Module 9 - Lecture 6 - CNS Synapses, Transmitters, Integration Flashcards
Understand the post-synaptic potential.
What is the difference between inhibitory and excitatory (ie their change on post-synaptic potential)?
- Excitatory (EPSP) pushes post-synaptic cell positively towards initiating an AP
- Inhibitory (IPSP) pushes the post-synaptic cell negatively away from threshold to negate the potential of an AP
Understand the post-synaptic potential. What is the ion most commonly conducted for these changes:
- EPSP
- IPSP
- Na+ (sodium) for an EPSP = Na+ is positively charged and is let into the cell to drive the potential positively
- Cl- (chlorine) for an IPSP = Cl- is negatively charged and is let into the cell to drive the potential negatively
What are the important features of the following common CNS neurotransmitters (what Ions are involved, what receptors open, are they open a long or short time, do they depolarize or hyperpolarize)?
- GLUTAMATE - AMPA receptor
Glutamate: main excitatory NT in the CNS
AMPA Receptor
Ions involved: NA+
Glutamate binds to Na+ ion pore in the membrane, which opens the pore allowing for Na+ to flow into the post-synaptic cell.
Time open: short
Depolarize/hyperpolarize: depolarize very quickly
What are the important features of the following common CNS neurotransmitters (what Ions are involved, what receptors open, are they open a long or short time, do they depolarize or hyperpolarize)?
- GLUTAMATE - NMDA Receptor
Ions involved: NA+, CA2+, Mg2+ (to an extent)
Glutamate binds to ion pore in the membrane, BUT big fat Mg2+ is blocking the channel. REceptor needs membrane to be depolarized so it can push out Mg2+, thus allowing Na+ and Ca2+ to enter the post-synaptic cell.
Time open: long
Depolarize/hyperpolarize: hyperpolarize
What are the important features of the following common CNS neurotransmitters (what Ions are involved, what receptors open, are they open a long or short time, do they depolarize or hyperpolarize)?
- GABA
GABA: Main inhibitory NT in the CNS
Ions involved: Cl-
GABA binds to pore, allowing for Cl- to flow into post-synaptic cell
Time open: short
Depolarize/hyperpolarize: hyperpolarize
Compare and contrast removal of the neurotransmitter vs acetylcholine.
ACh removal breakdown by enzymes in cleft, diffusion in cleft, reuptake into the cell.
NT removal Reuptake into glial cells or presynaptic neuron via transporters (EAATs) in cellular membranes to be recycled (glutamate) -OR- reuptake into glial cells or presynaptic neuron via transporters (EAATs) and then broke down by mitochondrial enzymes. By-products can then be recycled and used to make new GABA (GABA)
Compare and contrast the difference between a ligand-gated, voltage-gated, and ligand/ voltage gated ion channels.
- The channel types
- Their mechanism
What is the general concepts of G-protein coupled (Metabotropic) receptors. Compare and contrast them with ligand-gated ion channels in “speed”, duration and effect.
Speed: can take longer than a ligand-gated because of their physiology as a secondary messenger system. It can take longer for the secondary messenger signal to travel and act on a separate protein than if the protein channel the ligand was acting on was the actual channel that was going to be open.
Duration: GPCR’s can have longer lasting effects on the cellular environment because they are more diverse in mechanism that ligand-gated ion channels and also can contribute to a ‘amplifying’ effect (IE: a little NT goes a long way compared to a ligand-gated channel) on metabolic processes within its cellular target.
Effects: Open/closing/modifying other protein channels as a co-agonist, turn on/off biochemical pathways, turn on/off specific genes within the cell
What is the principles of summation for post-synaptic potentials? What determines the size of a single post-synaptic potential?
The influx of either a positively charged ion (EPSP) or negatively charged ion (IPSP) into the post-synaptic cell. One instance of either of these scenarios happening might not be of enough electrical magnitude to trigger/inhibit an AP in the post-synaptic cell, however. This is because one might not be enough ‘firepower’ to bring the post-synaptic neuron up to threshold
Why does temporal dispersion matters for the axon hillock?
The dendrites of the post-synaptic neuron cannot produce an AP (there’s no voltage gated channels there), only on its axon, starting at the axon hillock. EPSP/IPSP’s are also passive and decrease in magnitude as the propagate along the dendrites. They are able to reach the axon with enough summation (IE: multiple synaptic inputs add up in the dendrites, which then once they hit the axon hillock, they can trigger a response.) The only holdup to this is temporal dispersion, which is where these EPSP/IPSP’s don’t arrive at the axon hillock all at once and thus they won’t have enough summation to trigger an AP. This is known as phase cancellation.
What is the difference between convergent and divergent neuron networks and the implication?
Convergence
The # of inputs to a singular neuron
If high, it integrates the information from many neurons to perform a single action
Divergence
The # of targets from a single neuron
If high, has a wide sweeping action based on a sole signal
What is the clinical case of multiple sclerosis and how it impacts summation?
MS demyelination in the CNS = Without myelin, summated EPSP’s arriving at a target in-sync are much more difficult. This results in the inability to produce an AP because of the increased temporal dispersion. This leads to a lack of interpretation of a stimulus in the CNS.
