortex?

CNS with neuronal cell bodies

What includes white matter, lemniscus and capsule?

CNS with neuronal processes

Name the components of the CNS and PNS

CNS: Brain and spinal cord, The olfactory and optic nerve are part of CNSPNS: Enteric nervous system, Autonomic nervous system, Cranial and spinal nerves and their ganglia (not optic nerve and only a small portion of olfactory nerve) • Cranial nerves are generalized terms are part of PNS - not exactly correct ○ Visual cranial nerve II - the eye and optic nerve are extensions of CNS and NOT PNS ○ The olfactory nerve is a small portion § Top portion of nose through cribiform plate and connect with CNS in olfactory bulb (part of the CNS) § PNS part of olfactory nerve is where it picks up stimulants sends through cribiform plate and olfactory bulb is where CNS starts

What is Trigeminal Motor Nucleus (mid-pons)?

Cell bodies of both somatic & visceral motor neurons for CN 5Innervates the muscles of mastication, tensor tympani, tensor veli, palitini, mylohyoid and the anterior belly of the digastric muscle

When is glutamate used?

Central NT that primary nociceptors release when connecting to 2nd order neuron. The main excitatory NT in CNSExcitatory postsynaptic effects

What is the connection between the 3rd and 4th ventricles?

Cerebral aqueductImportant because cells surrounding cerebral aqueduct are important for production/contain a lot of cells that control involuntary function, pain pathways associated with these areasThe Periaqueductal Grey is associated with the cerebral aqueduct (grey = cell bodies)(peri = surrounding)The periaqueductal gray (PAG, also known as the central gray) is a nucleus that plays a critical role in autonomic function, motivated behavior and behavioural responses to threatening stimuli. PAG is also the primary control center for descending pain modulation. It has enkephalin-producing cells that suppress pain.

In general, what produces CSF and where is it absorbed?

Cerebrospinal fluid (CSF) is a clear, colorless body fluid found in the brain and spinal cord. It is produced by specialised ependymal cells in the choroid plexuses of the ventricles of the brain, and absorbed in the arachnoid granulations.Extra Notes: Where the arachnoid granulations contact venous blood sinusesCSF can exchange metabolites with venous bloodGets carried away to IJV getting back into circulatory system

What is the neuronal process of taste?

Chemicals from food and other sources interact, occur on the tongue in groups of 50-150. Each of these groups forms a taste bud, which is grouped together with other taste buds into taste papillae. The taste buds are embedded in the epithelium of the tongue and make contact with the outside environment through a taste pore. Slender processes (microvilli) extend from the outer ends of the receptor cells through the taste pore, where the processes are covered by the mucus that lines the oral cavity. At their inner ends the taste receptor cells synapse, or connect, with afferent sensory neurons, nerve cells that conduct information to the brain. Each receptor cell synapses with several afferent sensory neurons, and each afferent neuron branches to several taste papillae, where each branch makes contact with many receptor cells. The afferent sensory neurons occur in three different nerves running to the brain—the facial nerve, the glossopharyngeal nerve, and the vagus nerve. Taste receptor cells of vertebrates are continually renewed throughout the life of the organism.Taste sensations produced within an individual taste bud also vary, since each taste bud typically contains receptor cells that respond to distinct chemical stimuli—as opposed to the same chemical stimulus. As a result, the sensation of different tastes (i.e., salty, sweet, sour, bitter, or umami) is diverse not only within a single taste bud but also throughout the surface of the tongue.

What are the pros and cons of using Classical Cox inhibitors that are not selective versus those that selectively bind?

Classical COX inhibitors are not selective and bind to all types of COX. This results in reduced inflammation, antipyretic (reduced fever), antithrombotic (prevents blood clot) and analgesic effect- GI discomfort occurs because they inhibit PG which are used to coat GI mucosaOther NSAIDS selectively bind to COX-2 which is specific to inflamed tissue- This has less GI discomfort but increased risk of heart attack, thrombosis, stroke because there is an inbalance of COXRemember, you always want a balance of COX 1 and COX 2

What is the lowest portion of the spinal cord/where the spinal cord ends?

Conus medullarisEnds at L2

What reflex is triggered and what muscle is used to close your eye lids?

Corneal reflexCN 5 detects something touching the corneaTriggers CN 7 on BOTh sides to cause ORBICULARIS OCCULI MUSCLE to contractNote: orbicularis occuli muscle is the muscle responsible for closing your eyelids

Explain how it is in the cranial verus spinal - Pia Mater

Cranial: Attached to CNS surfaceSpinal: Attached to CNS surface, expanded as denticulate ligaments

Explain how it is in the cranial verus spinal - Arachnoid Mater

Cranial: Attached to inner surface of the duraSpinal: Attached to inner surface of dura

Explain how it is in the cranial verus spinal - Dura Mater

Cranial:double layered, attached to inner calvarial spaceSpinal: single layered, suspended in vertebral canal (it is single because there are no sinuses present)

Explain the major action that antipyretics are involved in with regard to NSAIDS

Decrease or inhibition of PGE2PGE2 is a mediator prostaglandin responsible for elevating the hypothalamic set-point for temperature control in fever and associated autonomic responses (promote autonomic mechanisms which cause fever)Induce cooling mechanisms via vasodilation and sweating

Codeine metabolism often varies by what ___. Explain this concept further.

