BSCI353 Exam 2

To which category of neurotransmitters does acetylcholine belong? Small-molecule neurotransmitters Biogenic amines Peptides Amino acids Purines

Small-molecule neurotransmitters

______ ______ propagates over the muscle

action potential

synapsin

a protein that reversibly binds to vesicles and is phosphorylated by CaMKII in order to move the vesicles closer to the plasma membrane

acetylcholine receptor

-cholinergic receptor -ACh is an excitatory and an inhibitory nt -nAChR: K+, Na+ --> cholinergic channel / receptors --> mAChR

clathrin and dynamin exocytosis

-clathrin: attaches to mem that is to be retrieved -dynamin: pinches off mem

metabotropic receptors

-G-protein coupled receptors -longer, slower, more widespread effect -amine and peptide receptors 1) nt binds 2) G-protein is activated 3) G-protein subunits or intracellular messengers modulate ion channels 4) ion channel opens 5) ions flow across mem

GABA receptor inhibitory effect- is GABAA inhibitory?

-GABAA opens to allow Cl- anions in -postsyn mem is hyperpolarized -when Cl- enters, the mem pot will actually depol to -60mV (Vrest = -65mV) --> does this mean that GABAA is still inhibitory? -yes! even though the activation of GABAA depolarizes the mem pot from its resting pot, it still prevents the neuron from reaching AP threshold! ***inhibitory and excitatory effects mean to compare Eion to threshold pot, not resting pot*** -excitation: increased prob of AP -inhibition: decreased prob of AP

GABA receptors

-GABAergic receptors -primary inhibitory receptor -GABAA allows Cl= ions in --> GABAergic receptors --> GABAB

halorhodopsin

-H and N also found other light channels that exhibited light sensitivity in bacteria -allowed Cl- in and would hyperpolarize the mem pot -called them halorhodopsin

optogenetics

-a modern method of manipulating neuronal activity

NMDA ionotropic receptor

-a type of glutamatergic receptor -both ligand and vg dependent properties -3 conditions to be open: 1) glutamate binding (ligand) 2) binding of glycine 3) Mg2+ that blocks channel at rest (Mg2+ is attracted to the closed channel at -meV -when open, Na+ and Ca2+ ions flow into the channel

why are metabotropic receptors needed if we always want a fast response

-bc metabotropic receptors allow for signal amplification in signal transduction pathways -> much more widespread effect -2nd messenger mediated long-term effect -metabotropic receptors may activate CREB

who created the 1st major neurophysiological experiment to describe nt release

-bernard katz

chemical synapses (general)

-discovered in 1921 by Loewi -20-50nm wide -unidirectional -nt released, ions flow through postsynaptic channels

electrical synapses (general)

-discovered in 1957 by Furshpan and Potter -3nm wide -bidirectional in invertebrate escape circuits, pacemakers, and liver cells (studied in crayfish) -ion current flows through connexon channels btw neurons (gap junctions) -fast and reliable -synchronize electrical activity

what revealed the presence of synaptic vesicles in presynaptic terminals?

-electron microscopy -nt's are packaged in vesicles and each vesicle contains a fixed amt of nt (a quantum) -subsequent biochemical studies have confirmed that each synaptic vesicle contains 10,000 ACh mc's, which matches the amt of ACh needed to elicit 1 MEPP -hypothesis: each vesicle releases its entire content during synaptic transmission, through the fusion of vesicles with the presynaptic plasma membrane

how do we test that each vesicle releases its entire content during synaptic transmission through the fusion of vesicles

-exp: record vesicle fusions using freeze-fracture e- microscopy and correlate with postsynaptic EPP's -fracture mem and pull back to see what's going on inside presynaptic terminal -results: when stimulated, we see "pits" (vesicle caught in the act of fusing) -count pits and correlate with EPP size -more postsynaptic pits results in more quanta of post synaptic EPP's -conclusion: Nt release is quantal, through the fusion of discrete synaptic vesicles with the presynaptic membrane (exocytosis)

glutamate receptor

-glutamatergic receptor -primary excitatory receptor in the brain -3 ionotropic glutamate receptor types: AMPA, NMDA, Kainate -AMPA, NMDA, Kainate --> glutamatergic receptor --> mGluR

