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Modulation of spontaneous quantal release of neurotransmitters in the hippocampus.
Presynaptic action potentials trigger the exocytosis of neurotransmitters. However, even in the absence of depolarisation-dependent Ca2+ entry nearby release sites, spontaneous vesicular release still occurs. Even though this happens at low rate, such spontaneous release may play a trophic role in maintaining the shape of dendritic structures. Like evoked responses, action potential-independent release is subject to modulation. This review describes some of the regulatory factors that rapidly and presynaptically regulate the ongoing Ca2+-independent release of neurotransmitters in the hippocampus. For instance, the electrical activity of the nerve ending, neurotransmitters, hypertonic solutions, neurotoxins, polycations, neurotrophic factors, immunoglobulins, cyclothiazide and psychotropic drugs can all modify the rate of spontaneous release. This can be achieved through various mechanisms that can be Ca2+-dependent or Ca2+-independent, protein kinase-dependent or independent. Since action potential-independent release contributes to the maintenance of dendritic structures, neuromodulators are likely to influence the density and/or length of dendritic spines, which in turn may modulate information processing in the central nervous system (CNS).[1]References
- Modulation of spontaneous quantal release of neurotransmitters in the hippocampus. Bouron, A. Prog. Neurobiol. (2001) [Pubmed]
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