Luteinizing hormone-releasing hormone (LHRH) neurons: mechanism of pulsatile LHRH release.

Many types of neurons and glia exhibit oscillatory changes in membrane potentials and cytoplasmic Ca2+ concentrations. In neurons and neuroendocrine cells an elevation of intracellular Ca2+ concentration is associated with neurosecretion. Since both oscillatory membrane potentials and intracellular Ca2+ oscillations have been described in primary LHRH neurons and in GT1 cells, it is evident that an endogenous pulse-generator/oscillator is present in the LHRH neuron in vitro. The hourly rhythms of LHRH neurosecretion appear to be the synchronization of a population of LHRH neurons. How a network of LHRH neurons synchronizes their activity, i.e., whether by the result of synaptic mechanisms or electrical coupling through gap junctions or through a diffusible substance(s), remains to be clarified. Even though LHRH neurons themselves possess an endogenous pulse-generating mechanism, they may be controlled by other neuronal and nonneuronal elements in vivo. NE, NPY, glutamate, and GABA are neurotransmitters possibly controlling pulsatile LHRH release, and NO, cAMP, and ATP may be diffusible substances involved in pulsatile LHRH release without synaptic input. Although synaptic inputs to the perikarya of LHRH neurons could control the activity of LHRH neurons, a line of evidence suggests that direct neuronal and nonneuronal inputs, especially those from astrocytes to LHRH neuroterminals, appear to be more important for pusatile LHRH release.