Berkeley Review Bology Chpt. 1 Questions! Yay!

[Filius]

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So, a few things that have come up in my review.


1) The text mentions that inhibitory post-synaptic potentials increase membrane permeability to Cl- and K+, which apparently makes the resting potential more negative by allowing K+ to escape and Cl- to enter in. However, it also mentions that extracellular [Cl-] is around 130 mM, and intracellular [Cl-] ranges from 5 to 40 mM. Plugging this into the Nernst equation (i.e.: -60log(130/40)) seems to give a resting potential of -85 mV to -31 mV. Thus, for a resting potential of ~-80 mV, I'd most often predict that Cl- ions would rush *out* of the cell upon an increase in PCl, causing an EPSP rather than an ISPS. What's going on here?

2) I find the text very unclear about what happens between dendrites and the axon hillock -- given that there's no action potential, am I to assume that it's just a sea of ions, with the electrochemical potentials generated in each dendrite mixing in the cell body, the output of which is summed at the hillock and converted into more action potentials?

3) I understand that pre-ganglionic neurons start in the CNS, and end in a ganglion, and post-synaptic neurons start in a ganglion, and end in the target organ. But what about neurons that start and end in non-CNS neurons? For instance, I'm under the impression that the columns of ganglion outside the spinal cord are not part of the CNS. But some neurons start here, and end in a second ganglion closer to the target region -- are these still considered pre-ganglionic neurons, though they originate in a ganglion? And, most importantly, do they release ACh or norepinephrine?

4) Do muscle fibres have normal endoplasmic reticulums in addition to sarcoplasmic reticulum? Or does the latter replace the former?

5) Axons generally seem to be defined as the "appendage" that carries action potentials away from the cell body. However, the extension originating from the Pacinian corpuscle -- is the cell body inside the corpuscle itself, or do axons in sensory neurons not necessarily conduct signals away from he cell body?


Thanks! 🙂

 

[hvairline]

1)When the chloride channels pop open in an IPSP Chlorine atoms will move in and out. Even though the electrical gradient does not favor Cl entry the concentration gradient does. Therefore due to a large concentration gradeint chlorine will move in causing membrane polarization up to the point where there is an equilibrium between the forces favoring Cl entry(concentration gradient) and the forces favoring Cl exit(electrical gradient).
2)Summation occurs in both the dendrites and axon hillock. Whether or not an action potential will fire depends on how positive the membrane of the axon hillock becomes. This depends on the mixing of the ions caused by the multiple signals received at the dendrites(integration).
Hope this helps!

 

[Filius]

Ah! Many thanks. But, for the first point, with the Chlorine ions -- I realize that these are the forces in play, but that's the purpose of the Nernst equation, which tells us which of the two forces are dominant. Thus, if the predicted *electro*chemical potential at in vivo concentrations is less negative than the actual electrical potential in the cell, would we not predict that electrical forces pushing ions out of the cell would be more powerful than diffusion pushing the ions inside?

Thus, opening Cl-channels would usually have a slight depolarizing effect, at least until the potential got closer to zero.

 

[Filius]

Bump!