Synaptic Transmission Flashcards
What are the 4 criteria for chemical neurotransmitters?
1 present in presynaptic terminal
2 releaed in response to stimulation - must be Ca dependent.
3 specific receptors for the neurotransmitter must be present on the postsynaptic cell
4 mechanism to inactivate neurotransmitter must be present (reuptake, breakdown etc.)
What do electrical synapses allow for?
Speed and synchrony. Gap junctions allow for the passage of ions between adjacent cells. Gap junctions connect glial cells. This does not seem to allow plasticity or learning.
What do chemical synapses allow for?
Directionality, amplification, potential for EPSP or IPSP, plasticity/ remodeling, integration in space and time (spatial/ temporal summation)
What does a rise in intracellular Ca do?
It is necessary and sufficient for neurotransmitter release.
What is facilitation? What causes it? Is it presynaptic or postsynaptic?
It is a form of short-term synaptic plasticity that results from prolonged elevation of presynaptic Ca. Facilitation is a PRESYNAPTIC event while summation is a POSTsynaptic event. These are very different from each other. Facilitation is driven by left over Ca that can’t be pumped out of the cell fast enough. It can alter postsynaptic events.
When does synaptic facilitation occur?
When two or more action potentials invade the presynaptic terminal within a few milliseconds of each other. Ca builds up and allows more NT to be released.
What are clear core vesicles?
small molecule NTs (amino acids). They are small vesicles synthesized in presynaptic nerve terminals.
What are dense core vesicles?
Neuropeptides. large vesicles synthesized in cell body and transported to the nerve terminal. Vesicular release often requires high frequency presynaptic activation.
What does high frequency signals at the presynaptic terminal cause?
A more generalized increase in Ca causing release of both types of vesicle (dense and clear). The postsynaptic target cell typically contains an electron dense area with many receptors called the postsynaptic density (PSD). They are aligned with active zones to promote efficiency across the synaptic cleft.
Experiments observing the NMJ found that ACh release leads to miniature end-plate potentials of the same size, what is this called?
Quanta. They are discrete packed of ACh each producing a so called MEPP. The fixed size of MEPPs is consistent with quantal release. Each vesicle contains ~10,000 ACh molecules.
Dendrites are said to be long and leaky, what does this imply about them?
Before EPSPs can reach the cell soma a large amount of the potential is lost by leakage through the membrane, a process called decremental conduction. Simultaneous firing of many synapses raises the summated potential to threshold for excitation and elicits an AP.
Discuss glutamate and its receptors in the CNS?
Glutamate is the major excitatory NT in the CNS, it binds to ionotropic and metabotropic receptors. Glutamate receptors are diverse and dynamic producing complex cell-specific responses that exhibit plasticity.
Glutamate binds to AMPA and NMDA receptors, describe how these receptors work:
EPSPs are mediated by a rapid component mediated by AMPA a slow component mediated by an NMDA receptor channel. NMDA receptors require glycine, glutamate a higher resting potential to fire compared to AMPA. AMPA will fire upon binding right away.
Discuss GABA in the CNS:
It is the major inhibitory transmitter and binds to ionotropic receptors that can be modulated.
What can inhibitory synapses allow?
Interposition of an inhibitory synapse in a neuronal circuit can prevent overactivity in the CNS, or underlie “reciprocal inhibition” as seen in the control of antagonistic muscles in a reflex. Stimulation of a presynaptic neuron releasing GABA can interfere with the generation of APs in the postsynaptic target neuron
