MMED1005 Lecture Notes - Lecture 6: Skeletal Muscle, Neuropeptide Y, Lipid Bilayer

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NEUROTRANSMISSION

Main points:

- Diversity of neurotransmitters and receptors

- Release mechanism for transmitter vesicles

- Postsynaptic mechanisms

o Ligand gated channels

o G-protein coupled receptors

- Presynaptic actions of neurotransmitters

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Information passes from a nerve cell to other cells by chemical signals (neurotransmitters)

- When an action potential (AP) reaches the ed terial of a erve, it releases a

neurotransmitter onto the next cell (another nerve cell or a muscle or a gland cell) in

the chain

- The neurotransmitter interacts with receptors on the target cell to cause an effect

- The effect may be

o Excitatory: causes an AP in the next nerve cell – makes a muscle cell contract

– causes the gland to secrete

o Inhibitory: prevents the next nerve cell from generating an AP – makes the

muscle cell relax – prevent secretion by a gland

Neurotransmitters:

- Presynaptic terminals store neurotransmitters ready for release in vesicles

o Most terminals contain more than one neurotransmitter

o **Some are too unstable to be stored

- E.g. Acetylcholine (ACh), amines, amino acids, peptides, purines (ATP)

How are they released?

- The signal is depolarisation of the presynaptic terminal

- This occurs when the AP reaches the terminal

- Depolarisation opens voltage-activated Ca channels in the terminal,

allowing a Ca influx and rise in intracellular Ca concentration in the

terminal

- Ca triggers the fusion of the vesicle to the membrane, and release of its

contents

- After the vesicle contents have been released, the vesicle is refilled and

recycled

- Acetylcholine, noradrenaline, glutamate, ATP, etc. are released in this

way.

- The neurotransmitter diffuses across the synaptic cleft to receptors || on

the postsynaptic membrane

- The neurotransmitter binds to the receptor, and initiates events in the cell

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Document Summary

Postsynaptic mechanisms: ligand gated channels, g-protein coupled receptors. Information passes from a nerve cell to other cells by chemical signals (neurotransmitters) When an action potential (ap) reaches the e(cid:374)d (cid:894)(cid:858)ter(cid:373)i(cid:374)al(cid:859)(cid:895) of a (cid:374)erve, it releases a neurotransmitter onto the next cell (another nerve cell or a muscle or a gland cell) in the chain. The neurotransmitter interacts with receptors on the target cell to cause an effect. The effect may be: excitatory: causes an ap in the next nerve cell makes a muscle cell contract. Inhibitory: prevents the next nerve cell from generating an ap makes the muscle cell relax prevent secretion by a gland. Presynaptic terminals store neurotransmitters ready for release in vesicles: most terminals contain more than one neurotransmitter, **some are too unstable to be stored. Acetylcholine (ach), amines, amino acids, peptides, purines (atp) The signal is depolarisation of the presynaptic terminal. This occurs when the ap reaches the terminal.

Related Questions

Tetraethylammonium (TEA) is a drug that blocks voltage-gated potassium channels. What effect would this have on an action potential?

(a)Prevent the rising phase

(b)Prevent the cell from reaching the threshold to trigger an action potential

(c)Prevent or prolong the falling phase

(d)None of the above

The hyperpolarization phase of the action potential is due to:

(a)The opening of voltage-gated Cl- channels

(b)Prolonged opening of voltage gated K+ channels

(c)The closure of resting Na+ channels

(d)Rapid inactivation of voltage-gated K+ channels

The period when it is difficult to initiate another action potential for several milliseconds due to voltage-gated sodium channel inactivation is referred to as the:

(a)Relative refractory period

(b)Absolute refractory period

(c)Resting period

(d)Hyperpolarization period

In the human central nervous system, Gap junctions are found:

(a)Only between neurons

(b)Only between astrocytes

(c)In both neurons and astrocytes

(d)In all cells

Small molecule transmitters such as acetylcholine are synthesized in:

(a)The nerve terminal

B) The cell body and transported to the nerve terminal

C) Synaptic vesicles

D) Endoplasmic reticulum

Prior to Otto Loewiâs classical experiment, which of the following was not known:

(a)stimulation of the vagus nerve slows the heart

(b)extracts of frog heart, made following vagal nerve stimulation, slow the heart

(c)some acetylcholine effects are similar to those produced by muscarine

(d)vagal nerve stimulation releases a substance which slows the heart

Which of the following is most important in determining if neurotransmission is excitatory or inhibitory?

