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Lecture 5

Dr. Sharif lecture 5.pdf

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PHGY 311
Reza Sharif

Dr. Sharif lecture 5 Saturday, December 01, 2012 5:42 PM Slide 8: - Relevance o phasic firing...tday will discuss mechanism 9: - Shift toward hyopertonic env...VP release to bring back to set point 10: - 3 regulatory mechanisms that increase firing rate from lect 1:taurine release from astrocytes etc... - If VP neurons were to increases there firing rate and fire continuously: this leads to a fatigue of the release process ○ You get a decrease in the amount of VP released very quickly even though the firing is maintained… 11: - No VP=no antidioreses 12: - Cells transition from irr firing to phasic firing to avoid secretory fatigue - As osmolarity around the cell increases, transition from irr to phasic, the mean firing rae increases and the frequency within the burst increases and the duration of the burst also increases 14: - Was not know if the same neuron was doing all these pattern transitions, found out yes… 15: - 2 neurons firing at the same frequ but diff pattern: one has clusters phasic firing other has a transient irr firng..the one with phasic firing releases a larger amount of VP in the blood stream...moreca entering the terminal thus more vesicles fuse… 17: - Mechanism responsible for secretoryfatigue: - Accumulation of K outside the neuron...bc of the outward movement of k during the repolarizing phase of the AP, and if u increase the frequ, the more the K outside Initially this would change the concentration gradient of K-less driving force for them to exit the cell...more + ions inside the cell means more depolarization (this means increase in hormone release also)..but then the amount of VP released starts decreasing...WHY? 19: - Initially though: if u depolarize the axonal memb. Enough level u get inactivationof V-gated Na channels...prevent the AP transmission - Other possibility, the nerve terminals cannot depolarize enough to get Ca influx.. - Stimulated the neural stalk and recorded current in the nerve terminal - Saw that applying trains of stimuli on stalk to get AP to generate, they could record AP in the nerve terminal. - But if they increased the stimulation frequency, they saw spike broadening and decrease in spike amp… - 1st they saw a memb depolarization which is that axonal spike, then u get the spike that occurs in the nerve terminal ○ Depolarization in the axon doesn’t change in from the 1 to the last ○ But the nerve terminal depolarization, the amp to the spike decreases until u start getting failures ○ As you increase the firing rate, u get more failures in thenerve terminal not the axon 20: - How does the rise in K external prevent the AP form entering the nerve terminal?? - Turns out: the terminals express a type of v-gated Na channel that is diff from the one on the axon - Thes channels transit into the inactive state with just a slight depolarization in the membrane ○ The slight depolarization U would get by increasing K outside would be enough to inactivate these channels ○ So when AP reaches the terminal these channels are inactivated and cannot it cannot propagate and drops in amp.. ○ These channels are not compartmentalized to the terminal...u have some just before the terminal Then, u don’t have the signals for
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