Thursday, June 22, 2006
Handouts for the neurophysiology lectures
Handouts for my neurophysiology lectures are now available in PDF format at PhysioBytes. You may also want to check out some links related to neurophysiology...
Sunday, January 8, 2006
Lecture handouts for applied CVS physiology lectures
At last... I have posted the handouts for the rest of my CVS lectures on PhysioBytes. I know it has been long overdue...my apologies. These handouts are in the form of PDF files which can be easily printed.
Monday, November 7, 2005
Lecture hand-outs for cardiac muscle physiology
I have put up the hand-outs for the lectures on cardiac muscle physiology at resources page in PhysioBytes. Those of you who could not get the photocopies can download it from there.
Thursday, October 13, 2005
A few objective-type questions...
I have posted some objective-type questions on nerve-muscle physiology at PhysioBytes (click to visit).
Give them a try. Objective -type questions are a great way to review a topic.
Besides, it pays to solve these type of questions - all postgraduate entrance tests are MCQ based.
Give them a try. Objective -type questions are a great way to review a topic.
Besides, it pays to solve these type of questions - all postgraduate entrance tests are MCQ based.
Sunday, September 25, 2005
Answers to the crosswords on membrane physiology
To check out the answers for the crosswords on membrane physiology, visit PhysioBytes (click here)
Saturday, September 24, 2005
Sodium-Potassium pump and action potentials
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Regulation of ACh release at neuromuscular junction
An interesting question was raised a few days ago by a couple of you regarding the neuromuscular junction (NMJ).
Is there any mechanism that regulates the amount of ACh released at the NMJ?
One of the most important factors that determine the amount of ACh release at the NMJ is off course the ECF Ca++ concentration. A fall in ECF [Ca++] will decrease ACh release as the Ca++ influx that occurs during a presynaptic potential is dependent on the out-to-in gradient for Ca++.
Other than that, in many of the central neural synapses there are additional presynaptic mechanisms that influnce neurotransmitter release. Receptors for the very neurotransmitter released at a synapse are often present on the presynaptic membrane. Such receptors are refered to as autoreceptors. The nerutransmitter released during synaptic transmission, in addition to its primary action on the postsynaptic side, also binds to these presynaptic autoreceptors and brings about changes in the presynaptic mechanisms thus influencing further release of neurotransmitters. For instance, consider the synapses in the sympathetic nervous system. Nor-adrenaline is a neurotransmitter employed by sympathetic nerve endings and acts upon different types of nor-adrenergic post synaptic receptors. A particular type of adrenergic receptor, the alpha2 adrenergic receptor, is found on the presynaptic membrane of these nerve terminals. The nor-adrenaline released during sympathetic activation acts on these presynaptic autoreceptors to reduce further release nor-adrenaline. Thus this is an example for a feed back regulation of neurotransmitter release. In some cases such feedback regulation may increase neurotransmitter release rather than decrease it. Such mechanisms are believed to be important in maintaining the sensitivity of the post-synaptic emmbrane to neurotransmitters and regulating the efficiency of synaptic transmission.
Coming back to the NMJ, it was traditionally believed that such feedback regulation of neurtransmitter release does not occur at the NMJ. But recent studies suggest that the release of ACh at NMJs may also be influenced by a feedback effect of ACh on presynaptic autoreceptors which belong to the muscarinic class of cholinergic receptors.It remains to be seen how important such regulation is and whether it has clinical significance.
Is there any mechanism that regulates the amount of ACh released at the NMJ?
One of the most important factors that determine the amount of ACh release at the NMJ is off course the ECF Ca++ concentration. A fall in ECF [Ca++] will decrease ACh release as the Ca++ influx that occurs during a presynaptic potential is dependent on the out-to-in gradient for Ca++.
Other than that, in many of the central neural synapses there are additional presynaptic mechanisms that influnce neurotransmitter release. Receptors for the very neurotransmitter released at a synapse are often present on the presynaptic membrane. Such receptors are refered to as autoreceptors. The nerutransmitter released during synaptic transmission, in addition to its primary action on the postsynaptic side, also binds to these presynaptic autoreceptors and brings about changes in the presynaptic mechanisms thus influencing further release of neurotransmitters. For instance, consider the synapses in the sympathetic nervous system. Nor-adrenaline is a neurotransmitter employed by sympathetic nerve endings and acts upon different types of nor-adrenergic post synaptic receptors. A particular type of adrenergic receptor, the alpha2 adrenergic receptor, is found on the presynaptic membrane of these nerve terminals. The nor-adrenaline released during sympathetic activation acts on these presynaptic autoreceptors to reduce further release nor-adrenaline. Thus this is an example for a feed back regulation of neurotransmitter release. In some cases such feedback regulation may increase neurotransmitter release rather than decrease it. Such mechanisms are believed to be important in maintaining the sensitivity of the post-synaptic emmbrane to neurotransmitters and regulating the efficiency of synaptic transmission.
Coming back to the NMJ, it was traditionally believed that such feedback regulation of neurtransmitter release does not occur at the NMJ. But recent studies suggest that the release of ACh at NMJs may also be influenced by a feedback effect of ACh on presynaptic autoreceptors which belong to the muscarinic class of cholinergic receptors.It remains to be seen how important such regulation is and whether it has clinical significance.
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