Calcitonin gene-related peptide potentiates synaptic responses at developing neuromuscular junction

Article Abstract:

Calcitonin gene-related peptide (CGRP), a neuropeptide in presynaptic motor nerve terminals, promotes postsynaptic reaction in maturing neuromuscular networks by extending the bursting period of embryonic ACh channels. The effect of CRGP on ACh channels is simulated by dibutyryl-cyclic AMP and cAMP-dependent protein kinase, obstructed by peptide inhibitor PKA. Postsynaptic inhibitions by PKA narrowed the amplitude and decay time of spontaneous synaptic current. Prolonging the burst duration raises postsynaptic activity at the bginning of the development stage, when time resolution is not too crucial.

Synapses, Neural conduction

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Regulation of synaptic responses to high-frequency stimulation and LTP by neurotrophins in the hippocampus

Article Abstract:

The brain-derived neurotrophic factor (BDNF) stimulates long-term potentiation induced by theta-burst (LTP(sub T)) by increasing the capability of the hippocampal synapses to respond to high-frequency stimulations. Hippocampal slices from postnatal day 12-13 are unable to respond to tetanic stimulation in the absence of BDNF. In the presence of BDNF, the slices show LTP(sub T). A TrkB-IgG fusion protein that removes BDNF suppresses synaptic responses to tetanus and LTP(sub T) level.

Hippocampus (Brain), Neural stimulation

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Nitric oxide mediates activity-dependent synaptic suppression at developing neuromuscular synapses

Article Abstract:

Nitric oxide (NO) acts as a retrograde signal in the activity-dependent synaptic inhibition at neuromuscular synapses. Spontaneous and invoked synaptic currents are blocked by NO donors and activators of the cyclic GMP channel. NO released from a postsynaptic myocyte induces synaptic suppression. The NO-binding protein hemoglobin and NO synthase inhibitors avert the synaptic suppression triggered by postsynpatic depolarization.

Physiological aspects, Nitric oxide

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