CN - Chapter 5 - Synaptic Transmission

Question 1

synaptic transmission

Answer 1

The process of transferring information from one cell to another at a synapse.

Question 2

electrical synapse

Answer 2

A synapse in which electrical current flows directly from one cell to another via a gap junction.

Question 3

chemical synapse

Answer 3

A synapse in which presynaptic activity stimulates the release of neurotransmitter(s), which activates receptors in the postsynaptic membrane.

Question 4

gap junction

Answer 4

A specialized junction where a narrow gap between two cells is spanned by protein channels (connexons) that allow ions to pass directly from one cell to another.

Question 5

postsynaptic potential (PSP)

Answer 5

A change in the postsynaptic membrane potential by the presynaptic action of an electrical synapse, or a synaptically released neurotransmitter.

Question 6

secretory granule

Answer 6

A spherical membrane-enclosed vesicle about 100 nm in diameter containing peptides intended for secretion by exocytosis; also called dense-core vesicle.

Question 7

dense-core vesicle

Answer 7

A spherical membrane-enclosed vesicle about 100 nm in diameter containing peptides intended for secretion by exocytosis; also called secretory granule.

Question 8

membrane differentiation

Answer 8

A dense accumulation of protein adjacent to and within the membrane on either side of a synaptic cleft.

Question 9

active zone

Answer 9

A presynaptic membrane differentiation that is the site of the neurotransmitter release.

Question 10

postsynaptic density

Answer 10

A postsynaptic membrane differentiation that is the site of neurotransmitter receptors.

Question 11

neuromuscular junction

Answer 11

A chemical synapse between a spinal motor neuron axon and a skeletal muscle fiber.

Question 12

motor end-plate

Answer 12

The postsynaptic membrane at the neuromuscular junction.

Question 13

glutamate (Glu)

Answer 13

An amino acid; the major excitatory neurotransmitter in the CNS.

Question 14

gamma-aminobutyric acid (GABA)

Answer 14

An amino acid synthesized from glutamate; the major inhibitory neurotransmitter in the CNS.

Question 15

glycine (Gly)

Answer 15

An amino acid; an inhibitory neurotransmitter at some locations in the CNS.

Question 16

acetylcholine (ACh)

Answer 16

An amine that serves as a neurotransmitter at many synapses in the peripheral and central nervous systems, including the neuromuscular junction.

Question 17

transporter

Answer 17

A membrane protein that transports neurotransmitters, or their precursors, across membranes to concentrate them in either presynaptic cytosol or synaptic vesicles.

Question 18

voltage-gated calcium channel

Answer 18

A membrane protein forming a pore that is permeable to Ca²⁺ ions and gated by depolarization of the membrane.

Question 19

exocytosis

Answer 19

The process whereby material is released from an intracellular vesicle into the extracellular space by fusion of the vesicle membrane with the cell membrane. See also <i>endocytosis</i>.

Question 20

endocytosis

Answer 20

The process by which a bit of the cell membrane is pinched off, internalized, and converted to an intracellular vesicle. See also <i>exocytosis</i>.

Question 21

transmitter-gated ion channel

Answer 21

A membrane protein forming a pore that is permeable to ions and gated by neurotransmitters.

Question 22

excitatory postsynaptic potential (EPSP)

Answer 22

Depolarization of the postsynaptic membrane potential by the action of a synaptically released neurotransmitter.

Question 23

inhibitory postsynaptic potential (IPSP)

Answer 23

A change in the postsynaptic membrane potential by the action of a synaptically released neurotransmitter, making the postsynaptic neuron less likely to fire action potentials.

Question 24

G-protein-coupled receptor

Answer 24

A membrane protein that activates G-proteins when it binds neurotransmitters.

Question 25

G-protein

Answer 25

A membrane-enclosed protein that binds guanosine triphosphate (GTP) when activated by a membrane receptor. Active G-proteins can stimulate or inhibit other membrane-enclosed proteins.

Question 26

second messenger

Answer 26

A short-lived chemical signal in the cytosol that can trigger a biochemical response. Second messenger formation is usually stimulated by a first messenger (a neurotransmitter or hormone) acting at a G-protein-coupled cell surface receptor.

Examples of second messengers are cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), and inositol-1,4,5-triphosphate (IP₃).

Question 27

metabotropic receptor

Answer 27

A G-protein-coupled receptor whose primary action is to stimulate an intracellular biochemical response.

Question 28

autoreceptor

Answer 28

A receptor in the membrane of a presynaptic axon terminal that is sensitive to the neurotransmitter released by that terminal.

