One why that nociception (the sensation of pain) is modulated is by presynaptic
ID: 84993 • Letter: O
Question
One why that nociception (the sensation of pain) is modulated is by presynaptic inhibition of transmitter release from the nociceptive sensory neuton onto its postsynaptic target that takes information to the central nervous system. Endogenous opioids (endorphins) are released onto the presynaptic terminal of the nociceptive sensory neuron. If endorphins eventually result in an increased probability of Ca^2+ channel closure, what will happento the amount of glutamate release from the sensory neuron? Increase or decrease ? Why ? What would happen to ca^2+ channels if a G protein were activated in the absence of endorphin release? If endorphin release happens at the same time as glutamate release from the sensory neuron, would endorphin result in synaptic facilitation or depression? Why?Explanation / Answer
Answer 26 a. Decrease in amount of glutamate
Justification: In normal conditions, activation of N-methyl-D-aspartate (NMDA) receptor results in opening of calcium channel which causes glutamate release from sensory neuron. When Endorphin causes Calcium channel closure, glutamate release from sensory neuron will stop resulting in decrease in amount of glutamate.
Answer 26b. Closure of calcium channels.
In neuronal cell membranes, G proteins direct certain calcium ion channels. In particular, several high-threshold, slowly inactivating calcium channels in neurons are found to be regulated by G proteins. The activation of G proteins has been shown to cause rapid closing of voltage-dependent Calcium channels, which causes difficulties in the firing of action potentials. G proteins short circuit the second-messenger pathway and gate the ion channels directly.
Answer 26c. Glutamate release triggers the opening of calcium gated channels while endorphin causes Calcium channel closure. Hence, calcium ions will remain depress
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