phys exam #2

ACh (inotropic effects)

(atria negative effected by ACh): (-) atria only → inotropic (-) (decreases calcium permeability so decreases force) Independent of volume and preload

catecholamine (inotropic effects)

(veins postively affected by NE or E): (+) inotropic (increases calcium permeability Independent of volume and preload

differences of cardiac muscle compared to smooth muscle

* Uninucleated (sometimes bi) * More mitochondria * Muscle fibers branch * Less well developed sarcoplasmic recticulum - Not sufficient for complete calcium needs generally *INTERCALATED discs

contractile cells

*99% of all cardiac myocytes *perform mechanical work *Normally do not initiate action potentials *Require action potentials to generate contraction

action potential of cardiac cells

*Action potential attributed to more than sodium and potassium ALSO includes calcium *Action potential duration is REALLY long compared to normal

excitation-contraction coupling cardiac muscle

*Action potential enters from adjacent cell *Voltage gated Ca2+ channels open. Ca+2 enters cell *Ca2+ induces Ca2+ release through ryanodine receptor channels (RyR) *Local release causes Ca2+ spark *Summed ca2+ sparks create a ca2+ signal *Ca2+ ions bind to troponin to initiate contraction *Relaxation occurs when ca2+ unbinds from troponin *Ca2+ is pumped back into the SR for storage *Ca2+ is exhcanged with na+ by the NCX antiporter *Na+ gradient is maintained by the Na+/K+ ATPase

why upward and downward deflections of EKG?

*An upward deflection on an ECG means the current flow vector is toward the positive electrode *A downward deflection means the current flow vector is toward the negative electrode *A vector that is perpendicular to the axis of the electrode causes no deflection (baseline) *mV= on Y axis and time on X axis

sinoatrial node

*Crescent shapes, located in wall right atrium *Generates impulses about 60-100 times a min → due to parasympathetic tone and other factors (HR → 55-80 BPM) *Hence pacemaker internodal pathways *connect SA node to AV node

compensatory hypertrophy

*Enlargement of preexisting cells *Asking sekelteal muscle to do more work than capable of → muscle fibers tear → cells respond to damage and repair and builds biggerrrr

I (f) channels (="funny")

*First half of pacemaker channel of autorhymic cell *Permeable to both sodium and potassium channels *When open Na+ influx > K+ efflux Open at membrane potentials

cardiac muscle similar to smooth muscles

*Gap junctions= single-unit smooth muscle *SR smaller than in skeletal muscle= suggest that outside Ca2+ is needed

anatomy of smooth muscle

*Higher organized into layers *Oblique filament layers as opposed to parallel (contraction pulls in many different directions *Relaxed smooth muscle cell= flare and longer and NO sarcomere are intermediate filament bundles attached to dense bodies *Contracted smooth muscle= scrunches up into little ball, like ringing out a towel

repolarization (contractile cells)

*Increase in K+ permeability (decrease in calcium permeability) *Slow K+ channels ALL open

skeletal muscles special characteristics

*Length-tension *All or none *Motor units (recruitment) *Summation

atrioventricular node

*Located at the base of the right atrium near the septum *Impulse delayed *Conducted more slowly about 40-60 (Smaller chamber wise and smaller density wise)

L-type Ca2+ channels

*Maintain plateau and *Where extracellular calcium enters cytoplasm of cell then enter SR -Results in significant increases in calcium [ ] or calcium sparks -So calcium has normal signal to initiate contraction

graded potential: cardiac muscle fibers

*More ca2+ → stronger force of contraction *Enhance cardiac muscle force by enhancing intracellular calcium - Not through AP frequency - Use other modulating pathways

cardiac muscle differs from skeletal muscle ?

*Muscle fibers smaller *Single nucleus *Branching of cells: creates an extensive network (intercalated disks join muscle cells)

peak of depolarization (contractile cells)

*Na+ channels close (at around +20, sodium permeability decreases) *fast-K+ channels open (repolarization starts but is very short)

K+ channels (repolarizing cardiac)

*Open at peak of depolarization *K+ efflux causes repolarization *I-f channels begin to open again to get us to another depolarization

working muscle (phosphocreatine)

*Phoscreatine + ADP (creatine/kinase) → creatine + ATP *(ATP needed from): myosin ATPase (contraction) → Ca2+ ATPase (relaxation) → Na+, K+ ATPase (restores ion that cross cell membrane during action potential to their original compartments)

length-tension relationship cardiac muscle fibers

*Similar to skeletal muscle *Come back towards end of lecture *Degree of overlap between actin and myosin

plateau (contractile cells)

*Voltage gated ca2+ channels open (L-type calcium channel, meaning LONG calcium channels) *Fast K+ channels close (some)

recruitment (nerve vs neuron)

- If applying a stimulus to nerve that depolarizes the membrane to -60 - EXAMPLE: Only the neuron that has a threshold of -65 will fire and AP because that is the only neuron that has reached its threshold (-55 and -45 have not become suprathreshold so still wont fire) - If change so that stimulus is now -40, we have recruited more neurons to fire AP because now it will fire -45, -55 and -65

nerve impulse: end depolarizaiton/begin repolarization

- Na+ voltage gated channels are triggered to close - Inactivation gate closes and Na+ entry stops - Negatively charged protein gate that is closing so that Na+ can't diffuse anymore but this is inactive gate

can smooth muscel regenerate ?