Typically, autoreceptors are G-protein-coupled receptors that stimulate second messenger formation. The consequences vary, but a common effect is inhibition of neurotransmitter release, and, in some cases, neurotransmitter synthesis.

Question 29

neuropharmacology

Answer 29

The study of the effects of drugs on nervous system tissue.

Question 30

inhibitor

Answer 30

A drug that blocks the normal action of a protein or a biochemical process.

Question 31

receptor antagonist

Answer 31

A drug that binds to a receptor and <em>inhibits</em> its function. (Think <i>antagonist</i> = against/blocking the actor).

Question 32

receptor agonist

Answer 32

A drug that binds to a receptor and activates it. (Think <i>agonist</i> = actor).

Question 33

nicotinic ACh receptor

Answer 33

A class of acetylcholine-gated ion channels found in various locations, notably at the neuromuscular junction.

Question 34

synaptic integration

Answer 34

The process by which multiple EPSPs and/or IPSPs combine within one postsynaptic neuron, in some cases triggering one or more action potentials.

Question 35

miniature postsynaptic potential (a “mini”)

Answer 35

A change in postsynaptic membrane potential caused by the action of neurotransmitter released from a single synaptic vesicle.

Question 36

quantal analysis

Answer 36

A method of determining how many vesicles release neurotransmitter during normal synaptic transmission.

Question 37

EPSP summation

Answer 37

A simple form of synaptic integration whereby excitatory postsynaptic potentials combine to produce a larger postsynaptic depolarization.

Question 38

spatial summation

Answer 38

The combining of excitatory postsynaptic potentials generated at more than one synapse on the same cell. See also, <i>temporal summation</i>.

Question 39

temporal summation

Answer 39

The combining of excitatory postsynaptic potentials generated in rapid succession at the same synapse. See also, <i>spatial summation</i>.

Question 40

length constant

Answer 40

A parameter used to describe how far changes in membrane potential can passively spread down a cable such as an axon or dendrite, represented by the symbol λ. The length constant λ is the distance at which the depolarization falls to 37% of its original value; it depends on the ratio of membrane resistance (r_m) to internal resistance (r_i).

Question 41

internal resistance

Answer 41

The resistance to electrical current flows [flowing?] longitudinally down a cable or neurite, represented by the symbol r_i.

Question 42

membrane resistance

Answer 42

The resistance to electrical current flow across a membrane; represented by the symbol r_m.

Question 43

shunting inhibition

Answer 43

A form of synaptic inhibition in which the main effect is to reduce membrane resistance, thereby shunting depolarizing current generated at excitatory synapses.

Question 44

modulation

Answer 44

A term used to describe the actions of neurotransmitters that do not directly evoke postsynaptic potentials but modify the cellular response to excitatory postsynaptic potentials and inhibitory postsynaptic potentials generated by other synapses.

Question 45

norepinephrine (NE)

Answer 45

A catecholamine neurotransmitter synthesized from dopamine; also called noradrenaline.

Question 46

adenylyl cyclase

Answer 46

An enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), a second messenger.

Question 47

cyclic adonosine monophosphate (cAMP)

Answer 47

A secondary messenger formed from adenosine triphosphate (ATP) by the action of the enzyme adenylyl cyclase.

Question 48

protein kinase

Answer 48

A class of enzyme that phosphorylates proteins, a reaction that changes the conformation of the protein and its biological activity (i.e., changing its shape changes its function).

Question 49

phosphorylation

Answer 49

A biochemical reaction in which a phosphate group (PO₄^2-) is transferred from adenosine triphosphate (ATP) to another molecule. Phosphorylation of proteins by protein kinases changes their biological activity.

Question 50

Question 1: What is meant by quantal release of neurotransmitter?

Answer 50

The elementary unit of a neurotransmitter release is the content of one synaptic vesicle.

Each vesicle contains several thousand transmitter molecules. The total amount of transmitter released at a synapse is a multiple of this number, depending on how many vesicles release their contents into the synaptic cleft.

The amplitude of an EPSP is a multiple of the response to the contents of one vesicle. It reflects the number of transmitter molecules in one synaptic vesicle and the number of postsynaptic receptors available at the synapse.

Question 51

Question 2: You apply ACh and activate nicotinic receptors on a muscle cell. Which way will current flow through the receptor channels when V_m = -60 mV?

When V_m = 0 mV?

When V_m = 60 mV?

Why?

Answer 51

Nicotonic ACh receptors are permeable to both sodium and potassium.

When Vm = –60 mV, net current flow through ACh-gated ion channels is inward, toward the equilibrium potential of sodium, causing depolarization.

At Vm = 60 mV, the direction of net current flow through the ACh-gated ion channels is outward, toward the equilibrium potential of
potassium, causing the membrane potential to become less positive.

