Somatostatin depresses excitability in neurons of the solitary tract complex through hyperpolarization and augmentation of IM, a non-inactivating voltage-dependent outward current blocked by muscarinic agonists.
AUTOR(ES)
Jacquin, T
RESUMO
The synaptic function of somatostatin-containing fibers in the nervous system is controversial. Therefore, we used a slice preparation of the rat brain stem to test the electrophysiological effects of prosomatostatin-derived peptides on neurons of the solitary tract complex, which contains an abundance of somatostatin-containing fibers and cell bodies. Superfusion of both somatostatin-14 and somatostatin-28 (the precursor for somatostatin-14), but not somatostatin-28-(1-12) or -(1-10), predominantly inhibited spontaneous spike and subthreshold (probably synaptic) activity. In intracellular recordings, somatostatin-14 and -28 hyperpolarized most neurons in association with a slight (10-35%) but reproducible decrease in input resistance. These hyperpolarizing responses were augmented in depolarized cells and persisted in cells in which spontaneous inhibitory postsynaptic potentials became depolarizing after Cl- injection. These data suggest that somatostatin receptors regulate a K+ conductance. In voltage-clamp studies, somatostatin-28 and -14 induced a steady outward current and augmented the voltage-dependent, nonactivating outward K+ conductance (IM) shown to be blocked by activation of muscarinic cholinergic receptors. These results suggest (i) that somatostatin-containing elements in the solitary tract complex play an inhibitory role through the activation of postsynaptic permeability to potassium ions and (ii) that the same ion channel type may be coregulated by two neurotransmitter candidates, somatostatin and acetylcholine, through a reciprocal control mechanism.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=279674Documentos Relacionados
- A non-inactivating K+ current sensitive to muscarinic receptor activation in rat cultured cerebellar granule neurons.
- Inactivating and non-inactivating dihydropyridine-sensitive Ca2+ channels in mouse cerebellar granule cells.
- Contribution of a non-inactivating potassium current to the resting membrane potential of fusion-competent human myoblasts.
- Muscarinic enhancement of the voltage-dependent calcium current in an identified snail neuron.
- Alpha 1-adrenergic agonists selectively suppress voltage-dependent K+ current in rat ventricular myocytes.