- YES and smooth muscle can ALSO divide and multiple Capable of division in adult *Can regenerate after injury *Can divide (pregnant uterus) *Abnormal growth of smooth muscle may ause blockage or coronoary artery (restenosis= correct;ed bu angioplast) *angioplasty

calcium release (excitation-coupling)

- action potential traveling down t tbulue (L type calcium channel or DHP)

role of caclium

- bind to troponin - complex pulls on tropmyosin - binding site for myosin now free - myosin binds (power stroke can begin)

muscle spindle location and how they happen

- buried among extrafusal fibers of muscles - sends info about muscle stretch to CNS

golgi tendon organ location and how it works

- consists of sensory nerve ending interwoven among collagen fibers - able to respond to tension or force - more tension muscle produces, muscle is forced into relaxation by golgi tendon reflex

where is neurotransmitter released into?

- interstitial fluid - bind to receptor, diffuses away, reuptake, break down by enzymes (MAO)

sliding filament theory

- myofilaments themselves don't actually change in contraction - They stay same length but slide past each other and make overall sarcomere length shorter but myofilaments same length

recruitment of smooth muscle cells ?

- no recruitment - blood vessels, smooth muscel in intestine etc

types of neurotransmission

- occurs at synapse - depolarize OR hyper polarize neuron (graded potential) at postsynaptic cell - electrical changes= graded potential - end plate potential = muscle cells (net depolarizing event) - receptor potentials = seen in receptor cell (graded potential more umbrella term)

phantom limb pain

- psychological trauma - circuitry still there and nerves could still be firing down - eventually down regulation of receptors but not like a neuron atrophy type of situation so nerves still excitable

AP created in muscle cell (excitation- coupling)

- travel down t tubule - ca2+ released from SR (starts at low resting level then increases 100 fold after AP)

sarcomere structure

- z line: zig sag protein, attachment site for actin - i band: occupied only by thin filament - a band: entire thick filament (outer edge include both thin and thick and middle only thick) - h zone: only thick filament - m line: divides each thick filament in half

all or none principle for skeletal muscle

-if a muscle fiber is timulated --> it will contract BUT force of contraction is varaible -stimulated by motor neuron: contraction is certain but force of this contraciton is variable

short duration maximal exertion fatigue

-increased levels of inorganic phosphate - may slow Pi release from myosin -decrease calcium release ex: doing jump squats

what is end plate potential ?

-net depolarizing event -all suprathreshold and specific to skeletal muscle and AP generated throug htis - activate motor neuron, skeletal muscle always contract and respond - skeletal muscle is voluntary so always want this signals to be suprathreshold so that they can occur

maximal exercise fatigue

-potassium leaves muscle fiber - leading to increased concentration that is delivered to decrease ca2+

rigor mortis

-stiffening of muscles 3-4 hours after death - after death, muscle fibers begin to die *Causes release of Ca2+ from SR *Cross bridges forms *Available ATP used (no more ATP produced, levels decline) *Relaxation prevented *Stays this way until relaxation is achieved by dying myofilaments (usually about 48-60 hours after death)

smooth muscle relaxation

1) free Ca2+ in cytosol decreases when Ca2+ is pumped out of the cell or back into the sarcoplasmic reticulum 2) Ca2+ unbinds from calmodulin (CaM) 3) Myosin phorphatase remvoes phosphate from myosin, which decreases myosin ATPase activity 4) Less myosin ATPase results in decreased muscle tension

starting smooth muscle contraction

1) intracellular Ca2+ concentrations increase when Ca2+ enters cell and is released from sarcoplasmic reticulum 2) Ca2+ binds to calmodulin (CaM) 3) Ca2+ calmodulin activates myosin light chain kinase (MLCK) 4) MLCK phosphorylates light chains in myosin head and increase myosin ATPase activity 5) Active myosin crossbridges slide along actin and create muscle tensions

mechanical events of heart cycle

1) late diastole 2) atrial systole 3) isovolumic ventricular contraction 4) ventricular ejection 5) isovolumic ventricular relazation

integration post synpatic neuron steps

1) one excitatory and one inhibitory neuron fire 2) modulated signal is below threshold 3) no action potential is initiated at trigger zone 4) no response occurs in any target cell

integrating inputs

1) one inhibitory and two excitatory neurons fire 2) the summed potnetials are below threshold, so no action potential is generated

efferent pathway types (reflex)

