I have some questions for basic medical physiology：
1. What's the ture reason for presynaptic inhibition from the 2 statements as follows
1) increase the chlorine ion permeability of presynaptic excitory ending tomake it depolarized
2) accumulation of potassium ion in ECF surrounding the excitory ending to produce partial depolarization of excitory ending.
2. Can you explain the formula:
osmolarity of blood = 2[Na+](meq/l)+0.055[Glu](mg/dl)+0.36[bUN](mg/dl)
and what's the meaning of [bUN]?
3 Can you explain the formula:
specific activity of sodium = radioactive sodium24 (counts/min/l) divided by the sum of Na24 and nonradioactive Na (meq/l)
and why there is a "min" unit in formula?
4 Could u explain:
"Evidence that a substance is a transmitter includes its uneven distribution in nervous system and a parallel distribution of enzymes responsible for substance's synthesis and catabolism"
5 In the synthesis of catecholamine:
Is tetrahydrobiopterin a cofactor for tyrosine hydroxylase, for phenylalanine hydroxylase, or for both of them?
6 In the presynaptic inhibition, how the mechanism works? In a book it said that the neurons producing presynaptic inhibition discharge to reduce the membrane potential of the excitory endings to a level closer to the firing level makes the endings more excitable, but it also reduces the size of the action potential reaching the ending "by an amount equal to the amount of depolarization". Consequently less mediator is released for reduced action potential.
can u tell me if the action reduction here means the frequency of it decrease? and how it is related to a higher firing level?
7 more detail about accommodation of the sensory nerve fiber to the generator potential, except the "slip back from distortion"
8 In the book it said: intensity discrimination of sensation R = K times S in the power of A. In next paragragh: current evidence indicates that in the central nervous system the relation between stimulus and sensation is linear... why?
Thannnnnnk you ！