Different ethnicities will have different metabolic rates Some codeine is converted to morphine in the mitochondriaCertain ethnic gorups are vulnerable to the toxic effects of codeine. Those who have ULTRARAPID METABOLISM may have an increase in morphine production from the same amount of codeine intake as regular metabolizers. Ultra-Rapid MetabolizersCaucasian 1-10%African Americans 3%Chinese or Japanese 1%Hispanics 1%North Africans, Ethiopians, or Saudi Arabians 16-28%Approximately 5% to 10% of codeine is metabolized via the hepatic microsomal enzyme cytochrome P450 2D6 (CYP2D6) to morphine. In patients with poor metabolizer phenotype at CYP 2D6 (∼5% to 10% of patients), there is greatly reduced morphine formation after codeine administration, leading to insufficient pain relief. In patients with ultrarapid metabolizer phenotype (∼1% to 2% of patients), there is greatly increased morphine formation after codeine administration, LEADING TO A HIGHER RISK OF TOXICITYExtra notes: Codeine is metabolized to morphine by the cytochrome P450 enzyme (CYP) 2D6. Inhibitors of this enzyme (such as fluoxetine and citalopram) can decrease or even abolish the effect of codeine.

How is noradrenaline/norepinhephrine disributed?

Distributed by a nucleus in the brain stem known as the locus coeruleus to the entire brain

How is serotonin distributed?

Distributed by raphe nuclei

Name the catecholamines

Dopamine, Epinephrine and Norepinephrine

What are the spaces in the CNS? (Hint there are 4)

Dura Mater, Epidural Space, Arachnoid Mater, Pia Mater

What are the connective tissues of the nerves? (Hint there are 3)

Endoneurium: covers the individual nerves including the axons and schwann cellsPerineurium: covers the fasicle bundlesEpineurium: covers the entire group of mutliple fasicles and blood supply

What keeps arterial blood away from contact with brain parenchyma? BLOOD BRAIN BARRIER

Endothelial cells and astrocytes

figure 15.9 (part 1)

Even though there are 400 active OR genes, these genes may be able to produce more than 400 different receptor molecules due to posttranslational modifications. The point of this slide is that there many variable regions in the molecule which can make the molecule more or less likely to bind to any given odorant. Sits on the ciliate.

1. Cranial nerve ganglia belong to the CNS and spinal nerve ganglia belong to PNS

F

11. Cranial motor nuclei UMNs and ventral horn of the spinal cord house LMNs

F

13. Cranial nerve ganglia belong to the CNS and spnal nerve ganglia belong to PNS

F

19. Olfactory receptor cells are modified epithellial cells

F

What innervates the Stapedius muscle?

Facial motor nucleus/Facial Nerve

The dorsal column/funiculi is divided into these 2

Fasciculus GracilisFasciculus Cuneatus

Which papillae does not have taste buds?

Filiform papillae

In the sympathetic and parasympathetic nervous system the 1st and 2nd order neurons vary in size. Describe the length for both systems.

For the sympathetic NS, the 2nd order neuron is much longer than the 1st order neuronFor the parasympathetic NS, the 1st order neuron is much longer than the 2nd order neuron

What are the openings at the base of the 4th ventricle and what may they be used for?

Foramen of Magendie (median apperture, opening at midline)Foramen(s) of Luschka (lateral appertures)CSF can flow through these openings into the arachnoid spaceCan go down and around spinal cord as well as up and around the brainThe foramen magendie and the foramen of luschka are the flushing system

Identify all the parts of the forebrain, midbrain and hindbrain

Forebrain aka Prosencephalon consists of the Telencephalon and Diencephalon. The telencephalon consists of the cerebral hemispheres and lateral ventricles. The diencephalon consists of the thalamus and 3rd ventricle.Midbrain aka Mesencephalon consists of the midbrain and aqueductHindbrain aka Rhombocephalon consists of the Metencephalon and Myelencephalon. The metencephalon consists of the pons, cerebellum and upper part of the 4th ventricle. The myelencephalon consists of the medulla and lower part of the 4th ventricle.See next tab for pic

What do Glycine and GABA do in the NS?

GABA and Glycine are the main inhibitory NT in NS

Explain General Afferents

GSA (somatic) & GVA (visceral - ANS): Single nerve cell carries info from target organ to the cell body in the DORSAL ROOT GANGLION- VA run with VE convey info from visceral (rather than somatic tissues)

Explain General Efferents

GSE: Single cell body in the ventral horn innervates the target organ by its axonGVE: 2 neurons, lateral horn of CNS sends out an axon that synapses with 1 or more cell bodies located outside CNS in a cluster of cell bodies called a Ganglion (then goes to target organ)2 neurons = preganglionic and postganglionic

What is the general mode of analgesia?

General Mechanism of Analgesia: 1) Increase pain threshold (spinal) and 2) Reduce perception of pain (brain or supraspinal)

Mesencephalic nucleus

General somatic affarent

What are the amino acid neurotransmitter receptor systems?

Glutamate receptors-Majority are ionotropic receptors (ligand-gated ion channels)-Three subtypes of ionotropic glutamate receptors:--> N-methyl-D-aspartate (NMDA) receptors--> α-Amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptors--> Kainate receptorsExtra Notes about Glutamate: • It also has G-protein coupled receptors• That's is why glutamate can do so many diff functions • You also have metabotropic glutamate receptors • Pretty much glutamate does a lot of work

What is Inferior Salivatory Nuclei (CN 9)?

Goes to the otic ganglion and then parotid glandSends preganglionic fibers into the glossopharyngeal nerveThese terminate in the otic ganglion, which in turn sends postganglionic axons to the parotid salivary gland

What is Superior Salivatory Nuclei (CN 7)?

Goes to the submandibular & pterygopalatin ganglionsSupplies preganglionic fibers to the facial nerve that terminate in the pterygopalatine and submandibular gangliaPostganglionic fibers from the pterygopalatine ganglion innervate the lacrimal gland and the nasal and oral mucous membranesThose from the submandibular ganglion innervate the submandibular and sublingual salivary glands

What is the difference between graded potential and all-or-none response? Be specific and include where it is located, what type of gates are there, what kind of ions are used and what type of signal each has.