1) somatic (muscle spindle, golgi tendon, nociceptive) 2) autonomic (visceral or vascular like baroreceptor)

integration center (reflex)

1) spinal (somatic and some visceral like urination) 2) cranial (visceral like baroreceptors) 3) both (urination and defecation)

summation: spatial and temporal steps

1) three excitatory neuron fire. Their graded potnetials separately are all below threshold 2) graded potentials arrive at trigger zone together and sum to create a suprathreshold signal 3) an action potential is generated

labeled line coding

1:1 association of a receptor with a sensation activate a particular reeptor and you will get that sensation - activate cold receptor adn you will feel "cold" - blow to head results in seeing flash of light (doesn't matter what stimulus is.. activated photoreceptor in eye)

how many voltage gated channels does Na+ have?

2 (inactivation and activation)

P-R or P-Q interval

= SA node depolarization to start of ventricular depolarization Flat line: representative of AV node delay

why autorythmic cells spontaneous depolarizaiton

= Unstable membrane potential - 60 mV *Pacemaker potential: never really "rests" *Don't have resting membrane potential (instead call it a pacemaker potential because they do NOT rest)

resting membrane potential of cardiac muscle cells

= about -90 *higher degree of postassium permeability *Resting membrane potential around -90 which is K permeability so higher than most other cells in body and potassium disturbances so dangerous for heart

p wave

= depolarization of the atrial muscle (0.16 sec) Mechanical event paired with this time= atria contracting

QRS complex

= depolarization of ventricular muscle (0.09 sec) Largest amplitude due to number of cells activated Represents ventricular depolarization/contraction

s-t segment

= depolarized state of ventricular muscle Ventricular muscle in depolarized state

frank-starling law of the heart

= heart contraction strength automatically increases to accommodate increased venous return -Aka: blood is equals blood out (Maintaining ESV as constant as possible) *Muscle length tension curve *Fibrous pericardium protects heart *Normal resting values → forced (indicated by stroke volume, mL)= 70 AND stretch (indicated by EDV, mL) = 135

muscular dystrophy

= improper protein folding in plasma membrane *Loses degrees of functionality *Chronic and fatal problem *Longer life span for this is around 20 *No treatment, just managment of systems to improve quality of life

temporal summation

= many ESPSs (and/or IPSPs) in rapid succession -From a single source but signals are arriving at different times -If rapid enough, won't fully repolarize to rest and will push to suprathreshold and allow AP to occur -Frequency matters because need to be close enough so repolarization doesn't happen inbetween signal deliveries

botulism disease

= neurotoxin, chemicals that target either motor neuron/circuitry attached with motor neuron pathways *Inhibiting motor neuron *Prevent ACh release from motor neuron → get paralysis of muscle *Then leads to respiratory failure, dropping look of face

tetanus

= neurotoxin, not allowing inhibitory interneurons to function properly *Can't facilitate normal coordinated movement *Can't inhibit motor neurons so over excitablity of motor neurons → over excitabliity of muscle → muscle spasms → excess contraction and respiratory failure (can't relax diaphragm) *Bacteria that carries toxin likes oxidized metal so that's why there is a correlation with rusty nails and such

wiggers diagram

= overlay of multiple concepts ECG, pressure changes, heart sound, volume changes, mechanical events

t-p interval

= refractory period, heart at rest (during this time, heart is filling) Not absolute and does NOT mean nothing is happening Filling time of the heart

t wave

= repolarization of ventricular muscle (0.15 sec) Represent ventricular repolarization/diastole

intercalated discs

= special electrical and mechanical junctions between adjacent muscle fibers *Contain desmosomes (biding cells together) *Contain gap juncitons: holes in plasma membrane, allow ions to pass (Behave like single unit skeletal muscles)

phosphocreatine

= strong contraction *ATP in cell only lasts a little while *High concentration in cell *Can regenerate ATP through catalyzed reaction

angioplasty

= the reconstruction of blood vessels cause by disease of injury

q-t interval

= total time for ventricular depolarization and repolarization

t-ca2+ (voltage gated calcium channel)

= transient Ca2+ channels (finishing pacemaker potential) *Open as potential becomes more positive *Bring cell to threshold *Depolarization continues → at threshold: T-Ca2+ close, L-Ca2+ channels open (long lasting ca2+ channels)

main function of cardiovascular system

= transport material to and from the cells of the body *Nutrients, water, and gases *Cell-cell communication *Wastes from cell

cardiac output

= volume of blood pumped by one ventricle in a given period of time CO= HR x SV average= 5 L/min

