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1

neurons communicate with one another by.....

releasing chemical messengers called neurotransmitters

2

main excitatory neurotransmitter

glutamate

3

main inhibitory neurotransmitter

GABA

4

how to evoke synaptic response

binding to and activating neurotransmitter receptors, yielding any possible modes of synaptic signalling

5

after activating neurotransmitter receptors, neurotransmitter are removed from synaptic cleft by...

neurotransmitter transporters or degradative enzymes

6

3 different classes of neurotransmitters

1) classical (small molecule transmitters
- ACh, amino acids, biogenic amines derived from amino acids, purines

2) peptides
- endorphins etc.


3) non-classical, small molecule
- NO

7

neuropeptides

- examples

- relatively large transmitter molecules (3-36 amino acids)

- endophrins, enkephalins, neuropeptide Y, vasoactive intestinal peptide, substance P, FMRDamide

8

small molecule transmitter

- individual amino acids (ex: glutamate, GABA)
and transmitters (ACh, serotonin, histamine)
- smaller than neuropeptides

- divided into: acetycholine, amino acids, purines, biogenic amines

9

what are biogenic amines

- examples
- subgroup

- small molecule transmitter (subgroup)

- similar chemical properties and postsynaptic actions
- examples: dopamine, norepinephrine, epinephrine, serotonin, histamine

- catcholamines (subgroup)

10

what are catcholamines?

- biogenic amine subgroup
- hydroxylated benzene ring

11

Acetylcholine
- basic processes to all chemical synapses (4)

- where is it made?

- synthesis
- package and release
- reception
- removal (simple slow diffusion)

- made in cytoplasm

12

synthesis of ACh

- precursors (2)
- enzyme
- transporter

- synthesized in nerve terminals, from precursors acetyl coenzyme A (kreb cycle) and choline

- enzyme: reaction catalyzed by choline acetyl transferase (ChAT or CAT)

- transporter: after synthesis in cytoplasm, vesicular ACh transporter loads ~10 000 molecules of ACh into cholinergic vesicle

13

how to determine the evolution of ACh?

(how do we know which tranmitter is used by which neuron for which function?)

- raise antibodies against ChAT (enzyme)
- knockout genes (synthesis of ChAT)
- any mutation of the enzyme is quickly lethal mutation

14

locations of ACh in vertebrate nervous system

- all motor neurons= spinal cord and brainstem
- autonomic nervous system (sympathetic and parasympathetic divisions)- fight or flight
- modulatory neurons in brainstem and basal forebrain- often involved with levels of activation (sleep/wake)- susceptible to Alzheimer's (boost ACh to relieve some symptoms)
- intrinsic neurons= basal ganglia, tectum

15

reception of ACh- 2 major types of receptors

1) nicotinic receptors
2) muscarinic receptors

16

nicotinic receptors

- example found..?
- iono/metabo
- conduct?
- made up of.. ?

- important for reception of ACh

- ex: found neuromuscular junction
- ionotropic
- conduct both Na and K (depolarizing- net flow of Na override outflow of K)

- composed of 5 subunits with 3-4 transmembrane domains which form a channel with central membrane-spanning pore
- ligand-gated channel - binding ACh, causes conformational change, rearranges receptor domains, opening gate, permittion ions to diffuse through pore

17

where does ACh bind on nicotinic ACh receptors?

on the alpha-subunit

(usually has 2 alpha subunits at neuromuscular junction )

18

muscarinic receptors

- example, found where?
- iono/metabo
- when do you want to use these?

- structure

- ex: targets of parasympathetic postganglionic neurones
- found on receptors of parasympathetic nervous system, heart muscles

- metabotropic receptor

- use ACh to speed up/slow down processes (ex: beating of heart)

structure:
- 7 transmembrane domains
- extracellular site to bind neurotransmitter
- intracellular site to bind G-protein
- activate inward rectifier K channels or Ca-activated-K channels, exerting inhibitory influence on dopamine-mediated motor effects

19

subtypes of muscarinic receptors

how does ACh bind?

M1, M2, M3, M4, M5
- different binding characteristics
- different reactions to drugs

- no subunits, each protein forms a complete receptor with its transmembrane domains

20

G-protein receptors
- iono/metabo
- how does it work
- 2 examples

- metabotopic receptor

- work indirectly to regulate activity in numerous other proteins including channels
- receptor lies within membrane, can mind to transmitter, has intercellular domain that can react to G-protein

- heterotrimeric or monomeric

21

2 differences between ionotropic and metabotropic receptors

1) speed (fast vs long lasting effects)
- fast= ionotropic
- slow= metabotropic

2) multiple actions

22

how any subtypes of muscrinic receptors are there?

5

23

removal of ACh

- post synaptic actions of ACh at many cholinergic synapses, is terminated by hydrolytic enzyme= acetylcholinesterase

- enzyme is concentrated in synaptic cleft, ensuring rapid decrease in ACh concentration after its release from presynaptic terminal

- choline produced by ACh hydrolysis, is RECYCLED by being transported back into nerve terminals, where it is used to re-synthesize ACh

24

Why is the process of chemical synapses of ACh important?

- differential effects of toxins and drugs-- pharmacology

- Agonists (drug mimics specific transmitter)
- antagonists (blocks transmitter)

- disease affecting cholinergic transmission

25

what is agonist and antagonist

- agonist= mimic endogenous ligand

antagonist= block endogenous ligand

26

example of nicotinic agonist

cholinergic substance

(nicotine)
- nicotine binds to nicotinic receptors

27

nicotinic antagonist

- a-bungarotoxin from krait (used by snake, paralyze prey), prevents ACh from opening postsynaptic ion channels

- A-neurotoxin from cobra (blocks nicotinic receptor)

- curare (used as poison on darts to kill animals, blocks nicotinic receptors)

28

3 examples of muscarinic agonist and antagonist

- muscarine from the Amarita mushroom

- Summer flower

- Atropine from deadly nightshade (autumn berry)

29

effects of myasthenia gravis on neurotransmission and basis of treatment

- myasthenia gravis= disease that interferes with transmission between motor neurons and skeletal muscle fibers

- effects: autoimmune destruction of nicotinic receptors
- immunse responses reduced number of functional receptors at neuromuscular junction, eventualyl destroys them, diminishing efficiency of synaptic transmission

- muscle weakness occurs b/c motor neurons are less capable of exciting the postsynaptic muscle cells

- inhibitors increase concentration of ACh at synaptic cleft, allowing more effective activation of postsynaptic receptors not yet destroyed by immune system

30

each transmitter must always have mechanism for (4)

- synthesis
- package and release
- reception
- removal