Graded Potential- Located in dendrites and cell body- Gates: Ligand-gated and GPCR ion channels (no voltage gated ion channels). In general, mechanically, chemically, or voltage-gated channels- Ions: Usually Na+, Cl-, Ca2+- Type of Signal: Input signal, Depolarizing or Hyperpolarizing - There is an exchange of ions and depolarization is created because the ion channels are open and closing. DOES NOT generate an action potential.All-or-None- Located or eminating from the axon hillock (trigger zone) to the terminus- Gates: Voltage-gated sodium and potassium channels- Ions: Na+ and K+ - Type of Signal: Conduction signal, Depolarizing *Important to remember is that graded potential can be summed but action potential cannot be summed. The strength of the signal for graded potential depends on the initial stimulus while the action potential is always the same giving it the title "all-or-none". Moreover, graded potentials are intiated by the entry of ions through its channel but all-or-none potential needs to have above-threshold graded potential at the trigger zone (axon hillock). Thus, the graded potential has no minimum requirement while AP has a threshold stimulus requirement.See next tab for pic

How is the spinal cord organized? Hint there are 2 divisions

Grey Matter: Mostly cell bodies, includes dendrites and terminals as well- Spinal reflex integrating center (patella reflex without any higher control from the brain)White Matter: Bundles of myelinated axons - Ascending tracts = sensory- Descending tracts = motor- Dorsal roots = sensory- Ventral roots = motor and autonomic

Define Nerve

Group of neuronal axons outside the CNS

Define Tract

Groups of neuronal bodies inside the CNS

Where do cell bodies reside in the head region and below the neck?

Head: Cranial nuclei Below neck: Dorsal horn ganglion

Where does histamine come from?

Histidine

What is the difference between hyperpolarization and depolarization?

Hyperpolarization is making the membrane potential more negative than usual while Depolarization makes the membrane potential less negative (more positive) than usualWhen you open chloride channels the neuron becomes hyperpolarized. Hyperpolarization inhibits AP.

What coordinates our circadian rhythm?

Hypothalamic suprachiasmic nuclei (in the hypothalamus of the diencephalon)we have a feedback loop: genes to regulate proteinsMost physiological systems have rhythmic patternsSleep: REM and deep sleepWhen we are awake - alpha waves have higher frequency and lower amplitude

17. Tylenol and NSAIDs exert their antipyretic effect in

Hypothalamus

What is a well known propionic acid derivative?

Ibuprofen

What cranial nerve innervates the posterior belly of the digastric muscle and what does it control?

Innervated by CN 7 (facial nerve)2nd order neuron cells bodies are in facial motor nucleiFacial motor nucleus = all muscles of facial expression & the stapedius

What cranial nerve innervates the anterior belly of the digastric muscle and what does it control?

Innervated by the mandibular branch of CN 5 (V3)2nd Order cell bodies are found in the Trigeminal Moto Nucleus

What is the difference between intragemmal nerve and Perigemmal nerve?

Intragemmal nerve fibers (gustatory) are found to innervate all regions of fungiform taste papillae (taste bud)Pergemmal nerve fibers (somatosensory) innervate the peripher of the taste budBDNF mRNA associated with TBNT-3 mRNA associated with periphery

If you cut the spinal cord at L7, what structures loses it's mechanosensors?

Ipsilateral leg to the lesion because the neuron has not yet crossed over

What is the reason the dura mater is two-layered (characteristics of the dura mater)?

It is at the top of the brainThe two layers separate from each other and it creates the venous sinusesSpecific projections of arachnoid membraneGoing into dural sinus areasArachnoid granulations - projections of arachnoid membrane that go into the venous sinuses for exchange of metabolitesCSF will never come in contact with bloodCSF metabolites drain into venous sinuses

How does the composition of CSF compare to plasma?

K+, Ca2+, HCO3-, glucose is lower than it is in plasma[H+] is higher than in plasma, thus, pH is lower (more acidic)Na+ is similarLittle protein and no blood cells compared to plasma (but enough to supply the brain)

What are all four types of opioid receptors coupled with?

KNOW THIS: Opioid receptors are coupled to INHIBITORY G PROTEINS (Gi or Go - G-protein coupled receptors) The G proteins are regulated by RGS proteins.ANALGESIA is attributed to the signal transduction through the G protein-mediated second messenger system initiated by the binding of an agonist to an opioid receptor. EXTRA: Agonist binding to opioid receptors - activates G subunits that activate downstream effectors:1) Opening of K+ channels2) Inhibition of Ca2+ channels3) Inhibit adenylyl cyclase (AC) that reduces cAMP.

Why is dopamine so important?

Leads to influences in the reward systemThe VTA (ventral tegmental area) and substantia nigra are two structures near each other in the brain stem that play an important part in rewardThe VTA has projections that lead into the nucleus accumbens

figure 16.8

Location and relative number of ORG's on human chromosomesThere are hundreds of genes that code for different olfactory receptor proteins. My notes:GCPR sit on the ciliate of olfactory neuronsWe have many olfactory genes on human chromosomesOlfaction is important evolutionary thing we have still keptMany diff olfactory genes compared to taste (which is limited number of genes encoding for GCPR detecting taste modalities)

Explain what happens when a loud noise occurs. What is the name of the reflex?

Loud Noise ReflexVestibulocochlear nerve (CN 8) detects a loud noiseTriggers Facial Nerve (CN 7) to contract the stapedius muscle which will dampen the noiseNote: The tensor tympani and stapedius muscles are protective reflexes. They reduce the amount of sound that gets into the inner ear. They are somewhat similar to the blink reflex. Thus they can be triggered by loud noise, and when they "go off", both ears can be involved.

What do MAO and COMT do?

MAO and COMT deactivate catecholamines

Explain analgesias mode of action

MOA: Increase pain threshold at the spinal cord and alter the brain's perception of pain - following therapeutic doses of morphine, patients report pain is less intense, less discomforting or entirely goneExtra: less pain perception is transmitted, more of C' fiber affect is dampened

What is similar to the optic chiasm but located in the brain stem?

