(06) Synaptic Transmission Flashcards
synaptic transmission occurs between neurons through either…
chemical synapses or electrical synapses (via pores called gap junctions)
in the developed mammalian brain, occurs almost entirely through CHEMICAL synapses
structure allowing transmission of a message from one neuron to another
axo-dendritic synapse
like a long axon extending from the pre-synaptic neuron to a post-synaptic neuron
structure for transmission from motorneuron to muscle fibre
neuromuscular junction = “end plate”
what type of transmission happens at a neuromuscular junction?
excitatory synaptic transmission
what is the neurotransmitter in a neuromuscular junction?
acetylcholine (ACh)
process occurring at a chemical synapse
depolarisation at the presynaptic terminal –> release of neurotransmitter, diffuses across synaptic cleft, binds to receptors in post-synaptic membrane
–> opening of a channel / current
three features of chemical synapses
specificity - specific neurotransitters have specific effects on postsynaptic membrane
complexity
plasticity - changes in synaptic structure/function with development / age / learning etc
process occurring at a neuromuscular junction
AP down pre-syn terminal
increased pre-syn Ca2+ permeability –> influx
release of neurotransmitter by exocytosis
reacts w/ post-syn receptors
activation of ligand-gated non-selective cationic channels (permeable to BOTH Na+ and K+) –> post-syn End Plate Potentials (EPP) + AP in both directions down muscle fibre
define suprathreshold
always triggers an AP (above threshold)
End Plate Potentials (EPP) always suprathreshold
name two types of chemical synapses
Excitatory
Inhibitory
what is an EPSP
Excitatory Postsynaptic Potential
= DEpolarisation of the postsyn membrane (so less negative)
what is an IPSP
Inhibitory Postsynaptic Potential
= HYPERpolarisation of postsynaptic membrane (so more negative)
neurotransmitters for EPSP
Glutamatic acid (glutamate), ACh
neurotransmitters for IPSP
gamma-aminobutyric acid (GABA) or glycine
ionic mechanism of EPSP
transient opening of ion channels for Na+, K+, sometimes Ca2+
ionic mechanism for IPSP
transient opening of K+ channels
name two classes of neurotransmitters
small molecule / “classical”
neuropeptides / modulators
how do classical neurotransmitters work?
Fast action (milliseconds), direct on postsyn receptors
examples of classical neurotransmitters
Amino acids: Glycine, GABA, glutamate
ACh
Amines: serotonin, noradrenalin, dopamine
how do neuropeptides work?
large molecules, slow (seconds-mins)
usually more diffuse action
indirect (metabotropic) action on postsyn receptors and modulatory action on the effects of other neurotransmitters
what three main factors affect synaptic action?
- type of neurotransmitter
- receptor / channel complex
- synaptic plasticity: amount of NT receptor in postsyn membrane
what are the four main types of glutamate receptors and how do they affect synaptic action?
Three are DIRECTLY gated ion channels:
AMPA receptor: fast response
NMDA receptor: slow
Kainate receptor
Second-messenger mediated: metabotropic glutamate receptor
three paths to neurotransmitter inactivation
- Diffusion - away from synaptic cleft. occurs in all NT to some extent
- Enzymatic degradation - eg. ACh esterase
- Re-uptake + recycling - for amino acids / amines. most common.
why is NT inactivation important?
to allow a new signal to follow rapidly
what must happen to depolarise the initial segment?
each neuron receives thousands of synapses, each producing only very small postsyn potentials
to reach threshold, EPSPs must be ENHANCED
= temporal / spatial SUMMATION at the axon initial segment
how does temporal summation of EPSPs work?
multiple accumulation of stimulus at presynaptic neuron causes the membrane potential to exceed threshold level, generating AP
how does spatial summation of postsynaptic potentials work?
multiple presyn attached to one postsyn neuron
EPSP + EPSP same time, causes large enough increase of MP to cause AP
EPSP + IPSP causes a tiny increase, no threshold reached
what is excitotoxicity?
overactivation of excitatory NT (eg. glutamate), causes Ca2+ accumulation, activates enzymes which kills the cell / neuron damage
what might happen if post-synaptic neurons are lacking GABA receptors?
GABA = inhibitory NT receptors
Post-syn potential increases
more firing of AP –> affects CNS w/ more activity than usual
a possible theory of schizophrenia
name two mechanisms NTs are involved in which gate ion channels
Direct gating
Indirect gating
describe direct gating by NTs
NT binds to receptor / ion channel
causes opening / passing of ions –> de/hyperpolarise membrane, making it more / less likely to generate an AP
typically FAST onset (<1ms), short-lasting effects
describe indirect gating by NTs
NT binds to receptors (eg. G-protein-coupled, known as metabotropic (indirect) receptors)
activates biochemical pathway involving G-prot
–> activates second messengers (eg. cAMP/ IP3)
–> activates protein kinases which phosphorylate specific ion channels causing them to open/close
SLOWER onset, longer lasting (sec-mins)
what is the main excitatory NT in the CNS?
Glutamate (L-glutamic acid)
