Question

Based on your excellent understanding and extensive knowledge of chemical synaptic transmission,

EXPLAIN what would happen in response in each hypothetical situation below….Assume you have an experimental set-up with two neurons connected via a chemical synapse – Neuron A is presynaptic and Neuron B is postsynaptic. Also assume that there is a stimulating electrode in Neuron A that brings it to threshold and produces an EPSP in Neuron B. In your answers, include all relevant events between this stimulus and response.

(1) First, state which specific mechanism(s)/event(s) involved in chemical synaptic transmission WOULD be affected, e.g., what would be stopped, disrupted, enhanced, diminished, etc,

(2) Second, state which specific mechanism(s)/event(s) involved in chemical synaptic transmission WOULD NOT be affected, i.e., what would happen as usual, e.g., still have APs, neurotransmitter release, etc, etc.

(3) Third, explain WHY these mechanism(s)/event(s) would be affected and/or would not be affected, i.e., explain your justification for your answers to (1) and (2).

You may combine any or all of these three parts as long as you clearly address each one.

(E) if rab3 proteins are inhibited or broken down, then…..

(F) if synaptotagmin is inhibited or broken down, then…..

(G) if external K+ concentration becomes equal to internal K+, then……

(H) if all extracellular Na+ is removed, then……

Answer 1

1. As the nuron A is being stimulated and brought to action potential with the help of an electrode, the gates which are responsible for transmission of nerve impulse ( situated at nodes of ranvier in case of medulated nurons and throughout the axon in case of nonmedulated nurons) are not doing any work ( that is the ion channels are not pumping in and out ions and creating the charge imbalance that they generally do to create the action potential), here the charge imbalance is beng created artifially. Second, the Channels which are responsible for bringinng the nuron back to resting potenctial will open in response to voltage, and will cause further imblence in ion concentration inside the nuron.

2. In this senario, some pathways will continue to function as usual, For example, the pathways responsible for voltage responsive Traffcing, Transport and fusion of Nurotransmitter filled vesicles to the synaptc membrane and their release in the synyaptic space will occur naturally.

opening of the ligand gated channels ( Nurotransmitters as Ligands) present in Nuron B and transmission of the action potential to Nuron B will happen naturally.

3. RAB-3 is a GTPase protein responsible for calcium mediated exocytosis of nurotransmitters to the synaptic space. Ifthe RAB-3 protein is mutated then even if there is action potential at Nuron A, ther nurotransmitters will not get released in the synaptic space and the ligand gated channels at Nuron B will not open and the Action potential will not be transmitted.

4. Synaptotagmins are Specific membrane trafficking proteins that are responsible for transport of nurotransmitter filled vesicles from ER and Golgi bodies to the membrane, it is also proposed to act as a sensor for Ca ion concentration and plays a role in release of nurotransmitters. So mutation of this protein will also mean the non transmissionn of nerve impulse.

5 & 6. The Na-K ATPase Protein plays a major role in menteinng the resting potential of the nurons. They pump out 3 molecules of Na+ from Inside to outside, while pumping in 2 molecules of K+. As a result a total +1 charge is transported out, resulting in a 'Inside -ve' potential.

if the K+ concentration Inside and Outside becomes the same, that will result in the total collapse of resting potential. and when nerve impulse will come and the gates open, there will be no exchange of ions thus no action potential will be propagated.

Same will happen In case if extracellular Na+ gets delepeted, No action potential can get transmitted.