Medullary pyramids have pyramidal nerve tracts known as the corticospinal (and corticobulbar tracts). At the pyramids' most caudal end, the corticospinal axons decussate (or cross over) the midline and continue down the spinal cord on the contralateral side.The primary purpose of the corticospinal tract is for voluntary motor control of the body and limbs.In short, pyramids have nerve tracts that crossover

Notochordal Process

Mesenchymal cells migrate from the primitive knot to form a midline cellular cord known as the notochordal process. The notochordal process grows cranially until it reaches the prechordal plate, the future site of the mouth. In this area the ectoderm is attached directly to the endoderm without intervening mesoderm. This area is known as the oropharyngeal membrane, and it will break down to become the mouth. At the other end of the primitive streak the ectoderm is also fused directly to the endoderm; this is known as the cloacal membrane (proctodeum), or primordial anus.The oropharyngeal membrane and cloacal membrane become the only bilaminar structures that remain at week 3.See pic on next tab

What glial cells originate from bone marrow (mesenchymal cells produce bone marrow, monocytes)?

Microglial Cells

What type of cells are taste cells?

Modified epithelial cells

When is analgesia most effective?

Most effective for CONTINUOUS DULL PAIN and SEVERE & VISCERAL pain of pathologic origin or "spontaneous" pain

right controls left, vice versa

Motor decisions in limb come from opposite side of brain

Explain the function of hypoglossal nerve, what it innervates and what nuclei are involved

Motor function ONLY - innervates the extrinsic and intrinsic muscles of the tongue- Neurons originate from the HYPOGLOSSAL NUCLEUS-Stimulating by signals from SOLITARY NUCLEUS and TRIGEMINAL MAIN SENSORY NUCLEUS to coordinate chewing, sucking and swallowing reflexes- Also receives signals via CORTICOBULBAR PATHWAY to help produce speech Axons travel between the PYRAMIDS and the OLIVES

What motor neurons control the Nucleus ambiguous (medulla) and what happens?

Motor neurons of CN 9, 10 and 11Sends motor fibers in the glossopharyngeal, vagus and cranial part of the accessory nerve to innervate the muscles of the pharynx and larynx

How are motor signals communicated out from the brain?

Motor signals:Motor neurons in ventral horn --> ventral root --> dorsal ramus of spinal nerve --> innervate muscle that is found in back OR skeletal muscle

What are the three subtypes of ionotropic glutamate receptors?

NMDAAMPAKainate receptorsN-methyl-D-aspartate (NMDA) receptorsα-Amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptorsKainate receptors

NT Receptor Systems

NT Receptor systemso Dopamine is a ligand that comes and bind to g coupled protein receptors (but you have many of these receptors for dopamine); so dopamine binding to one receptors leads to one reaction and binding to other reactions give another function/reaction o Norepinephrine and epinephrine --> There are two subtypes of alpha receptor and three subtypes of beta receptors --> Just know that there are alpha and beta receptors --> In lungs you have beta 2 receptors your bronchial will dilated o For serotonin you have tons of receptors: some g protein receptors and some ligand gatedo For histamine are all g protein receptorso Amino acids --> NEED TO KNOW RECEPTORS FOR THIS ONE --> Glutamate is one ligand; in CNS glutamate is the neurotransmitter --> Know the three ionotropic glutamate receptors • All three are ioniotrophic receptors • NMDA receptors (addition molecules can bind to this)• AMPA receptors• Kainite receptors • It also has G-protein coupled receptors• That's is why glutamate can do so many diff functions • You also have metabotropic glutamate receptors • Pretty much glutamate does a lot of work --> GABA binds to Cl channel • Cl can go into cell and hyperpolarizes • GABA is inhibitory AA• GABA main inhibitory in CNS• Glycine is more at the spinal cord level inhibitory NT

Explain the pharmacokinetics of naloxone

Naloxone is given to patients who have overdosedPHARMACOKINETICS:- Naloxone is NOT effective orally - - - undergoes rapid first-pass metabolism to glucuronide & has a short duration of action (1-4 hrs)- Naloxone given by repeated injections to patients. - Naltrexone has high oral bioavailability - Naltrexone: Long duration of action (24-48 hr) -- Given every other day; Also available in extended-release formulation for once monthly IM injection.

What are the opioid antagonists? What are the pharmacological effects?

Naloxone, Naltrexone, MethylnaltrexonePharmacological effects: Competitive ANTAGONISTS at m & other opioid receptors - kicks out the actual agonist & bind itself to receptor Example: Compeition of nalaxone with opioid agonists- Binding of naloxone (rather than opioid agonists) does not activate the opioid receptor. Therefore, naloxone reverses the effects of opioid agonists, such as morphine and heroin.

What happens if there is a large tumor in the pituitary gland?

Narrowed vision, headache, pressure on sella turcica, bone resorption

What are the steps of norepinephrine release and recycling?

Norepinephrine release at a variscosity of a sympathetic neuronTyrosine is a precursor for catecholamines (NE, E, dopamine)1) Action potential arrives at the variscosity2) Depolarization opens voltage-gated Ca2+ channels3) Ca2+ entry triggers exocytosis of synaptic vesicles4) NE binds to adrenergic receptor on target5) Activity ceases when NE diffuses away from the synapse6) NE is transported back into the axon7) NE can be taken back into synpatic vesicles for re-release8) NE is metabolized by monoamine oxidase (MAO)Note on 7&8, NE can either be RECYCLED or DESTROYED

figure 15.13 (part 2)

Note that the olfactory receptor cells terminate on glomeruli in the olfactory bulb.Notes: related to last slideORC --> specific areas in Olfactory Bulb known as Glomeruli (glomerulus is singular) Polar neurons that contact same receptors (whether lateral or medial) they will go to same glomerulus --> Somatotropic mapping preservation within olfactory cortex

Presynaptic inhibition

Occurs at axo-axonic synapsesNeurotransmitter released from the upstream terminal decreases release from the other

Presynaptic facilitatoin

Occurs at axo-axonic synapsesNeurotransmitter released from the upstream terminal increases release from the other

Opioids can have both what?

