Neurotransmission and Neuromuscular Junction

Question 1

Electrochemical Neurotransmission Def.

Answer 1

Conversion of electrical to chemical signal in the synapse

Question 2

Synaptic Transmission (Electrochemical Coupling) Outline

Answer 2

Action potential depolarizes axon terminals. Ca2+ channels open. Ca2+ entry triggers synaptic vesicles fusion to membrane and exocytosis of neurotransmitters from them. NTs bind to synaptic cleft. NTs bind to post-synaptic or auto receptors and elicit response. NTs are inactivated

Question 3

Neurotransmitters Def.

Answer 3

Small, rapid-acting chemical messengers. Specific to neuron in both development and action (neurons can accept many different NTs but NTs have specific receptor shape)

Question 4

Excitatory Neurotransmitters

Answer 4

Acetylcholine and Glutamate

Question 5

Inhibitory Neurotransmitters

Answer 5

GABA, Glycine and Serotonin

Question 6

Neurotransmitter Lifecycle

Answer 6

Precursor (amino acid) uptake, NT Synthesis, NT vesicle uptake, NT release into synaptic cleft, receptor binding (post-snaptic or auto receptors), NT inactivation

Question 7

2 Types of Neurotransmitter Receptor

Answer 7

Ionotropic (ligand - gated) and metabotropic (g-protein coupled)

Question 8

Ionotropic Receptors Outline

Answer 8

NT binds, channel opens, ions flow through. Fast synaptic neurotransmission

Question 9

Metabotropic Receptors Outline

Answer 9

NT binds to g-protein and it either modifies ion channel function or triggers intracellular signaling. Slower transmission used in both short and long term effects

Question 10

Different methods of NT Inactivation

Answer 10

Enzymes in synaptic cleft, taken up by presynaptic neuron (via transporter protein, reused), glial cell uptake and diffusion to periphery

Question 11

Glutamate Desc.

Answer 11

Major excitatory NT. Essential in plasticity, learning, memory and higher processing. Inactivated by astrocytes (expressing glutamate transporters)

Question 12

4 Glutamatergic Ionotropic Receptors

Answer 12

N-methyl-D-asparate (NMDA), Amino-3-hydroxy-5-methylisoxazoleproponic (AMPA), Kainte and Delta

Question 13

8 Glutamergic Metabotropic Receptors

Answer 13

mGluR1 …. mGluR8

Question 14

Function of NT at an excitatory synapse

Answer 14

Depolarises post synaptic membrane

Question 15

Result of Glutamate binding to NMDA receptor

Answer 15

Influx of Ca2+ ions, depolarisation of the post-synaptic membrane

Question 16

GABA (Gamma amino butyric receptors) Function

Answer 16

Major inhibitory NT, counterbalances glutamate. Dysregulation causes epileptic symptoms.

Question 17

2 Types of GABA Receptors

Answer 17

GABAa (ionotropic (Cl-)) and GABAb (metabotronic)

Question 18

NT inactivation Def.

Answer 18

Reuptake of NTs into pre-synaptic neuron (astrocyes) vis GABA transporters

Question 19

Function of NT at Inhibitory Synapse

Answer 19

Hyperpolarizes post synaptic membrane. GABA induces Cl- influx

Question 20

Acetylcholine (ACh) Function

Answer 20

CNS: learning and memory. PNS: Neuromuscular junction motion and automatic NS

Question 21

Substances that stop effect of acetylcholine

Answer 21

Acetylcholinterase (inactivates, on post-synaptic memebrane) and Botox (acts as antagonist)

Question 22

2 Types of Cholinergic Receptors

Answer 22

Nicotinic (Ionotropic, Na+, Ca^2+ and K+) (excitatory) and Muscarinic (metabotropic) (slower-acting)

Question 23

Muscarinic Receptor Types

Answer 23

M1 - M5. Most cholinogenic CNS pathways

Question 24

2 Types of Nicotinic Receptors

Answer 24

N(m): skeletal neuromuscular junction. N(n): postganglionic ANS cell bodies

Question 25

Skeletal Muscle innervated by

Answer 25

Somatic NS and Motor neurons

Question 26

Motor Unit Def.

Answer 26

1 motor neuron branching and innervating multiple muscle fibres

Question 27

Neuromuscular Junction Def.

Answer 27

1 motor synapse on a muscle fibre

Question 28

Neuromuscular Junction Outline

Answer 28

Action potential travels down motor axon, Ca^2+ influx causes ACh release into synapse, ACh diffuses across synaptic cleft and binds to nicotinic receptors on motor end plate (muscle fibre), triggers Na+ influx and K+ eflux ( ligated-gated ion), Threshold (-50) mV is reached and action potential is generated (Muscle rmp = -90), ACh is degraded

Question 29

End Plate (muscle fibre) Potential Function

Answer 29

Partially depolarises muscle membrane. Multiple push membrane potential past threshold to generate action potential

Question 30

Neuromuscualr Junction Chemical Agents Results and Examples

Answer 30

Paralysis and cessation breathing. Botox (ACh antagonist), Curare (ACh antagonist) and Sarin (inhibits AChe), BW venom (ACh agonist)