(a)The structure of the synapse

(b)The neurotransmitter released by the presynaptic neuron

(c)The neurotransmitter receptor

(d)The strength of the stimulus

Benzodiazepines such as Valium allosterically regulate GABA receptors by:

(a)Binding at receptor sites other than the transmitter binding site

(b)Binding at the transmitter (GABA) binding site on the receptor

(c)Blocking the action of the endogenous transmitter

(d)Mimicking the action of the endogenous transmitter

GABA-A receptors are ligand-gated Cl- channels. The equilibrium potential of Cl- is -65 mV. At the neuronal resting membrane potential of -65 mV, GABA binding to the GABA-A receptor would result in the opening the Cl- channel, resulting in:

(a)no net flow of Cl- ions

(b)Cl- inflow and hyperpolarization

(c)Cl- outflow and depolarization

(d)Cl- outflow and hyperpolarization

At the mammalian neuromuscular junction, the released neurotransmitter acts on:

(a)muscarinic receptors

(b)nicotinic receptors

(c)adrenergic receptors

(d)Beta receptors

Neurotransmitters are packaged into synaptic vesicles by:

(a)endocytosis following transmitter release

(b)presynaptic membrane transporters

(c)vesicular transporters

(d)all of the above

. Which of the following are NOT types of ion channels?

Voltage-gated

(a)Ligand-gated

(b)G protein coupled receptor (GPCR)-gated

(c)Leak channels

(d)NONE of the above

NMDA receptors are unique in that their ion channel is:

(a)Ligand-gated

(b)Voltage-gated

(c)Ligand- and voltage-gated ion channels

(d)GPCR-gated

. Which of the following is INCORRECT regarding Catecholamine neurotransmitters

(a)Includes Dopamine, Norepinerphrine, and Epinephrine

(b)Contain a Catechol Ring

(c)Synthesized from Tryptophan

(d)Are produced by neurons whose cell bodies are located in the upper brainstem

The largest and most diverse group of receptors in eukaryotes is:

(a)Ligand gated receptors

(b)Glutamate receptors

(c)G-Protein coupled receptors

(d)Allosteric receptors

The most abundant G-protein coupled receptor in the brain is:

(a)Glutamate receptors

(b)Acetylcholine receptors

(c)Cannabinoid receptors

(d)Dopamine receptors

Which of the following drugs DOES NOT block voltage-gated Na+ channels

(a)Lidocaine

(b)Riluzole

(c)Reserpine

(d)Tetrodotoxin

Sarin, a nerve gas, exerts its toxicity by:

(a)blocking nicotinic receptors

(b)inhibiting choline acetyltransferase

(c)inhibiting acetylcholinesterase

(d)inhibiting voltage-gated Na+ channels

Botulinum Toxin (BoTox) interferes with transmitter release by:

(a)cleaving protein(s) involved in transmitter release

(b)blocking voltage-gated Ca2+ channels

(c)blocking voltage-gated Na+ channels

(d)blocking voltage-gated K+ channels

Atropine is:

(a)An agonist of the acetylcholine ionotropic receptor

(b)An antagonist of the acetylcholine ionotropic receptor

(c)An agonist of the acetylcholine metabotropic receptor

(d)An antagonist of the acetylcholine metabotropic receptor

MMED1005 Lecture Notes - Lecture 6: Skeletal Muscle, Neuropeptide Y, Lipid Bilayer

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