Opioids can have both STIMULATING and INHIBITING effects on the human body and this is due to the wide distribution of opioid receptors in various organs of the human body.- CNS, GI, Renal- Opioids have stimulant effects, dampening effects and analgesic effects on the CNS (antidiarrheal and antitussive too)

How do opioids induce analgesia?

Opioids induce analgesia by hyperpolarizing nerve cells and inhibiting neurotransmitter release

Pharmocoptherapy of PAIN

Opioids produce analgesia by acting on receptors located on the DESCENDING and ASCENDING pathways of painNSAIDS lower level of inflammation mediators so pain is not generated or transmittedOpioids influence many areas of CNS

Pharmocoptherapy of PAIN - The difference between how Opioids and NSAIDS handle pain

Opioids produce analgesia by acting on receptors located on the DESCENDING and ASCENDING pathways of painNSAIDS lower level of inflammation mediators so pain is not generated or transmittedOpioids influence many areas of CNS

Explain the olfactory bulb size relationship for different species

Ours is small compared to mouse (huge portion of brain). Sense of olfaction for mouse is important.- Large part of CNS (mice, dogs, etc) versus Smaller part of CNS (Us)- The number of olfactory receptor cells is increased in mammals that need it such as bloodhounds, rats, etc.Olfatory neurons detect odorants (molecules that go through the air) and dissolve in the mucous layer in the nose and go to receptors GCPR receptors and activate neurons)review 15.2 (part 1)

What is oxycodone?

Oxycodone is a semi-synthetic derivative of morphine used for moderate to severe pain

What is Salivatory Nuclei?

Parasympathetic cell bodies for CN 7 & 9The superior and inferior saivatory nucle in pontine tegmentum.

Acute toxicity regarding morphine overdose can be identified by the pathognomic triad. What is this? What treatment can be administered?

Pathognomic Triad1) Pinpoint pupils, 2) Respiratory Depression ((hypoventilation) is a breathing disorder characterized by slow and ineffective breathing), 3) Coma- low BP and shock may result with prolonged hypoxia and hypothermiaTreatment1) Establish patient airway & ventilate2) Administer Opioid Antagonists IV as needed

What is euphoria as experienced through opioids?

Patients that use opioids for pain or abused (e.g., drug users) experience a pleasant floating sensation with ↓ anxiety & distress (endorphins - m receptors)Extra Notes: EUPHORIA, indifference to stimuli, and sedation usually caused by the opioid analgesics, especially when injected intravenously, tend to promote their compulsive use (POSITIVE REINFORCEMENT).

Is the trigeminal a segmental or peripheral nerve?

Peripheral nerve

What innervates the sphincter pupillae and ciliary muscles within the eye?

Postganglionic fibers from Ciliary Ganglion Edinger-Westphal nucleus is where it starts basically

Postsynaptic Effect of NT

Postsyn effect of NTo At syn, one of these release NT that is then picked up by receotprs by post-syn membraneo That effect is caused by NT that comes ino This is something you need to memorize o You have inhibitory post syn potential if it is a inhibitor NT releasedo If you poke post syn neuron you will see that it was inhibited o The IPSP shows up on board exam (inhibitory post syn potential) --> Generated post-syn potential in the next neuron o Slow IPSP is hyperpolarization (meaning it is slow) o Post syn effects of NT -- > EPSP (excitatory post-syn potential)o Post syn of AMPA and NMDA receptors --> Long-term potentiation

What is the most important part of what makes a NT a NT?

Postsynaptic effect mimicked by exogenous application

What produces CSF? Where does it reside? What does it fill? Briefly describe the exchange transport

Produced by the choroid plexus which resides in each of the four ventriclesFills the ventricles and the subarachnoid spaceFluid pillow floats the brainThe exchange transport - from blood to brain tissue

Olfactory neurons bipoilar

Project to olfactory bulb

What is the difference between prostacyclin and thromboxane?

Prostacyclin - anti-coagulation, VD, decrease platelet aggregationThromboxane - pro-coagulation, VC, increase platelet aggregation

Explain the pathway of the Vagus Nerve (X)

Receptors for general sensation end up in the trigeminal main sensory nucleusVisceral afferents end up in the solitary nucleusMotor neurons arise from the NUCLEUS AMBIGUS of the medulla- for this reason the nucleus ambigus is very important for swallowing and speechThe PS fibers of the vagus nerve originate from the dorsal motor nucleus of the vagus, which lies in the medulla - they are distributed throughout cardiovascular, respiratory and GI systems

Glossopharyngeal nerve (CN IX)

Receptors for general sensation of: PharynxPosterior 1/3 of tongueAuditory canal & middle earReceptors for tasete of : posterior 1/3 of tonguepharynxChemoreceptors in carotid bodyBaroreceptors in the carotid sinusSensation neurons synapse in the Trigminal Main Sensory NucleusTaste neurons synapse in the Solitary NucleusNeurons for Gag Reflex synapse in the Nucleus Ambigus (9, 10, 11)and Hypoglossal Nucleus (12)Motor component is very small - only controls the stylophyarngeus which is needed for swallowing- these neurons arise from rostral part of the Nucleus Ambiguus in the medullaSalivation- neurons arise from the Inferior Salivatory Nucleus of the medulla- these Preganglionic Parasympathetic fibers synapse with postganglionic neurons in the Otic Ganglion and then innerate the Parotid Gland

7. preganglionic parasympathetic neuronal cell bodies are located in

Salivatory nuclei, dorsal motor vague nerve, Edinger-Westphal

What glial cells originate from neural crest cells?

