University:
Binghamton University
Course:
BIOL 313 | Cellular Neurobiology
Academic year:

2024
Views:

262

Pages:

2
Author:

CrystalMintah

October 9th, 2024 How neurotransmitters are released from the presynaptic side Half a second delay for chemical release in the synapse. Experiments done to show Na+ and K+ are not directly responsible for action potentials In the 1960s applied Tx to a neurotransmitter junction. If only a very tiny amount of TTX is applied not all the sodium channels are blocked so you end up with a lower amplitude action potential. This led to a lower amplitude PSP. If you apply a high dose of TTX there is no PSP. But even if all Na+ channels are blocked, if a depolarization is applied to the presynaptic terminal, you will get a PSP. (Sodium is usually responsible for depolarization) This tells us that it is not the Na+ itself but the depolarization it brings to the terminal that causes neurotransmitter release. It even works if TTX and TEA are applied then the terminal is artificially depolarized in the electrode. So: NA+ and K+ are not directly responsible The ion associated directly with neurotransmitter release is calcium 1.) When the presynaptic terminal depolarizes, voltage-gated calcium channels open 2.) Calcium has a strong driving force to enter the terminal 3.) Calcium concentration in the terminals can increase up to 200x when an action potential reaches it. Experiments done to show calcium is responsible for the release of vesicles To show calcium is what is needed for neurotransmitter release, put “caged” calcium into the terminal to bypass the voltage-gated calcium channel. This example uses entropion which holds calcium Until you apply UV light, then it releases the caged calcium If you reduce the amount of calcium extracellularly by replacing it with magnesium (which does not have the same effects as CA++ but maintains the osmotic balance of the saline) Then stimulate the presynaptic terminal electrically you will find that you get: similar amplitude PSPs in the postsynaptic cell The lower the calcium the lower the PSPs When calcium levels get very low you find the PSP amplitude declines in steps and eventually, there is a minimal size for them-minimum or nothing These are miniature end plates potential or “minis” A Mini - the PSP you got for the release of 1 vesicle of Ach this preparation, sometimes referred to as quanta or called this quantal release So, as far as we see: the postsynaptic cell depolarizes when the action potential reaches sit, this opens voltage-gated calcium channels which allow an influx of Ca ++........... Which causes vesicles of neurotransmitters to be released each vesicle containing molecules of neurotransmitters. The terminal contains 2 groups of vesicles 1.) Those in the storage pool are anchored to the cytoskeleton 2.) Those in the releasable pool are available for docking to the terminal membrane and releasing contents into the cleft Now storage pool vesicles can be added to the releasable pool by activating a protein kinase that cuts the protein that holds the vesicles to the cytoskeleton - Synapsin is this protein - The protein kinase that releases synapsin's hold on the vesicle is captivated by calcium Oce a vesicle is in the releabsable pool - It needs to “dock” at the terminal , membrane then open to the synaptic cleft to release it;’s contents. d