Loewi's experiment

-had the idea of chemical transmission already in 1903, but he didn't know how to do an experiment to test the idea --> case up w/ one in his dreams -exp: researchers knew of the vagus nerve in frog hearts -injection of current would slow hr -therefore, if 1 heart is stimulated, an unstimulated heart in a connected chamber will then also be stimulated -result: stimulatiton causes 1 heart to slow down, transfer of fluid to 2ns heart causes 2nd heart to slow down too! -conclusion: soluble stuff, not electrical impulses, mediates this vagus nerve effect (this nt was ACh!)

gap junctions

-hemi-channel (connexon) made up of 6 connexins on each cell -2 hemi-channels are aligned -channel pore is large, permitting ions and small proteins to go through -current directly flows through the connexon pores

exp to find how channel rhodopsin works

-injected channel rhodopsin into xenopus oocyte and analyzed with voltage clamp method -blue light --> inward current detected --> Na+ and K+ allowed in --> excitatory depolarization of mem pot -bc the retinol mc changes shape when blue light is sensed --> channel opens -this ultra-fast appearance of the rhodopsin current suggested that the rhodopsin and ion channel were intimately linked, forming a single protein complex

ionotropic receptors

-ligand gated ion channels -fast 1) nt binds 2) channel opens 3) ions flow across mem

exp to lower external Na+ conc and increase external K+ conc

-lowering external Na+ conc = decreased Na+ conc diff across mem --> reversal pot is also decreased (shift left) -confirmed that the channel is permeable to Na+ -increased external K+ conc = decreased K+ conc diff across mem --> reversal pot increased and shifts right -confirmed that K+ can go through the same channel

CREB

-metabotropic receptors may activate CREB (cAMP Response Element Binding protein), which can change gene expression to have long term effects -activation of CREB can create new synapses for new pathways, allowing for long term memory

metabotropic receptors (more specific)

-no pores -use G-proteins to activate other proteins to initiate a response --> cascade of intracellular signaling -there is an extracellular nt binding site and an intracellular G-protein binding site -2 effect pathways from activating a metabotropic receptor

MEPP's

-not evoked, just occur every now and then -appear to be similar in size -when bathed in a low-Ca2+ solution, stimulating the motor neuron evokes much smaller EPP's, similar to the sized of MEPP's --> occasionally, EPP's are doubled or tripled the size of EPP's

Katz' experiment

-record lots of EPP's in low-Ca2+ solution and plot size vs number of size -the sizes of EPPs are integer multiples of MEPPs -data fit Poisson distribution, suggesting that synaptic transmission is in discrete quanta (packets) of 0.4 mV -but where are those packets?

Hegemann and Negel discovery of light-gated ion channels

-single-celled algae have an eye spot that allows them to swim towards dim light and away from bright light -they wanted to find the gene responsible for this -a protein channel in the DNA sequence was found --> channel rhodopsin

where are small nt's and neuropeptides synthesized

-small nt's are synthesized loally -neuropeptides are synthesized in the cell body and transported to the terminal

sparkers theory vs soupers theory

-sparkers: said electrical current flows from 1 neuron to the next -soupers: said that chemical substances transfer info from 1 neuron to the next at synapses -both types exist!

temporal summation

-sum of 1 EPSP multiple times -if 1 neuron is stimulated multiple times v quickly, the EPSPs can be added together to stimulate AP at next neuron

spatial summation

-sum of all the EPSPs and IPSPs -all the synaptic potentials (EPSPs and IPSPs) on dendrites are combined at axon hillock to try to reach threshold

important proteins covering the synaptic vesicle

-synapsin: helps mobilize vesicles towards synapse -synaptotagmin: Ca2+ sensors -synaptobrevin -SNARES: help dock and prime vesicles -Clathrin and dynamin: retrieve membrane to recycle

what happens to all the vesicle membranes that fuses to the presynaptic terminal membrane