Schwann Cells and Satellite Cells

Slide 7

Slide 7: Know combination of these receptors for sweet (T1R2 & T1R3), umami (T1R1 & T1R3), sour (PKD). For salty tastants: Amiloride-sensitive Na+ channels detect Na

16. Primary chemosensory neurons connect to second order neurons in

Solitary nucleus

Solitary nucleus

Solitary nucleus: chemoreceptors & visceral afferents project to it

Where do touch, pain and temperature afferents (SA) coursing in CN 7, 9 and 10 terminate?

Spinal trigeminal nucleus

Spincerebellar tract lesions

Spinocerebellar tract lesions usually part of more complex lesions such as brown-Sequard in which spinocerebellar lesions are masked clinically by muscle paralyses

SP and CGRP

Substance P & CGRP are dental nociceptors in periphery. After activation in CNS there is Substance P & glutamate

What portion of the spinal cord is where see the lateral horn?

SympatheticThoracic OnlyT1-L1 you would see the lateral horn, this is where sympathetics neurons come from. Cervical and lumbar enlargement is b/c of increase in sensory and motor neurons needed for limbs, which could lead to larger dorsal and ventral horn

What is meperidine?

Synthetic strong agonists

What is methadone?

Synthetic strong agonists

18. Bitter taste receptors are G-protein coupled receptors from the

T2R

An interneuron stays within a region or segment. T or F?

TRUE

What is the diencephalon, telencephalon and mesencephalon?

Telencephalon is the most anterior portion of the forebrain, diencephalon is also the forebrain and mesencephalon is the midbrainThe diencephalon sits between the telencephalon and mesencephalon

Termination of NT action

Termination of NT actiono We said we have catecholamine family produced by cells from precursors and it had receptors that we talked about o There has to be a termination mechanismo There is a way of re-uptake and taken to MAO so it become deactivatedo The other way is in the post-syn there is molecule called COMT which is enzyme that deactivates catecholamineso Some of the epinephrine can defuse away o REMEMBER COMT AND MAOo there are ppl with diff pain threshold bc they have diff COMT o some types of COMT are associated with ppl who have higher pain threshold and same versions associated with ppl with low thresholdo for serotonin you have re uptake and take it to MAO and it deactivates o SSRI: selective serotonin reuptake inhibitors (these are the first great anti-depressant drugs with less side effects)o NO COMT bc it is not a catecholamine o Glutamate use glutamate transporter; glutamate comes in and lets NA in and glutamate is metabolized (deactivate) o Acetylcholine has acetylcholinesterase that terminates it (hydrolysis)SSRI = influence the reuptake of sertonin so its present for longer period of time in synapses (i.e. antidepressants)

What kind of neurons are found in the ventral tegmentum/tegmental area?

The VTA has dopaminergic neurons and dopamine is released in the nucleus (leads to euphoric state)

What type of ganglion is the adrenal medulla and what is it derived from?

The adrenal medulla is a modified sympathetic ganglion and is derived from neural crest cellsNote, the adrenal cortex is a true endocrine glandThe chromaffin cell is a modified postganglionic sympathetic neuron (it is used because there are no post ganglionic neurons in the adrenal medullaEpinephrine is the neurohormone that enters the bodyCNS --> Spinal cord --> Adrenal Gland --> Target Tissues

Does the adrenal medulla have ganglia or chain? If not, explain how messages travel

The adrenal medulla is a special case (compared to the sympathetic and parasympathetic NS) as it has no ganglia or chainThe medulla is surrounded by the adrenal cortex, which is a true endocrine glandThe medulla is a modified ganglia and preganglionic neurons synapse on the medulla itselfThe Chromaffin cells are modified postganglionic neurons and neurons synapse hereThe Chromaffin cells release epinephrine directly in the blood streamExtra Notes: In order to activate chromaffin cells, the splanchnic nerve of the sympathetic nervous system releases acetylcholine, which then binds to nicotinic acetylcholine receptors on the adrenal medulla. This causes the release of catecholamines. The chromaffin cells release catecholamines: ~80% of adrenaline (epinephrine) and ~20% of noradrenaline (norepinephrine) into systemic circulation for systemic effects on multiple organs (similarly to secretory neurones of the hypothalamus), and can also send paracrine signals. Hence they are called neuroendocrine cells.* Medulla comes from neural crest cells (recall, it is a modified sympathetic ganglion)

What structures does the neural tube give rise to?

The brain from it's anterior portion, the spinal cord from the posterior portion and the hollow ventricles from it's cavity

Define the cauda equina. What is the region known for?

The cauda equina (from Latin horse's tail) is a bundle of spinal nerves and spinal nerve rootlets, consisting of the second through fifth lumbar nerve pairs, the first through fifth sacral nerve pairs, and the coccygeal nerve, all of which arise from the lumbar enlargement and the conus medullaris of the spinal cord.There is no spinal cord tissue just dorsal root, ventral root and CSFAnestheticsThis is where you get the lumbar shot

What anti-inflammatory action is taken by NSAIDS?

The decrease in vasodilator prostaglandins (PGE2, PGI2) means less vasodilation (widen blood vessels, decrease blood pressure) which indirectly means less edema (swelling)INHIBITION OF ADHESION MOLECULES (PGE2, PGF2)Accumulation of inflammatory cells (a source of cytokines, GF, etc.) is also reduced

Explain the Parasympathetic Pathway

The parasympathetic pathway differs from the sympathetic pathway in that it only releases one type of NT1) Release Acetylcholine (ACh) from BOTH the Preganglionic and Postganglionic NeuronsNOTE: The pre and post neurons synapse in an autonomic ganglia very close to the target2) The target organ has Muscarinic Receptors that receive ACh- Muscarinic receptors are ionotropic receptors so their action happens very quickly

What is the difference in myelination for the preganglionic neuron versus the postganglionic neuron?