ACh: parasympathetic modulation

=from PNS Binds to mscarinic-cholinergic receptors (autorhymic cells) Increases permeability to K+ → causes more to leave, hyperpolarization Decreases cAMP production Affect if channels as welt-Ca2+ channels → longer time to depolarization

autorhythmic cells

=pacemaker= nodal cells *Few contractile fibers (do not contribute to contractile force of heart) * Specialized: initiating, transmitting action potentials (contractile cells) *Spontaneously depolarize

neurotransmitter released by POST gang of parasympathetic

ACh

neurotransmitter released by PRE gang of parasympathetic

ACh

neurotransmitter released by PRE gang of sympathetic

ACh

excitation-contraction coupling

ACh binding to nicotinic receptors (set off a series of events) AP created in muscle cell --> calcium release --> calcium back to SR through ATPase --> power stroke

diff between AP and ECG

AP are INTRAcellular recording vs ECG is EXTRAcellular recording

summation of contraction

AP from motor neuron keep coming --> not enough time for ca2+ to be pumped back into SR (twitches add on top of one another)

contractile cells AP

AP reaches contractile cells (all suprathreshold events) Open voltage-gated Na+ channels (causes initial depolarization)

muscle at rest (phosphocreatine)

ATP from metaolbism + creatine (creatine/kinase) → ADP + phosphorcreatine

If pressure in aorta falls from 80 → 60 (same force of ventricle, 120, will remain)

Afterload goes down → increases stroke volume and decreases ESV

If pressure in aorta rises from 80 → 100 (same force of ventricle, 120, will remain)

Afterload goes up → decrease stroke volume and increases ESV

afterload ESV

Afterload: necessary force needed to eject blood from ventricle afterload= load that comes after heart, load outside of heart that heart has to try and get out Large ESV=lower stroke volume (inversely proportional)

cardiac muscle fiber regenerating/dividing

DO NOT regenerate/divide in an adult *Replaced with scar tissue *If they die, will not be replaced but can still strengthen through compensatory hypertrophy

purkinje fibers

Deliver final AP to contractile cells Very paid= 4m/s Generate AP of 25-40/min

LACKs hyperpolarization (contractile cells)

Falls to -90 which is already the resting membrane potential for potassium so it doens't want to fall anymore than it already is

phasic receptor

Fire rapidly Not constantly firing Only begin firing when stimulus begins or arrives adapt/cease fire really quickly as long as stimulus doesn't change Cease fire if stimulus intensity does not change (smell, kinda same with touch)

nerve impulse: repolarization and refracy period

Increase in potassium permeability results in eflux and potassium flows out and potassium gated channels are slow especially in comparison to sodium channels

modality/nature of sensory physiology

Indicated by → which sensory neurons are activated AND where the neurons terminate in the brain Specific to receptor type → receptor or neurons are sensitive to specific modalities

subthreshold graded potential

Ion leakage causes decreases is strength through traveling down cell body Stimulus not strong enough and ends up being subtreshold by time we reach trigger zone

neurotransmitter released by POST gang of sympathetic

NE and E

can you change AP duration/amplification in non-disruptted circumstances ?

NO - can influence AP frequency - can alter amp/duration if you change the condition or alter the situation

are graded potentials all or nothing ?

NOT all or nothing and can vary in duration and amplitude Action potentials will still remain the same

DHP channels (aka L type calcium channel)

NOT calcium release channels - mechanically gated to calcium release channels (Ryr)

nerve impulse: threshold reached

Na+ "rushes" into cell making it even more positive With activate gate open, Na+ enters the cell - Concentration gradient isn't changing significantly, electrical gradient changing wayyy more ("rushes" is just term to understand direction but not a lot of Na+ ions actually coming in to cell)

fibers contract and relax in response to many diff stimuli ?

Neurons, hormones, CO2 and O2 concentrations, chemicals, stretching irritation

L-ca2+ channels: symapthetic modulation

Open for longer period of time Increase ca2+ participation in excitation-contraction coupling For contracile cell= enhance permeability and increase sodium influx providing more intracellular calcium and stronger force

bundle of his

Originate from AV node Enter interventricular septum

ANS modulation for contractile cells

PNS (parasympathetic)= none SNS (sympathetic)= increase L-type channels function Therefore increase intracellular ca2+ and increase forced of contraction

right and left bundle branches

Part of bundle of His Come down into right and left ventricle wall

preload (EDV)

Preload: stretching of the cardiomyocyctes (before contraction) AND altered by venous return preload= load inside the heart that the heart has to try and mobilize Higher the preload, more stretch you have (contribute to immediate changes in contraction force) If preload goes up, stroke volume increases (directly proportional)

ca2+ channels: sympathetic modulation

T-ca2+ and greater influx (enhacne calcium permeability)

comparison of ECG and myocardial AP

The ECG represents the summed electrical activity of all cells recorded from the surface of the body The ventricular action potential is recorded from a single cell using an intracellular electrode. Notice that the voltage change is much greater when recorded intracellularly

composition of EKG

Waves: deflections (above or below) Segments: baseline sections between waves Intervals: combination of waves and segments