-there must be a way to recycle the vesicle -coated HRP at synapses after stimulation, and they were later seen in vesicles inside the presynaptic terminal --> so, and endocytosis must be occurring in order to recycle the vesicle membrane

Ca2+ injection exp

-to see if Ca2+ alone causes the nt release -injecting Ca2+ into the presynaptic terminal alone triggers a rise of the postsyn mem pot -shows that the presence of Ca2+ alone is sufficient for synaptic transmission to occur

Ca2+ imaging exp

-to see if Ca2+ really does enter the presynaptic terminal after stimulation -using Ca2+ sensitive dyes (fura-2) under a fluorescence microscope, we can directly observe a rise in Ca2+ conc (ca2+ influx) at the presynaptic terminal following a chain of AP's in the presynaptic neuron -shows that Ca2+ ions really do flow into the terminal

Ca2+ blockers exp

-to see if the nt release would be prevented by blocking Ca2+ -blocking Ca2+ with Cd2+ prevents rise of postsynaptic mem pot (EPSP), demonstrating that Ca2+ influx is necessary for synaptic transmission -voltage clamp used to do this -with TTX and TEA applied to presyn mem --> Ca2+ still worked and postsyn mem pot was normal -with TTX, TEA, and Cd2+ applied to presyn mem --> no rise in postsyn mem pot -shows that is Ca2+ is blocked, nt release will be prevented

exp to hold mem pot above Na+ equil pot with patch clamp method

-used patch clamp method to hold mem pot above Na+ equil pot -outside - out method: ACh applied to outside --> saw small inward current --> this is the inflow of Na+

Takeuchi's exp

-used voltage clamp on postsyn muscle cells -found large inward current after stimulation of presynaptic axon -when mem pot is held at 0mV, there was no current --> must be this ion's equilibrium pot -but, no ions have an equil pot of 0 --> thought that maybe this channel let multiple ions through, not just 1 -therefore, its channel would be at equil btw K+ and Na+'s equil pit -how do we prove this?

exps to know which ions caused excitatory signals

-we already know that Na+ is responsible for the early inward current 1) Takeuchi used voltage clamp on postsyn muscle cells 2) lower external Na+ conc and increase external K+ conc 3) patch clamp to hold mem pot above Na+ equil pot

SNARE complex

-when vesicle is sent near the presyn mem (by synapsin), SNAP-25 protein pulls vesicle to mem 1) free snares on vesicle and plasma mem 2) snare complexes form as vesicle docks 3) synaptotagmin binds to snare complex 4) entering Ca2+ binds to synaptotagmin, leading to curvature of plasma mem, which brings the mem's together 5) fusion of the membranes leads to exocytotic release of nt

what is the role of Ca2+ in the NMJ

-when vg Ca2+ channels open when the mem is depolarized, Ca2+ enters the presynaptic terminal --> hypothesized that Ca2+ influx causes nt release -experiments to test this: a) Ca2+ b) block Ca2+, c) Ca2+ injection into presynaptic terminal

dopamine metabotropic receptor pathway

1) dopamine binds to D2 receptor 2) Gi activation 3) decreased adenylyl cyclase activity 4) decreased cAMP production 5) decreased pkA activation 6) decreased protein channel phosphorylation

2 types of events that occur from the NMJ

1) evoked EPP's that occur after stimulation 2) spontaneous minuature EPP's (MEPP's), not evoked, just occur every now and then -led Katz to think that synaptic transmission is quantal (in discrete packets)

glutamate metabotropic receptor pathway

1) glutamate binds to mGluR 2) Gq activation 3) activates phospholipase C 4) path a: diacylglycerol --> protein kinase C path b: IP3 --> Ca2+ release 5) increased phosphorylation and activation of Ca2+ binding proteins

