L4: Synapses&neurotransmitters

Types of neurones: motor neurones, pyramidal neurone (hippocampus), purkinje neurone (cerebellum)

Synaptic Trasmission (chemical): e.g. neuromuscular junction (synapse between motor neurones&skeletal muscle)

neurotrasmitters are released resting neuromuscular junction
voltage gated Ca++ channel: open in response to changes in membr. depolarisation

ACheR=> ligand gated ion channels, non-specific cation channels

vesicles containing neurotransmitter (ACh)

activated neuromuscular junction:

1) AP generated <>

2) depolarisation

3) open Ca++ cause: Ca++ entry to presynaptic

4) cause ACh vesicles fuse with membr. to release ACh in synapse

5) let Na+ ion generates local potential /AP

6) when open -->> muscle-->>contraction

7)in skeletal muscle Ca++ release=>contraction

Neurotransmitters:

a.a.=>γ-aminobutyric acid (GABA), Glutamate, Glycine

amines=>ACh, Dopamine, Histidine, Noradrenaline, 5-HT (Hydroxytryptamine)

peptides=> Cholecystokinin, Dynorphin, Enkephalins, Neuropeptide Y, Somatostatic

gases=> NO, (CO)

Criteria for Identifying neurotransmitter:

1) Localisation

2) Synthetic/catabolic mechanisms: occurs in dif.ways

• Neurotr. synthesis:e.g. peptide neuron/DNA protein (all body), RER, Golgi apparatus, vesicle, transported in axon terminal, synaptic vesicles nerve terminal



• synthesis&degradation of ACh: catalyses synthesis ACh transporter=>

ChAT(cholic acetyl transferase)--> formation of Ach<Ch+Ac.CoA

AChE (acetyl choline esterase) breakdown ACh-->> acetic acid+choline (recycled for synthesis of ACh)

Ach=> package up inside vesicle to be trnsferred release<>

3)Release from terminal

release of neurotransmitter (e.g. ACh)by exocytosis: synaptic vesicle: protein-protein interactions binding to membr., once membrane depolarised, entry Ca++ allows vesicles to release content, neurotrasmitter molecules molecules : vesicle pinches back to presynaptic.

neurotransmitter receptors:

• ACh: ligand-gated ion channel=> ionotropic receptors: allow movements of ions: 1) signal proteins open, 2)allow ions in, 3) causes hyperpolarisation/depolarisation


• G-protein-coupled receptors => metabotropic: reflecting much slower on cellular metabolism, more time consuming process

Active G: activate ions->change in excitability-> cellular effects

Active G: activate E-> cause 2nd msg->Ca++ release/protein phosphorylation

4) Synaptic mimicry->stimulate nerve

5) Pharmacological identity of action: block effect of suspected neurotr. in the same way of directly stimulating nerves

Synapses in the CNS:

1) Variety-Types of synapses in the CNS:

2)Size &Shape of CNS synapses:

• presynaptic terminals contain vesicles arranged @ active zones => RELEASE
• postsynaptic membr.=> specialized&contains clusters of neurotransmitters receptor&signalling molecules

3) Excitatory/inhibitory synapses:

e.g. glutamate generates excitatory post synaptic potential (EPSP) Na+ entry causes local/ small depolarisation

/ e.g. γ-aminobutyric acid generates inbitory post synapric potential (IPSP) entry to cell more (-) inside cell, hypepolarisation

4)Synaptic integration:

temporal summation: adding 2gether local potentials that occur @ same synapse, but dif. times

spatial summation: adding 2gether local potentials that occur @ dif. sites on neurone=> more often cuase loc. potentials dont travel v. far

5)Electrical synapses: --> gap junctions: brain&heart

apart<>

formed<>

elec. synapses affect integration: generate elec. pot. although no enzyme released: If record Vm of cell 1 and cell 2 elect. PSP

lower curve than AP @ same time

6) network of neurones: convergence/ divergence