Physiological Basis of Behavior

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Eg. K ions channels open, K flows out an makes the potential membrane even more negative (called hyperpolarization, as we are making the polarized state even more severe).

-IPSP

*also get IPSP by opening the chloride channels (will only happen, if the membrane is already polarized due to other channels in the last 8 milliseconds because when membrane is at rest, outflow or inflow of chloride doesn’t affect the balance).

^if EPSP & ISP happens simultaneously, neurons have to integrate it all and decide and tally up the net effect- excitatory, inhibitory or other; then check the magnitude, if it is high enough, then fire the neurotransmitter or no.

EPSP and IPSPs

Image 1: depolarization and then return

Image 2:hyperpolarization first and then return

3: already EPSP is happening and the effect of simultaneous IPSP, EPSP reduces and results in small blip. Would’ve had a bigger effect, if it were closer to the synapse.

Amplify the impulse effect

- Spatial Summation

- We can have 3 different presynaptic impulses in a neuron, each producing a similar ESP arriving simultaneously, adding on top of one another. Much greater depolarization towards a more positive value from the resting value.

- Similar for IPSP, just invert the graph.

- Temporal Summation (last from 5 to 10 milliseconds, an impulse).

- Firing impulses after a particular time, one after another. Fastest a neuron can deliver nerve impulses is 1 second. So one after another, to amplify.

- Similar for IPSP, just invert graph.

Next Up: Unique nerve impulses in living being, arising from cell body.

An electrical impulse once initiated, never weakens, never dies, and travels along the axon. Speed ranges from 1m/s to 100m/s, longer the neuron the faster the impulse, the more myelin sheath the stronger impulse.

*Ionic composition of extracellular fluid-glial cells controls it, otherwise seizure disorders.

Class 4:

Na (sodium) is under pressure to enter the cell in the resting situation, and K is under pressure to exit.

If membrane permeability to NA increases, it will rush in and depolarization will occur.

If membrane permeability to k increases, it will rush out and hyperpolarization would occur.

IPSP and UPSP happen simultaneously.

The electric nerve impulse is initiated in the Axon Hillock (spike trigger zone, initial segment). In the axon there are voltage affected ion channels.

We are looking at the functions of a gated ion channels that can be opened by the electrical potential across the membrane due to action potential. Threshold amount (15mV).

When the action potential is initiated, and net effect is such that the membrane potential is less than 15mV, it will fire off the signal and it goes to the terminal endings. If initiated, it will end at the point of termination (it doesn’t die but HAS to be regenerated along the way).

Slide: Trigger Zone

*Generated action potential (initiation).

There is decay of passively spreading impulse due to cytoplasm as it doesn’t conduct electricity in the membrane. The job of the input (and the EPSP that it produces) is to depolarize the synaptic terminal by 15mV. If that doesn’t happen, there will be no signal fired. EPSP moved membrane potential from -70mV to nearly -40mV, further, It created depolarization but it diminishes along the cell body. Once at the trigger zone, it shows that it only till -60mV, due to which the action potential is decaying. So no depolarization of axonal membrane, it dies.

Next slide:

EPSP is stronger and there is still depolarization until the trigger zone. So action potential goes to all synapses.

(in reality, one cannot do this, summation of initiations)

Slide: Action Potential Stages

Describes the whole process.

*The sudden increases in membrane potential happens in milliseconds and the entire action potential happens within milliseconds.

Why is there is a rise & decay, why is there reversal of potential?

*at -55mV, there are Na channels that open up and NA comes rushing into the cells until it has diminished and has no reason to come in any more (membrane potential has reached or is very close to Enerst’s potential). [there is membrane potential reversal in between].

*second population, slowly opening up as membrane potential is been rising up; at the peak when Na channels are coming down, the K channels are opening up. K is under 2 gradients (usual concentration gradient and briefly under electro positivity), to which K responds and rushes out of the cell until it has no reason to do.

K is under so longer to move inside the cell if the temperate is

Everything comes back to normal, K-NA pump,

*when Na is reducing after the peak for about 3/10 of a millisecond or 1 millisecond; the channels close and do not open (sodium inactivation), no matter how excitatory the impulse is. This is the refractory period, when it is impossible to generate a signal.

After this there are about 1-2 milliseconds, when it is harder to bring it to threshold as K is entering now (relative excitatory period). It would need abut 20mV, instead of 15mV.

*Time consuming process involved in leading the potential from point of origin to termination point (hillock to terminal ending).

Slide: Notebook style, graphs (right side, domino effect)

We are saying that action potential will be regenerated by conversion, passively spreading current that regenerates by passing trigger zones.

Side: Action

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