2 types of post synaptic nt receptors

1) ionotropic receptors (ligand gated ion channel) 2) metabolic receptors (G-protein coupled receptor)

work led to 3 criteria to define nt's

1) must be synthesized and stored in the presynaptic neuron 2) must be released by the presynaptric axonal terminal following AP's 3) the mc alone (or its agonists) must produce a response in the postsynaptic neuron that mimics the response in number 2, and the response is blocked by an agonist

2 types of synapses

1) neuron-neuron (like in the brain) 2) neuron-muscle (NMJ)

norepinephrine metabotropic receptor pathway

1) norepinephrine binds to beta receptor 2) Gs activation 3) adenylyl cyclase converts ATP to cAMP 4) cAMP activates protein kinase A 5) increased phosphorylation opens ion channels

steps of a chemical synapse

1) nt is synthesized and stored in vesicles 2) an AP invades the presynaptic terminal 3) depolarization of presynaptic terminal causes opening of vg Ca2+ channels 4) influx of Ca2+ through channels 5) Ca2+ causes vesicles to fuse with presynaptic membrane 6) transmitter is released into synaptic cleft via exocytosis 7) nt binds to receptor mc's in postsynaptic membrane 8) opening or closing of postsynaptic channels 9) postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of the postsynaptic cell 10) removal of nt by glial uptake or enzymatic degradation 11) retrieval of vesicular membrane from plasma membrane 12) nt binds to postsynaptic channels 13) opening or closing of postsynaptic channels 14) postsynaptic current makes EPSP or IPSP 15) summation determines whether or not an AP will occur 1-11: presynaptic membrane 12-15: postsynaptic membrane

steps to synthesize an nt

1) precursor peptide is synthesized in rough ER (from mRNA from nucleus) 2) precursor peptide is split in the golgi apparatus to yield the active nt 3) secretory vesicles containing the peptide bud off from the golgi apparatus 4) the secretory granules are transported down axon to terminal where the peptide is stored

2 types of nt degradation and recycling

1) reuptake by transporters into presynaptic axon terminal 2) degradation by enxymes and metabolites reuptake

2 effect pathways from activating a metabotropic receptor

1) short cut pathway: G-protein activated/gated ion channels 2) G-protein coupled 2nd messenger cascase

2 types of vesicles

1) small: 20-40nm in diameter; house ACh, glutamate, and GABA 2) dense core: 90-250nm in diameter; house neuropeptides (larger nt's)

***updated: 4 major classes of ion channels

1) vg ion channels 2) ligand gated ion channels 3) stretch and heat activated ion channels 4) light gated ion channels (discovered recently!)

What is the neuromuscular junction?

A chemical synapse formed by the contact between a motor neuron and a muscle fiber and is the site at which a motor neuron is able to transmit a signal to a muscle fiber, leading to a muscle contraction.

What step in synaptic transmission would a-latrotoxin impact? How would that affect communication at the neuromuscular junction (NMJ)? What would happen to the postsynaptic muscle?

A-latrotoxin is the toxin found in widow spider venom. This toxin would affect the step of synaptic transmission at which neurotransmitters are released via exocytosis to the synaptic cleft. It affects the communication at the NMJ by causing the continuous release of ACh at the NMJ. This would then cause a rush of ACh into the postsynaptic muscle, causing the muscles to contract violently until the input of ACh is depleted.

metabotropic receptors of ACh, glutamate, and GABA

ACh: mAChR Glutamate: mGluR GABA: GABAB

ionotropic receptors of ACh, glutamate, and GABA

ACh: nAChR glutamate: AMPA, NMDA, Kainate GABA: GABAA

_____ gets released from the vesicles into the synaptic cleft by the process of _______

Acetylcholine; exocytosis

Which observation would indicate a role for calcium in transmitter secretion? Observation of presynaptic depolarizing currents after blockade of sodium channels All of them Blockade of transmitter release by injection of calcium blocker into the presynaptic terminal None of them Induction of transmitter release by injection of calcium into the presynaptic terminal Voltage clamp experiments showing voltage-gated calcium channels in the presynaptic terminal