The preganglionic neuron is lightly myelinateThe postganglionic neuron is not myelinated

What are the types of refractory periods?

The refractory period is a period of time after the action potential occurs where a 2nd AP is not able to occur1) Absolute refractory period: No AP can be generated and most of the voltage-gated sodium channels are still inactive (unable to re-open)2) Relative refractory period: A smaller than normal AP can be generated if there is a large enough stimulus and enough voltage-gated sodium channels are capable of opening- Intensity of required stimulus and magnitude of AP are time dependent

What happens at week 6 with regard to the brain?

The region that are present at birth have been differentiated

When does the rostral pore end and caudal pore end close? What happens if either don't close?

The rostral and caudal pore are the cranial/anterior and posterior opening ends, respectively. The anterior/rostral end closes first during the 4th week followed by the caudal/posterior end at the end of the week. If the rostral end does not close than the brain can fuse/develop properly and this is normally lethal. If the caudal pore does not close than spina bifida.

What does the Sulcus Limitans separate?

The sulcus limitans is found in the fourth ventricle of the brain. It separates the cranial nerve motor nuclei (medial) from the sensory nuclei (lateral). It can also be located by searching laterally from the medial eminence. It is parallel to the median sulcus.

What is the function of the suprachiasmic nucleus?

The suprachiasmic nucleus/nuclei is a tiny region of the brain in the hypothalamus that is responsible for controlling circadian rhythms

What is the role of the trigeminal complex and the general organization?

The trigeminal complex has sensory and motor portions--> Sensory Role (Portio major) (GSA)1) Exteroceptive - touch, pain and thermal sense (temperature)Serves the:- skin of face and forehead- mucous membranes of nose, nasal sinuses and oral cavity - the teeth- extensive portions of cranial dura2) Proprioceptive - deep pressure & kinesthesis (position sense)Allows you to know where jaw and muscles of mastication are in space- Teeth, periodontium, hard palate, TMJ- afferent fibers from stretch receptors in muscles of mastication--> Motor Role (Portio minor) (SVE to muscles of branchial arch origin)These neurons, part of CN 5, are called SVE neurons even though they go to skeletal muscles NOT visceral muscles They are named that way because they innervate muscles of branchial arch origin- 1) muscles of mastication- 2) Anterior belly of digastric- 3) Tensor Tympani and Tensor Veli PalatiniThe above 3 all innervated by brachial motor neurons (special visceral efferent)Definitely know the 3 above

The taste transduction mechanisms vary depending on taste. What are the receptors used for 1) Salt and Acid, 2) Sweet, Bitter and Umami

There are many genes that encode receptor proteins that are able to bind substances that are sweet, bitter, umami, salt or acid. More than one of these receptors can occur in the same cell, but not all of them in one cell. Intracellular Signaling Pathways Used by different Taste Receptors1. Salt and Acid (Sour) = Ion Channel2. Sweet, Bitter, Umami = G-Protein Coupled Receptors - T2R for Bitter- T1R2 and T1R3 dimerize for Sweet- T1R1 and T1R3 dimerize for Amino Acid/UmamiT1R3 is the common receptor for Sweet and Amino Acid/Umami

What does the marginal zone nuclei and substantia gelatinosa nuclei have in common?

They are both in the dorsal hornSubstantia gelatinosa is a collection of cells in the gray area (dorsal horns) of the spinal cord. Found at all levels of the cord, it receives direct input from the dorsal (sensory) nerve roots, especially those fibers from pain and thermoreceptors.

How do we characterize opioids?

They are classified by their interaction with receptors in the CNS as well as the ability to activate those receptorsReceptor Sub-Types1) Mu (m) - analgesia, sedation, GI effects, miosis, respiratory depression, EUPHORIA2) Kappa (k)- analgesia, sedation, GI effects, DYSPHORIA3) Delta (d)- analgesia, sedatinOpioids are also characterized by how well they activate receptors. Opioids can be full (or strong) agonists that produce a maximal effect when bound or they can produce a reduced response as a partial agonist. Lastly, they can occupy the receptor as an antagonist, but not activate the receptor.

What is unique about the oropharyngeal membrane and the cloacal membrane?

They both are bilaminar structures (2 layers of cell) until they disintegrate or, in the case of the oropharyngeal membrane becomes the boundary between the ectoderm (front part of embryo) and endoderm (which starts in pharynx, larynx and continues down)

What causes Bell's Palsy? How does this compare to Ramsay Hunt Syndrome?

This disease of the lower motor neurons represents a unilateral inflammatory lesion of CN 7 leaving the muscles of facial expression paralyzedNote: Both the above reflexes will not work since they both rely on CN 7Ramsay Hunt Syndrome is a peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth. In Ramsay Hunt Syyndrome, this inflammation is caused by the Herpes Zoster Virus (Chicken pox in kids and shingles in adults). A rash of the external auditory canal & mucous membranes of the oropharynx will be seen.

What must be reached in order for an action potential to be activated?

Threshold potential - a level of depolarization that must be reached to trigger an action potential

What are the removal mechanisms of catecholamines?

Transporters, MAO, COMTTwo important enzymes of this type are catechol-O-methyltransferase (COMT) and monoamine oxidase A (MAO-A). COMT is an Mg2+-dependent enzyme involved in the inactivation of certain catecholamines (norepinephrine, epinephrine, and dopamine).

What are some treatments of withdrawal?

Treatment of Withdrawal- METHADONE (Onset: 0.5-1h; Duration: 22-48h): For withdrawal or maintenance: Cross-dependence & Tolerance --- tolerance and physical dependence may develop more slowly; withdrawal symptoms are milder, but more prolonged- Buprenorphine (Duration: 20-36h): High affinity for m receptors & also weak k receptor antagonist--> Clonidine: a-2 adrenergic agonist - - reduces autonomic hyperactivity (i.e., sympathetic syndrome) --> Naltrexone: For maintenance

What forms the general somatic afferent (GSA) column?