The critical value of membrane potential at which the direction of current flow reverses is called the reversal potential. In this case, the reversal potential is 0 mV because this is the value between the equilibrium potentials of sodium and potassium. At 0 mV, no current flows.

Question 52

Question 3: In this chapter, we discussed a GABA-gated ion channel that is permeable to Cl^–.

GABA also activates a G-protein-coupled receptor called the GABA_B receptor, which causes potassium-selective channels to open. What effect would GABA_B receptor activation have on the membrane potential?

Answer 52

Activated GABA-gated Cl^– ion channels bring the membrane toward the equilibrium potential for Cl^–, which is –65 mV.

If the membrane potential was less negative than –65 mV when the transmitter was released, activation would cause hyperpolarization.

The activation of GABAsub>B receptors causes potassium-selective channels to open. As a result, GABA_B activation brings membrane potential toward the equilibrium potential of potassium, which is –80 mV. If the membrane potential was less negative than –80 mV when the transmitter was released, activation would also cause hyperpolarization.

This channel might also impact the neuron by shunting inhibition, allowing a depolarizing current from an excitatory synapse to leak out. This, in turn, decreases the likelihood of action potential.

The action of a G-protein-coupled receptor is, however, slower than that of the GABA-gated Cl^– ion channel or a typical excitatory synapse. Therefore, its effects would be slower to occur and would last longer.

Question 53

You think you have discovered a new neurotransmitter, and you are studying its effect on a neuron. The reversal potential for the response caused by the new chemical is –60 mV. Is this substance excitatory or inhibitory?

Why?

Answer 53

If the new chemical has a reversal potential of –60 mV, the substance is likely to be inhibitory.

The reversal potential reflects the types of ions the membrane is permeable to after the application of the neurotransmitter. A reversal potential of –60 mV suggests that the neurotransmitter activates ion channels that make the membrane more negative. If a neurotransmitter causes the membrane to move toward a value that is more negative than the action potential threshold, the neuron becomes less likely to fire an action potential, which means it is inhibited.

Question 54

Question 5: A drug called strychnine, isolated from the seeds of a tree native in India and commonly used as rat poison, blocks the effects of glycine. Is strychnine an agonist or an antagonist of the glycine receptor?

Answer 54

Strychnine is an antagonist of glycine at its receptor. Mild strychnine poisoning enhances the startle and other reflexes and resembles hyperekplexia. High doses can eliminate glycine-mediated inhibition in circuits of the spinal cord and the brain stem. This leads to uncontrollable seizures and unchecked muscular contractions, spasms, and paralysis of respiratory muscles. It might ultimately result in painful, agonizing death from
asphyxiation.

Question 55

Question 6: How does nerve gas cause respiratory paralysis?

Answer 55

Nerve gases interfere with synaptic transmission at the neuromuscular junction by inhibiting AChE. Uninterrupted exposure to high concentrations of ACh for several seconds leads to a process called desensitization. In this process, transmitter-gated channels close despite the continued presence of ACh. Normally, the rapid destruction of ACh by AChE prevents <i>desensitization</i>. However, if AChE is inhibited by nerve gas, ACh receptors will be desensitized and neuromuscular transmission will fail, causing respiratory paralysis.

Question 56

Question 7: Why is an excitatory synapse on the soma more effective in evoking action potentials in the postsynaptic neuron than an excitatory synapse on the tip of a dendrite?

Answer 56

A current entering the sites of synaptic contact must spread to the spike-initiation zone and this zone must be depolarized beyond its threshold to generate an action potential. In addition, depolarization decreases as a function of distance along a dendrite. As a result, the
effectiveness of an excitatory synapse for triggering an action potential depends on how far the synapse is from the spike-initiation zone. Because the soma is closer to the spike-initiation zone, an excitatory synapse on the soma is more effective for evoking action potentials than an excitatory synapse on the tip of a dendrite.

Question 57

Question 8: What are the steps that lead to increased excitability in a neuron when NE is released presynaptically?

Answer 57

he steps that increase the excitability of a neuron when NE is released presynaptically are:

1. The NE receptor bound to a Β receptor activates G-protein in the membrane.
2. G-protein activates the adenylyl cyclase enzyme.
3. Adenylyl cyclase converts ATP into the second messenger cAMP.
4. cAMP activates a protein, kinase.
5. Kinase causes a potassium channel to close by attaching a phosphate group to it.

This produces little change in membrane potential but increases the membrane resistance and increases the length constant of dendrites. This enhances the response that a weak or a distant excitatory synapse produces. This effect can last longer than that of the presence of the
transmitter.