All of them

Which feature of an electrical synapse allows synchronizing the electrical activity of multiple neurons? Ability of neurons to form gap junctions with glial cells Fast speed of transmission Bidirectional transmission of electrical signals Slow transmission of signals Bidirectional transmission of chemical signals

Bidirectional transmission of electrical signals

In what way are GABA and glutamate similar in the adult brain? Both are excitatory neurotransmitters. Both are synthesized from glucose in the presynaptic terminal. Both are transported into synaptic vesicles via the vesicular inhibitory amino acid transporter. Both are inhibitory neurotransmitters. Both are common in the nervous system.

Both are common in the nervous system.

What step in synaptic transmission would botulinum toxin impact? How would that affect communication at the neuromuscular junction (NMJ)?

Botulinum toxin blocks the exocytosis/release of ACh at the NMJ by preventing the function of SNAREs that allow for the fusion of synaptic vesicles with the presynaptic plasma membrane. This then leads to absence of communication at the NMJ, because ACh will not reach the postsynaptic membrane and lead to an action potential occurring in the postsynaptic neuron (leading to muscular contraction), ultimately resulting in muscular paralysis and asphyxiation.

vg channels open, allowing _______ to enter the cell

Ca2+

You conduct a voltage clamp experiment in which you hold the presynaptic terminal of a glutamatergic neuron (a neuron that releases glutamate) at 0 mV. When you treat the terminal with TTX, an inward current is recorded. Which ion and ion channels are responsible for the current you observe? Calcium; voltage-gated calcium channels Potassium; voltage-gated potassium channels Sodium; ligand-gated non-specific cation channels Calcium; ligand-gated non-specific cation channels Sodium; voltage-gated sodium channels

Calcium; voltage-gated calcium channels

Cell X fires an action potential and releases GABA onto Cell Y. Assuming only GABA A receptors are present on the postsynaptic membrane, which is at rest at -55mV, which ion is responsible for the changes that would be observed? Magnesium Calcium Sodium Chloride Potassium

Chloride

What step in synaptic transmission would curare impact? How would that affect communication at the neuromuscular junction (NMJ)?

Curare blocks postsynaptic acetylcholine receptors and thus would interfere with the ability of the neurotransmitter to elicit an endplate potential in the associated muscle fiber. This would result in the inability of the presynaptic neuron to elicit muscle contraction.

At which point during signal transmission at a chemical synapse is exocytosis occurring? As neurotransmitter binds to its receptors During reuptake, as synaptic vesicles are reformed from the plasma membrane As voltage-gated Ca 2+ channels are opening During neurotransmitter release into the synaptic cleft While Ca 2+ enters the presynaptic terminal

During neurotransmitter release into the synaptic cleft

Which molecule binds NMDA receptors and prevents the flow of ions at resting and hyperpolarized membrane potentials? Glycine Ca 2+ NMDA Glutamate Mg 2+

Mg 2+

What is the source of the quanta that make up the EPP? Pulses of current that flow through the electrical synapse Short-term increases in membrane permeability Current through a single ion channel Fusion of individual synaptic vesicles with the plasma membrane Individual action potentials

Fusion of individual synaptic vesicles with the plasma membrane

What is the main excitatory neurotransmitter in the adult brain? Glutamate GABA Dopamine Norepinephrine Serotonin

Glutamate

How would the effect of botulinum toxin (BOTOX) at the NMJ make it useful for removing wrinkles?

In diluted forms, botulinum toxin is called BOTOX, and it is able to enter the NMJ's of facial muscles, locally paralyzing them to thus inhibit muscle contractions that develop into wrinkling.