Integration (in presynaptic inhibition)

a modulatory neuron synapses on one collateral of the presynaptic neuron and selectively inhibits one target

integration (pre synaptic inhibition)

a modulatory neuron synapses on one collateral of the presynaptic neuron and selectively inhibits one target

neurotransmitters for ANS

acetylcholine (ACh), epinephrin (E) and norepinephrine (NE)

types of myofilaments

actin (thin) and myosin (thick)

nerve impulse: beginning depolarization

activation gates open when membrane potential reaches "threshold" (around -50mV), depolarizing stimulus arrives at the channel, activation gate opens

sympathetic modulation: where does epinephrine come from

adrenal medulla Activate beta1- adrenergic receptors (only on heart) Use cAMP messengers Alter transport properties of ion channel

good strengthening of cardiac muscle fiber

aerobic exercise and will decrease resting heart rate (leads to lower resting heart rate)

a mutated gene prevents t-tubulues from conducting action potentials. Which of the following would most likely results? SARCOLEMMA DEPOLARIZES NORMALLY EXCITATION CONTRACTION COUPLING IS IMPAIRED CYTOSOLIC CA2+ REMAINS LOW WEAK OR ABSENT CONTRACTIONS ALL OF THE ABOVE

all of the above

stroke volume

amount of blood pumped by one ventricle during a contaction EDV-ESV= stroke volume

relative refractory period: nerve impulse

another action potential may be generated only if stimulus is suprathreshold - mid to late stages of hyperpolarization, sodium inactive gates have been reset

type of control most internal organ under during homeostasis ?

antagonisitic control - one autonomic branch is excitatory and other branch is inhibitory - homeostasis is a dynamic balance between autonomic branches

inotropic effects

any chemical affecting contractility (but not through length, instead through calcium permeability → then alters crossbridge formation → eventually altering force)

receptive fields

area in which sensation can be picked up

sarcomere

arrangment of thick and thin filament in parallel

isovolumic ventricular relaxation

as ventricles relax; pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed Ventricules do not fully eject all blood (at rest only about 75%) ESV

ventricular ejection

as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected

activated Na+ gate

at rest this is the one that is close, needs to be stimulated to open and once stimulated and open, start of depolarization phase (inc sodium permeability)

atrial systole

atrial contraction forces a small amount of additional blood into ventricles EDV

special senses ?

balance, sight, smell, taste, hear

late diastole

both sets of chambers are relaxed and ventricles fill passively

exception of brain using location for receptive field ?

brain uses timing difference rather than neuron to localize sound

I(f) channels sympathetic modulation

cAMP binds → channels forced to stay longer and more open → increased sodium permeability

cardiac muscle autorhythmicity

can contract without nerve stimulation Nerves may alter rate and strength of contraction Do not initiate it

cardiomyocytes

cardiac muscle cells -autorythtimic cells and contractile cells

autonomic innervation of heart (sympathetic)

cardiac nerves → innervates authorymthic cells and contractile cells and increases heart rate adn contractions Impacts BOTH rate and force of contraction (innervating nodal cells and muscles)

L-ca2+ channels (cardiac)

channel is continuing out rest of action potential of autorhymic cell

inactivation Na+ gate

close to stop depolarization phase

duration of receptive fields

coded by duration of AP and some receptors can adapt or cease to respond

intensity of receptive field

coded by number of receptors activated and frequency of action potentials

twitch definition

complete contraction-relaxation phase

unmyelinated axons

conduction is slower and travels along axon stopping at every receptor along the way - Loss in resistance to leakage, so ions are going to leak out → don't have charge to keep action potential going - Reducing strength to point that it is below threshold so by time it reaches next voltage gated channel, AP threshold too low for AP to actually occur → this is what happens in like MS or unyelinated degeneration/diseases

myofibrils

contain contractile proteins arranged into sarcomeres - several myofibrils make up muscle cell

contractility ESV

contractility= describes forcefulness of heart contraction Increased contractility= increased forced contraction Large ESV=lower stroke volume (inversely proportional)

what is happening during muscle latent period ?

contraction isn't starting even though muscle fully excited - representative of time it takes for excitation of muscle membrane and when calcium is high enough to move tropomyosin/troponin before muscle can fire

isotonic contractions defintion

create a force and move load

isometric contraction definition

create force without moving a load - series elastic elements, sarcomeres shorten while elastic elements stretch resulting in little change in overall length

muscle contraction definition

creation of tension in muscle

extended submaximal exercise fatigue

depletion of glycogen stores - long hike

how can conduction velocity speed be influenced?

