Physiology of Excitable Cells - Anatomy physiology of synapse

Electrical synapse key info

symmetrical, bidirectional, gap junctions (connexins), very fast no synaptic delay, Ca2+ dependent, temp insensitive, large synapse, limited functions, synchronised activity

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Chemical synapse key info

highly developed structure, polarised, slow synaptic delay, Ca2+ dependent, temp sensitive, thousands of small synapses, versatile E and I, specific point to point activity

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Principles of chemical synaptic transmission

neurotransmitter synthesis, neurotransmitter storage into synaptic vesicles, vesicles fuse to presynaptic terminal, nt released into synaptic cleft, nt binds to postsynaptic receptors, response in postsynaptic cell, removal of nt from synaptic cleft

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Types of chemical synapse

Axo dendritic - between axon of one neuron and dendrite of another, Axo somatic - between axon of one neuron and soma of another, Axo axonic - between axon of one neuron and axon of another

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Transmitter examples

glutamate (CNS PNS) - excitatory, GABA (CNS PNS) - inhibitory, Acetylcholine (neuromuscular junction) - excitatory, Noradrenaline and Dopamine - excitatory and inhibitory

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1. Neurotransmitters and Biosynthesis

amino acids, amines, peptides. Peptide neurotransmitter synthesis: synthesis in cell body from pre pro peptides --> pro peptides--> peptide - packaged into vesicles in cell body and transported to axon terminal

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2. Neurotransmitters stored in synaptic vesicles

stored in vesicles to achieve high concentration, protect from degradation by cytoplasmic enzymes, allows for regulation of synaptic release

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3. Synaptic vesicle cycling and exocytosis

vesicles in reserve pool undergo priming to enter readily releasable pool. primed vesicles - fuse with plasma membrane by sustained depolarisation - elevated cytoplasmic Ca2+

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SNARE complex

Vesicular fusion mediated by SNARE complex, core SNARE complex formed by 4a helices. Synaptotagmin - calcium sensor: regulates SNARE zipping which is triggered by Ca2+ entry, zipping bridges bilayers of vesicle and plasma membrane -proximity- fusion

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Botulinum Toxins

they cleave various components of SNARE complex - so vesicular fusion and transmitter release is inhibited - muscle unable to respond to motor neurones - muscle paralysis. BOTOX - relaxes muscles ( no wrinkles )

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Quantal transmitter release

binding of neurotransmitter to postsynaptic membrane generates electrical signal proportional to amount of neurotransmitter released

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4. Transmitters bind to receptors

Ionotropic receptors - (ion channels) opened by binding agonists e.g. nicotinic Ach, glutamate (EPSP), GABAa (IPSP). Metabotropic receptors - GPCRs ( G protein coupled receptor) e.g. muscarinic Ach, adrenoceptors

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Response in post synaptic cell

Glutamate (Na+/Ca2+) - EPSP - depolarisation, inward current (Na+/Ca2+), increased firing rate. GABA (Cl-) - IPSP - hyperpolarisation, inward Cl-, decreased firing rate

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Hierarchy of neurotransmitters

amino acid transmitters - mediate excitatory and inhibitory transmission via ionotropic receptors. Catecholamine and peptide transmitters modulate transmission via metabotropic receptors by altering probability of release. Ach E - ionotr, I - metabo

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How do GPCRs modulate release of mediating transmitters?

1. Facilitate transmitter release (Gs coupled receptors) - Gs - AC - cAMP - binds directly to and opens HCN channel - cation influx - depolarisation - increased transmitter release

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2. Diminish transmitter release (Gi coupled receptors ) - i) binds/opens K+ channels - K+ efflux - hyperpolarisation ii)binds/inhibits VOCC - diminished Ca2+ influx - both together = less transmitter release

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5. Removal of Transmitters from synaptic cleft

1. Reuptake - taken back into pre synaptic terminal, 2. Enzyme - Ach by Ach esterase - binds to and degrades it, 3. Diffusion - out of cleft into extracellular space - blood vessels to be carried away in bloodstream

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Are Chloride channels always inhibitory?

If ECl < Vm - net influx of Cl- ions = hyperpolarisation. If ECl > Vm - net efflux of Cl- ions = depolarisation

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Dorsal column medial lemniscal (touch)

Afferent aB fibres from DRG ascend ipsilateral dorsal column. Synapse 1 at medulla, decussate then follow medial lemniscus. Synapse 2 at thalamus Synapse 3 at primary sensory cortex - ascending

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Spinothalamic (pain)

Afferent A@ and C fibres from DRG synapse 1 on entering spinal cord, decussate then ascend via contra lateral spinothalamic tract. Synapse 2 at thalamus Synapse 3 at primary sensory cortex

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Why pressure painful when focused

If C and aB fibres of one dermatome activated simulataneously, aB fibre activation of interneuron can inhibit projection neuron of spinothalamic tract. Presence of inhibitory interneuron prevents light touch causing pain

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Mechanical allodynia

normal light touch = painful. tissue is inflamed sensitises peroperal receptors - deep tissue injury. Tissue injury increases [Cl-] in projection neuron, now aB fibres via interneuron causes [Cl-] efflux - depolarisation - activation of pain pathway

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SIgnal passed from nerve to muscle?

neuromuscular junction is the synapse between a nerve and skeletal muscle fibre - chemical synapse

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Transmitter release

Ca2+ entry through Ca2+ channels, Ca2+ binds to synaptotagmin, vesicle brought close to membrane, SNARE complex make a fusion pore, transmitter released through this pore

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How to study events experimentally at synapse

record from neuromuscular junction, measure skeletal contraction in response to nerve stimulation, measure smooth muscle contraction in response to nerve stimulation, determine effects of agents that act at NMJ on locomotion

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Physiology of Excitable Cells - Anatomy physiology of synapse

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