In the sequence of events in neurotransmission, which event occurs just after the action potential arrives at the presynaptic terminal? Packaging of the neurotransmitter Delivery of the neurotransmitter to the presynaptic terminal Fusion of the synaptic vesicles with the presynaptic membrane Influx of Ca 2+ into the presynaptic terminal Release of the neurotransmitter

Influx of Ca 2+ into the presynaptic terminal

How would application of a Ca 2+ channel blocker affect the function of a synapse? It would decrease the magnitude of postsynaptic potential. It would eliminate the postsynaptic potential but have no effect on presynaptic neuron. It would increase the magnitude of postsynaptic potential. It would eliminate the postsynaptic potential and the presynaptic Ca 2+ current. It would eliminate the presynaptic Ca 2+ current but have no effect on the postsynaptic potential.

It would eliminate the postsynaptic potential and the presynaptic Ca 2+ current.

How would loss of voltage-gated Na+ channels affect action potential generation? How would that impact synaptic transmission?

Loss of VG Na+ channel function would result in the inability of Na+ to rapidly influx when the membrane depolarizes. This would make it so that the action potential's rising phase would be missing and no action potential would be generated because the threshold would not be reached. This would also impact synaptic transmission because action potentials wouldn't be passed on along the axon to the terminals, eliminating the potential needed at the synaptic terminal to open VG Ca2+ channels needed for the release of neurotransmitters for synaptic transmission. No potential at the synaptic terminal would lead to no signal transmitted from the synapse.

nt's bind to nicotinic acetylcholine receptors on the junctional folds along the motor end plate of the muscle. Ion channels open and _____ enters the muscle, which increases the membrane potential

Na+

Why do you suppose that ingestion of tetrodotoxin can cause death?

TTX interferes with sodium channels and prevents axonal depolarization. This results in the inability of neurons to communicate via action potentials and thus the nervous system would no longer be able to coordinate complex bodily functions necessary for survival.

Compare and contrast tetanus toxin's effect on synaptic transmission at the neuromuscular junction (NMJ) to that of botulinum toxin. How might the inflicted symptoms differ between the two toxins?

Tetanus toxin is chemically similar to botulinum toxin and causes tetanus poisoning or lockjaw. It binds to the NMJ at presynaptic terminals and is then transported via motor neurons to the spinal cord. Tetanus toxin then degrades synaptobrevin, causing inactivation of inhibitory neurotransmission that would normally suppress motor neuron activity and muscular activity. This causes enhanced excitability and activation of these motor neurons, leading to involuntary muscle contraction. The symptoms of tetanus toxin differ from those of botulinum toxin in that tetanus toxin causes over-excitability of muscles because of prevention of inhibitory neurotransmitter release instead of excitatory neurotransmitter release and thus muscle contraction, while botulinum toxin causes inhibition of muscle contraction.

clathrin

a protein that aids in the endocytosis of vesicles from the plasma membrane by forming a coat that molds the plasma membrane into a coated pit

Which statement about postsynaptic currents at the neuromuscular end plate is false? The end plate channels show a regenerative opening pattern that propagates an action potential along the length of the muscle fiber. The end plate potential is due to the opening of thousands or millions of channels. Acetylcholine can induce openings of ligand-gated ion channels. Individual channels tend to stay open for no more than a few milliseconds. Depolarizing currents can be recorded from outside-out patches of the postsynaptic membrane.

The end plate channels show a regenerative opening pattern that propagates an action potential along the length of the muscle fiber.

dynamin

a protein that forms a ring-like structure in order to pinch off vesicles from the plasma membrane to conclude endocytosis

Which is not a feature of glutamate signaling systems? Voltage-dependent gating of certain types of glutamate receptor The use of specialized proteins for loading glutamate into vesicles The presence of multiple glutamate receptor families with different ionic selectivities The use of specialized proteins for removing glutamate from the synaptic cleft The passage of large amounts of magnesium and calcium by NMDA receptors

The passage of large amounts of magnesium and calcium by NMDA receptors

Which statement about muscarinic acetylcholine receptors is true? They are metabotropic receptors. They control a ligand-gated channel. They mediate the effects of acetylcholine at neuromuscular junctions. They mediate a rapid response to acetylcholine. They are ionotropic receptors.