diameter of axon, resistance of axon membrane to ion leakage

graded contraction

different motor units responding to different threshold lead to different degrees of contraction *inc stimulus intensity (to motor neurons --> activation of more motor units (recruitment) --> inc tension in muscle) *used to chane relative force of contraciton * have to activate more motor units once all of the previous units have all met their maximum intesity

reflex types

efferent pathways, integration center, innate v learned, mono v polysynaptic

electrocardiogram (ECG or EKG)

electrical events of the heart → give insight into mechanical events (does not quantify mechanical events, only electrical events)

gap junctions of smooth muscle cells

electrically connects all cells - contract as a single unit

EDV

end diastolic volume, pushing all blood out of atria (fullest heart can be) If we constrict veins, we can make EDV go up and make stroke volume go up because directly proportional

ESV

end systolic volume, Some blood stays behind, blood left over after systole -afterload and contractility

varicosity

enlargement at end of axon - mitochondria - synaptic vesicles

role of somatic NS

excitatory

role of ANS

excitatory or inhibitory

EPSP

excitatory postsynaptic potential Monovalent cation channels open (Na+) causing sodium influx Membrane is partially depolarized → Does NOT make it to threshold due to outward movement of K+ Facilitation →Neuron is now more excitable →More sensitive to any stimulus and occurrence of AP is greater →Makes neuron more excitable so that if another AP comes it is now more likely to reach threshold

cardiac muscle

exclusive to JUST the heart (atria and ventricles, not vessels

brain regions specific to receptive fields

experiment stimulating the cerebral cortex

nicotinic receptors (cholinergic)

expressed on postganglionic cell bodies - excitatory - ligand gated channels location= preganglionic synaspe, CNS, motor end plate

muscarinic receptors (colinergic)

expressed on target cells - can be excitatory or inhibitory - metabotropic so secondary messenger and be excite/inhibit location= cardiac and smooth muscle, digestive organs, glands, CNS

nerve impulse: hyperpolarization

falls all the way down to -80 Falls below the starting resting potential

sympathetic ANS

fight or flight -thorocolumbar - energy consuming - fibers are short (pre ganglionic short and post are long)

small motor units

fine movement, 2-3 muscle fibers innervated by a single neuron

tonic receptors

fire rapidly, constantly firing, slow adapting, but never really cease firing Capability to slow down but don't cease fire EX: Baroreceptors (like blood pressure regulation) or proprioceptors

isovolumic ventricular contraction

first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves Blood pressure not high enough to open SL valves but strong enough to push closed AV valves (so all 4 valves closed)

muscle tension

force created by muscle

golgi tendon organ

found at connect between muscle and bone (the tendon itself) - prevent overforce, overwork of muscle

circular layer

further inner to hollow organ

nodes of ranvier

gaps in the myelin sheath - AP only occurs here and makes conduction velocity faster

nodal cells

generate action potentials without input from nervous system

proprioceptors definition AND main focuses

generation info about body position and change main focuses= muscle spindle and golgi tendon organ (both skeletal muscle) AND joint receptors

ways heart can change force

graded potentials and length-tension relationship

beta 1/beta 2 (adrenergic)

greater affinity for E (epinephrine)

alpha 1/alpha 2 (adrenergic)

greater affinity for NE (norepinephrine)

large motor units

gross movement, many muscle fibers innervated by one neuron

strength of signal initiation is dependent on?

how close you are from signal ex: furtehr you are from initiation of signal, weaker singal will be (fade as it continues deleivery)

which lines/bands shorten in sarcomere

i band= shortens h zone= shortens (can even disappear) a band= consistent m line = consistent

effect of increasing frequency of firing ?

increase cytosolic ca2+ (inc muscle tension)

lateral inhibition

increases contrast between activated receptive fields and inactive neighbors (enhances precision)

IPSP

inhibitory post synaptic potential K+ and Cl- channel open K+ OUT and Cl- IN (due to diffusion) Membrane is hyperpolarized →Goes in the opposite direction of threshold and cell is made more negative →Decreased chance of generating an AP because we are further from threshold

innate v learned (reflex)

innate= baroreceptor reflex learned= walking, cranial component to urination

motor neuron definition

innervates many muscle fibers - due to this organizaiton they function as a single unit

sensory system responsibility ?

integration of info from periphery to the brain

reflex definition

integration of sensory info into an involuntary response

actions of ANS

involuntary (unconscious)

saltatory conduction of myelinated axons

jumping/skipping regions of ion so AP stays above threshold to keep AP generated

synaspes defintion

junction of communication between a neuron and another cell

types of receptive fields

large and small

diameter of axon influence on AP speed

larger axons with more SA are faster conduction velocity - more SA = more voltage-gated channels = better ion flow (faster conductance)

precision of sensory pathways

lateral inhibition and population coding

how are resting permeabilities maintained ?

leak channels

eccentric action (isotonic)

lengthening action

large receptive field

less precision to sensory info and less sensitivity (thigh)

what type of receptor is a nicotinic receptor ?

