Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GABAA receptors mediate the inhibition of somatostatin release in hypothalamic neurones. To study the possible effect of GABA on somatostatin biosynthesis, somatostatin and preprosomatostatin mRNA levels were evaluated after exposure of hypothalamic neurones to muscimol or bicuculline. Muscimol (50 microM) decreased preprosomatostatin mRNA levels, by 25% after 4 h and 30% after 24 h treatment. Bicuculline (50 microM and 100 microM) increased preprosomatostatin mRNA levels by 1.4 and 1.5 fold after 4 h and by 1.3 and 1.7 fold after 24 h treatment. Somatostatin content was not modified after muscimol or bicuculline exposure. Total DNA content, used to control cellular viability, was not modified under any experimental conditions. Our findings suggest that the GABAergic inhibition of mRNA levels could be a consequence of the GABA inhibition of somatostatin release, thus allowing limited changes in peptide steady-state levels.
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PMID:GABA inhibition of somatostatin gene expression in cultured hypothalamic neurones. 809 10

Neuropeptide Y-containing interneurons in the dentate hilar area play an important role in inhibiting the activity of hippocampal circuitry. Hilar cells are often among the first lost in hippocampal epilepsy. As many types of neurons are found in the hilus, we used a new transgenic mouse expressing green fluorescent protein (GFP) in a subset of neurons that colocalized neuropeptide Y (NPY), somatostatin (SST), and GABA for whole-cell, perforated, and cell-attached recording in 240 neurons. As these neurons have not previously been identifiable in live slices, they have not been the focus of physiological analysis. Hilar NPY neurons showed modest spike frequency adaptation, a large 15.6 +/- 1.0 mV afterhyperpolarization, a mean input resistance of 335 +/- 26 M Omega, and were capable of fast-firing. Muscimol-mediated excitatory actions were found in a nominally Ca(2+)-free/high-Mg(2+) bath solution using cell-attached recording. GABA(A) receptor antagonists inhibited half the recorded neurons and blocked burst firing. Gramicidin perforated-patch recording revealed a GABA reversal potential positive to both the resting membrane potential and spike threshold. Together, these data suggest GABA is excitatory to many NPY cells. NPY and SST consistently hyperpolarized and reduced spike frequency in these neurons. No hyperpolarization of NPY on membrane potential was detected in the presence of tetrodotoxin, AP5, CNQX and bicuculline, supporting an indirect effect. Under similar conditions, SST hyperpolarized the cells, suggesting a direct postsynaptic action. Depolarizing actions of GABA and GABA-dependent burst-firing may synchronize a rapid release of GABA, NPY, and SST, leading to pre- and postsynaptic inhibition of excitatory hippocampal circuits.
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PMID:GABA excitation in mouse hilar neuropeptide Y neurons. 1720 5