They are metabotropic receptors.

Why might curare have been used as an anesthesia in early medical practices?

To paralyze the motor nerves so that patients don't move around and reduce the likelihood of muscle contraction during surgical procedures.

To date, which observation is not part of the experimental evidence favoring the vesicular release hypothesis of neurotransmission? Visualization of acetylcholine molecules diffusing out of the neck of the membrane-fused vesicle Visualization of synaptic vesicles using electron microscopy Quantized distribution of events occurring at the neuromuscular junction Fixed size of MEPPs Correspondence between a vesicle's acetylcholine content and MEPP size

Visualization of acetylcholine molecules diffusing out of the neck of the membrane-fused vesicle

Which event is the first in the series of events that take place during chemical synaptic transmission? Synaptic vesicles fuse with the presynaptic membrane. Neurotransmitter is released into the synaptic cleft. Neurotransmitter binds to its receptors. Influx of Ca 2+ in the presynaptic terminal. Voltage-gated Ca 2+ channels open.

Voltage-gated Ca 2+ channels open.

SNAP-25

a plasma membrane SNARE protein that forms a helical SNARE complex with other SNARE proteins to bring the vesicle close to the plasma membrane

syntaxin

a plasma membrane SNARE protein that forms a helical SNARE complex with other SNARE proteins to bring the vesicle close to the plasma membrane

synaptobrevin

a vesicular SNARE protein that forms a helical SNARE complex with other SNARE proteins to bring the vesicle close to the plasma membrane

synaptotagmin

a vesicular protein that binds Ca2+ along with the SNARE complex on the plasma membrane in order to initiate vesicle fusion

Compare and contrast electrical and chemical synapses.

a) Chemical i) Nerve impulses are transmitted via chemical signals (neurotransmitters) ii) In higher-functioning vertebrates iii) One way transmission of signals from the presynaptic to postsynaptic neuron iv) Chemoreceptors present on postsynaptic membrane v) Slow transmission of information vi) Found in most neuron junctions vii) Utilize endocytosis and exocytosis for delivery of neurotransmitters and recycling of the vesicles respectively b) Electrical i) Nerve impulses are transmitted via ions ii) In lower-functioning vertebrates and invertebrates iii) Transmission of electrical signals through gap junctions iv) No vesicles used v) No chemoreceptors present on postsynaptic membrane vi) High-speed transmission vii) Can have bidirectional transmission viii) Can lead to synchronous activity ix) Rare in the nervous system, present in pacemaker cells in the heart c) Both i) Stimulated by an action potential ii) Exist in many of the same neuronal paths

the muscle _____

contracts

Action potential enters presynaptic axon terminal, which causes ___________ of the terminal

depolarization

Presynaptic and postsynaptic neurons that form _______ synapses are connected via _______. electrical; synaptic vesicles electrical; gap junctions electrical; the synaptic cleft chemical; neurotransmitter release chemical; connexons

electrical; gap junctions

EPSP

excitatory post synaptic potential

IPSP

inhibitory postsynaptic potential

vesicles filled with _____ fuse with the membrane of the presynaptic neuron

neurotransmitters

Precursors of peptide neurotransmitters are synthesized in the _______ and packaged into vesicles in the _______. rough endoplasmic reticulum; trans-Golgi network rough endoplasmic reticulum; endosome rough endoplasmic reticulum; presynaptic terminal nucleus; presynaptic terminal smooth endoplasmic reticulum; trans-Golgi network

rough endoplasmic reticulum; trans-Golgi network

Small-molecule neurotransmitters are _______ for _______. taken back into the presynaptic terminal; degradation scattered in the synaptic cleft; reuse taken up by the postsynaptic cell; reuse taken up by the postsynaptic cell; degradation taken back into the presynaptic terminal; reuse

taken back into the presynaptic terminal; reuse