ligand-gated - gate opens when ACh binds to receptor - Na+ overpowers K+ so get an excitatory event

bad strengthening of cardiac muscle fiber

like pathologies causing heart to get too thick and chambers being narrowed (like congestive heart failure)

regeneration definition

limited capacity to divide * mesenchymal (satellite) cells (endomysium decreases with age)

what does smooth muscle line?

lining all hollow organs

types of cross section of intestines

longitudinal and circular layers - good for segmentation and peristalsis

2 stages of crossbridges

low force= relaxed muscle high force= contracting muscle

autonomic division function (ANS)

maintain homeostasis (regulates smooth muscle contraction, cardiac muscle, glands and VISCERA of human body) visceral reflex effects (intense and rapid responses)

spatial summation

many (2 or more) synapses over a broad area simultaneously More than one presynaptic sources that are simultaneously delivering signals from two different spaces or locations

conduction velocity

measure of speed in which AP travels down the axon

neurotransmitter release compared to neuron-neuron synapse

mode of relase from axon terminal same - not as specific as neuron-neuron synpase

muscle spindle definition

modified set of muscle fibers located in belly of muscle - designed to prevent overstretch of muscle and protect from damage

mono v polysnaptic (reflex)

mono= afferent to efferent (no interneuron) poly= uses interneuron (ALL autonomic are, some somatic are)

small receptive field

more precision and more sensitivity (face, hands)

population coding

multiple receptors functioning and analyzed together (pulling info from lots of senses and pulling all together to create singular thought)

types of cholinergic receptors

muscarinic and nicotinic

threshold stimulus definition

must be met to generation action potential

resistance of ion leakage influence on AP speed

myelinated axon are faster (less leakage = faster movement)

adrenergic

neurons that release NE and E (like adrenaline and sympathetic is fight or flight so like adrealine) - only found on target tissue

cholinergic

neurons which release ACh

smooth muscle electrical properties

no need for action potential to initiate contraction results in many different pathways

multi unit smooth muscle cells

not electrically linked, and each cell must be stimulated independently - no gap junctions (cells do not electrically communication) -Axons weave throughout (ensures that all cells are close, independent stimulation) - Very fine control - Recruitment

botox

not the neurotoxin but functions same way that it paralysis the muscles of the face so no longer pulling on droopy skin and then wrinkles eventually relax and even out Or for excessive sweating, inhibits ACh which triggers sweat glands so sweating no longer happening or triggered

neurotransmission definition

occurs between the axon of one neuron and the dendrite/cell body of another neuron

terminal cisterna

on either side of t tubulue and contain large amount of ca2+

all or non principle of action potential

once threshold is reached --> full AP generated

# of neurons from CNS to effector in somatic NS

one

tetanus definition

one smooth contraction, max amplitude

triad (muscles)

organization of t tubulues and SR -SR largest when closes to t tubule and that's where store the most ca2+ - communication allows for propagation of AP

smooth muscle control

paracrine, hormones and neurotransmitters

what dominates homeostasis for rest and digest ?

parasympathetic

length tension relationship of skeletal muscle

physical length of sarcomere impacts amount of tension capable of being able to be produced - crossbridge tension decrease --> tension decreased

where does integration of EPSP and IPSP occur ?

post synaptic neuron each post synpastic neuron is an integration center (changes in RMP spread down axon hiilock when an AP either will or will not be generated)

general senses ?

pressure, touch, pain, tickle etc (through post-central gryus)

longer refractory period of contractile cells

prevents summation

2 circuits of the cardiovascular system

pulmonary and systemic pulmonary= heart → lungs → heart (Right ventricle lungs, left atria) systemic= heart → body → heart (Left ventricle, whole body, right atrium)

varicosities of nearby smooth muscle cells

release neurotransmitter in general area

muscle relaxation

release of tension

parasympathetic ANS

rest and digest - restore body function, energy conserving - craniosacral - fibers are long (preganglionic are long and post is short)

repolarizatioin

return cell to negative charge (opening K+ voltage gated channels and closing Na+ voltage gated channel)

depolarization

reverse membrane potential (inside neuron becomes positive relative to outside)

longitudinal layers

run LENGTH of hollow tube

concentric action (isotonic)

shortening action

motor unit defintion

single motor neuron and all the muscle fibers that it innervates

structure of somatic nervous system

single neuron from CNS out to skeletal - CNS origin, myelinated - NT= ACh and nicotinic receptor - always excitatory

effectors of somatic NS

skeletal muscles

what does somatic nervous system control

skeletal muscles - branches, neuromuscular junction

types of muscle fibers

slow oxidative(type 1), fast oxidative (type 2a), fast glycolytic (type 2b)

effectors of ANS

smooth muscle, cardiac muscle, glands

acetylocholinesterase (AChE)

special enzyme destroys ACh

how is cardiac depolarization spontaneous

special ion channels I(f) channels and t-ca2+

suprathreshold graded potential

stimulus being strong enough and elicits an AP as it is suprathrehold

contraction of skeletal muscle is achieved when .. ?