Trigeminal nuclei

Where does serotonin come from?

Tryptophan aka 5-hydroxytryptophan

What is a well known para-aminophenol derivative?

Tylenol - no anti-inflammatory effectAnalgesia and antipyretic activityUsed in patients with bleeding disorders

What is a popular para-aminophenol derivative? Give all it's characteristics

Tylenol - used in patients with bleeding disorder, peptic ulcer or ASA intoleranceImportant to know...Analgesia and antipyretic activityChronic Ingestion: Large doses (>4 g/d) of acetaminophen may result in liver damage, especially in malnourished or alcoholic patients. CONTRAINDICATIONS & CAUTIONS • Known hypersensitivity to acetaminophen • Individuals with impaired liver function or alcoholism Drug Interactions • Alcohol • Barbiturates, PhenytoinExtra from slides: - Coal-Tar analgesics- Active metabolite of phenacetin- PK: Well-absorbed; Largely conjugated to glucuronide & sulfate; HIGH DOSE - - some is oxidized to toxic metabolite: N-acetyl-p-benzoquinone. - Weak inhibitor of COX-1 & COX-2 in peripheral tissues; Analgesia and Antipyretic activity comparable to ASA; Advantage: NO GI irritant vs ASA; Disadvantage: NO anti-inflammatory or anti-platelet effects. - Clinical Uses: Preferred substitute for analgesia or anti-pyresis when 1) ASA is contraindicated & anti-inflammatory action is not needed (e.g., headache). 2) Patients with bleeding disorders, peptic ulcer or ASA intolerance; 3) children and infants with fever and at RISK for Reye's Syndrome. - Adverse Effects: MINIMAL - Hypersensitivity reactions (RARE) HEPATOTOXICITY: Dose-dependent, POTENTIALLY FATAL---- MINIMAL LETHAL DOSE ~ 15 g (adult) • Initially (12-24 hr): NVD, anorexia, abdominal pain • Latent (2-7d): Jaundice, hepatic failure, coma, & death can follow

Which type of synapse is excitatory and which is inhibitory?

Type I --> ExcitatoryType II --> Inhibitory

What is the rate-limiting step in synthesis?

Tyrosine hydroxylaseTyrosine hydroxylase (TyrH) is the rate-limiting enzyme of catecholamine synthesis. It catalyzes the hydroxylation of tyrosine to L-DOPA (1). ... Phenylalanine hydroxylase converts phenylalanine to tyrosine, tyrosine hydroxylase hydroxylates tyrosine to L-DOPA.

What is the precursor to catecholamines?

Tyrosinetyrosine can increase brain synthesis and release of catecholamines, especially norepinephrine and also perhaps dopamine

When is acetylcholine used?

Used in somatic motor system and used in PS and S NS as well

6. where would you find gamma motor neuron cell bodies?

Ventral horn

14. Nerve in brachial and lumbosacral plexus have their origin from

Ventral rami

3. Nerves in brachial and lumbosacral plexus have their origin from

Ventral rami

5. which one is a putr motor nerve

Ventral root

What are the sites of action and MOA (mode of action)?

Ventral tegmentum area (VTA) and Nucleus Accumbens (NAc) in Mesolimbic DA PathwayMOA: Opioid activation of the mesolimbic DA pathway - Reward and Pleasure circuits in brainOpioid peptides and receptors are involved in the brain network that mediates the REWARD and REINFORCING properties (i.e., Mesolimibic DA pathway).Extra Notes: - Reward system - structures activated when using something rewarding (i.e. addictive drug)--- Rewarding stimulus --> Releasing NT dopamine--- Structures part of reward system found along major dopamine pathways- Mesolimbic DA Pathway starts in a part of spinal cord known as VTA- VTA is one of principal dopamine producing areas in the brain- Mesolimbic DA Pathway connects VTA with Nucleus Accumbens (found in a part of the brain associated with reward, motivation)- Now if we take a drug then dopamine neurons in VTA are activated project to nucleus accumbens via Mesolimbic pathway and causes dopamine levels in NAc to rise- Dopaminergic input from VTA modulate the activity of GABAergic neurons within the nucleus accumbens. These neurons are activated directly or indirectly by euphoriant drugs. - Mu and K receptors on nucleus accumbens

What 2 tracts are part of the secondary trigeminal pathways?

Ventral trigeminal thalamic tractDorsal trigeminal thalamic tract

Which potential is real and which is theoretical?

Vm, membrane potential, is a real value that can be measured at any given timeEx, equilibrium potential, is a theoretical value used to estimate Vm assuming all ions are at equilibrium

What are the two areas associated with language?

Wernicke's Area and Broca's Area

10. A primary sensory neuron could be (No gamma)

a. nociceptor a mechanoreceptor a proprioceptor a psudo unipolar

What is the reversible equation to synthesize acetylcholine?

acetyl co enzyme A (Acetyl CoA) + choline <-- --> CoA and ACh

What about dysphoria?

an unpleasant state w/restlessness & malaise occurs upon Withdrawal (dynorphins - k receptors)ParanoiaExtra Notes: • DYSPHORIA, due to kappa receptors on dopaminergic neurons vs. mu receptors on GABAergic neurons (Figure 32-2, Katzung's) (NEGATIVE REINFORCEMENT)Withdrawal induces Dynorphins that activate kappa receptors in NA GABA neurons (see also slide 17).

12. GVE neuronal cell bodies are located in

dorsal motor nucleus of vagus - is also parasympathetic nucleus

Explain the cingulate gyrus of lymbic system

evolutionary one of the oldest parts of the brainpain, chronic, processinglarge part of brain in higher mammals