Message transmission between neurons takes place through the release of chemical substances which, inter-acting with specific receptors, behave as neurotransmitters; they are termed classical or putative when they repectively meet fully or partially a set of recognised criteria. Concomitantly with neurotransmitter release, a wide spectrum of peptides is released. As demonstrated for neurotransmitters, such peptides are synthesized and stored within neurons and later released, so they are denominated neuropeptides.
Oxidative metabolism is very active in brain, mostly required to maintain cellular Na+/ K+ gradients involved in nerve impulse propagation, in neurotransmitter release and in cation hemeostasis. The sodium pump or Na+, K+-ATPase, its enzymatic version, regulates K+ entry with Na+ exit from neurons, and therefore is responsible for Na+ / K+ equilibrium maintenance through neuronal membranes. Thus, it is essential in the normal cell cycle, for preventing cell membrane osmotic rupture as well as for nervous system differentiation.
Sodium pump modulation by neurotransmitters has been reviewed elsewhere and the purpose of the present article was to summarize available evidence on Na+, K+-ATPase modulation by neuropeptides.
Experimental approaches employed to study Na+, K+-ATPase modulation by neuropeptides are dealt with and the effect of neurotensin, calcitonin, insulin, angiotensin system peptides, vasopressin, amyloid ß- peptide and other peptides reviewed. Findings indicating the invlovement of Na+, K+-ATPase in neuropeptide release, as well as the ability of some peptides either to protect enzymatic activity or else to exert ouabain-like properties were included.
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