stimulus is at threshold or higher, smallest stimulus needed to excite a muscle (all signals are suprathreshold) ** all or none principle applies to stimulus not force of contraction

graded potentials types

subthreshold and suprathreshold

t tubulues

surround every myofibril and conitinuation of sarcolemma and important for action potentials - portions that extend down from muscle fibers

muscle fiber

surrounded by sarcolemma - synonymous with muscle cell

muscle cramp definition

sustained painful contraction hyperexcitable neurons

power stroke

swivel of myosin hinge (pulls actin filament toward M line)

what dominates homeostasis for flight or fight ?

sympathetic

sympathetic modulation: where does norepinephrine come from

sympathetic nervous system

neuromuscular junction definition

synapse between sarcolemma and motor neuron -where we release ACh onto nicotinic receptor

neuroeffector junction

synaspe between postganglionic autonomic neuron and target cell

patellar tendon (knee jerk) reflex

test to make sure muscle spindle reflex is firing properly

what type of contraction does muscle undergo ?

tetanic contraction

tetany of skeletal vs cardiac

tetany skeletal= good tetany cardiac= death (Would stay in contracted state, and cardiac tetanus wouldn't allow heart to fill with blood so we would die)

skeletal muscle fast twitch fiber

the refractory period (yellow) is very short compared with the amount of time required for the development of tension

cardiac muscle fiber (refractory period)

the refractory period last almost as long as the entire muscle twitch

autonomic innervation of heart (parasympathetic)

the vagus nerve → innervating authrorythmic cells ONLY and decreases heart rate Only impact rate (only innervating nodal cells)

how does calcium return to SR ?

through use of ATP - myosin heads detach (require ATP) - TN-TM covers binding sites - thin filaments slip back to resting length -sarcomere lengthens back to resting

absolute refractory period: nerve impulse

time at which another action potential can NOT be generated - inactive sodium gate is closed and therefore inactive NO amount of stimulus will allow for another AP to occur

latent period definition

time between muscle action potential and begin of contraction

receptor types

tonic and phasic

optimal length of length-tension relationship of skeletal muscle

total crossbridge formation is capable of being 100% so can produce stronger tension contraction - as length increases, pull thin filament so far away from myosin head, reduce overlap and crossbridges worse (greater forces= more crossbridges

# of neurons from CNS to effector in ANS

two

slow-oxidative/slow twitch

type 1 *Lots of myogobin - Related to hemoglobin, provides a lot of O2) *Slow twitch/ long distance run, LOW fatigue rate

fast twitch oxidative

type 2a *Fast twitch/ 400m or 800m sprints *Fatigue rate in the middle of type 1 and type 2B *Fine movements

fast glycolytic

type 2b *Fast twtich/short sprints *HIGH fatigue rate *Fine motor movement

actions of somatic NS

voluntary (conscious)

muscle load

weight that opposes contraction

refractory period in nerve impulse definition AND types

when it is possible to elicit another action potential and what are the requirements to be able to do this types = absolute and relative

trigger zone definition

where action potentials are initiated

axon hillock

where the cell body meets the axon - for multipolar neurons, is also trigger zone that initiates AP to propagate down axon

if the absolute refractory period increase in duration, would there be any effect on peak firing rate (number of action potentials delivered per second)?

yes the peak firing rate would decrease - increasing time which voltage sodium gated channels are inactive, take longer for channels to reset and for another AP to occur

full heart cycle

→ marked by beginning of systole (contraction phase) and end of diastole (relaxation phase)

4 major steps of power stroke

1) ATP bidns to myosin, myosin release actin 2) myosin hydrolyses ATP, myosin head rotates and binds to actin 3) power stroke 4) myosin releases ADP *doesn't matter which step you start at just follow correct order

steps leading up to muscle contraction ?

1) Events at the neuromuscular junction 2) Excitation-contraction coupling (--> then Ca2+ signaling) 3) Contraction-relaxation cycle (--> leads to muscle twitch or sliding filament theory)

conduction pathways steps

1) SA node depolarizes 2) electrical activity goes rapidly to AV node via internodal pathways 3) depolarization spreads more slowly across atria. Conduction allows through AV node 4) Depolarization moves rapidly through ventricular conducting system to the apex of the heart 5) Depolarization eave spreads upward from the apex

neurotransmission steps

1) action potential depolarizes the axon terminal 2) the depoliarization open voltage-gated Ca+2 channels and Ca+2 enters the cell 3) calcium entry triggers exocytosis of synaptic vesicle contents 4) neurotransmitter diffuses aross the synpactic cleft and bidns with receptors on the postynaptic cell 5) neurotransmitter binding initiates a response in the postynaptic cell EPSP OR IPSP

integration pre synpatic neuron steps

1) an excitatory neuron fires 2) an action potential is generation 3) an inhibitory neuron fires, blocking neurotransmitter release at one synapse