Lecture 10 Synapse Flashcards
Electrical synapses
Occur at gap junctions
Important during embryonic development of brain
Present in adult brain- synchronisation of the activity of groups of neurones
Gap junctions also occur between non-neuronal cells e.g. smooth and cardiac muscle
Chemical synapse
Most synapses use chemical neurotransmitter
Require:
Synthesis and vesicle packing (storage)
Release mechanism
Ability to bind to post synaptic membrane
Ability to rapidly remove neurot from synapse
Sequence of events
Action potential depolarises presynaptic membrane
Voltage gated Ca2+ channels open
Influx of Ca2+ ions cause vesicles to fuse to presynaptic membrane
Release of neurotransmitter (exocytosis)
Diffusion of neurotransmitter to receptors on post synaptic membrane
-receptor activation
Generation of post synaptic potential - triggers action potential
Rapid removal of neurotransmitter from cleft by : diffusion/ enzyme segregation/ reuptake or autoreceptors
Pre/post terms
Presynaptic axon terminal button
Post synaptic dendritic spine
Neuromuscular junction (NMJ)
A ‘model’ synapse
Motor neurones>skeletal muscle
Linked by chem synapse
Neurotransmitter is acetylcholine
EPP magnitude
Partial depolarisation
Post synaptic receptor
At NMJ post synaptic receptors are ligand gated ion channels
Binding of ligand (acetylcholine) triggers opening of channels
Cations (mostly Na+) flow into the cell inducing partial depolarisation (epp)
Neurotransmitters
Amino acids - glutamate, glycine, GABA
Amines - acetylcholine, noradrenaline etc.
Peptides - enkephalins, cholecystokinin etc.
Others - adenosine, ATP, nitric oxide
Postsynaptic receptors
Ionotropic - ligand gated ion channels v. Fast operation
Metabotropic- G protein-coupled receptors (GPCR’s). Comparitively slow operation.
Excitatory or inhibitory neurotransmitter
Excitatory - induces a partial post-synaptic membrane depolarization an EPSP
Inhibitory- induces a postsynaptic hyper polarisation an IPSP
EPSP - excitatory postsynaptic potential
Neurotransmitter at excitatory synapse depolarises the post synaptic membrane
E.g. acetylcholine (ACh)
Binding opens ligand gated Na+ channels
Allows influx of Na+ ions reducing membrane potential
Reduced membrane potential is called an EPSP
If depolarization of post synaptic membrane reaches threshold an action potential is generated in the post synaptic cell
IPSP- inhibitory post synaptic potential
Neurotransmitter hyperpolarises the postsynaptic membrane making action potential less likely to occur
E.g. gamma aminobutyric acid (GABA)
Binding of GABA
To GABA-A receptors on the post synaptic neuron open up ligand gated chloride (Cl-) ion channels
To GABA-B receptors activates an internal G protein and a “second messenger” that leads to opening of nearby K+ channels
Inhibitory vs. excitatory
Most synapses in the brain are inhibitory
Epilepsy may involve a deficit in inhibitory neurotransmission
- treat by enhancing GABA transmission
Smooth operation of skeletal muscle requires inhibitory as well as excitatory transmission
Synapse summation
In case of GABA-A and GaBA-B facilitated diffusion of ions changes the membrane potential (to as much as -80mv)
- this is IPSP as it counteracts any excitatory signals that may arrive at neuron
Production of an action potential is simply whether depolarization produced by excitatory synapse on cell minus any hyperpolarising effect of inhibitory synapses can reach threshold value or not
Summation = additive effects
Ending a response - removal of neurotransmitter
Vital for normal synaptic transmission
Removed by: enzyme degradation, diffusion or reabsorption - reuptake/uptake via neurotransmitter transporter
If neurotransmitter lingers in synaptic cleft it would continue to influence post synaptic neuron/muscle/gland indefinitely
- basis for the dopamine “high” associated with some drugs of abuse
