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)

Recent findings indicate that excitatory amino acids (EAAs) can modulate growth hormone (GH) secretion in several mammalian species in vivo and in vitro. In this study, we examined the effects of EAA receptor antagonists [N-methyl-D,L-aspartate (NMDA), kainic acid, L-glutamate] on GH secretion by the reverse hemolytic plaque assay (RHPA). Anterior pituitary cells of adult male Sprague-Dawley rats were enzymatically dispersed and subjected to RHPA. EAA receptor agonists increased the mean plaque area in a dose-dependent manner: the maximal increase was observed at 10 microM and increased the fraction of somatotrophs forming large plaques. NMDA (10 microM) did not increase the mean plaque area in the presence of the NMDA receptor antagonists 10 microM AP-7 and 10 microM MK-801. Coincubation of kainic acid with the non-NMDA receptor antagonist CNQX blocked the kainic-acid-stimulated increase in GH secretion. The addition of MK-801, AP-7 or CNQX to glutamate caused a partial reduction of the mean plaque area. Ten micromoles per liter glutamate with 10 nM GH-releasing hormone (GHRH) produced an additive effect on GHRH-induced GH release. Somatostatin suppressed the stimulatory action of glutamate. We speculate that glutamate plays a role in the regulation of GH secretion.
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PMID:Effect of excitatory amino acid receptor agonists on secretion of growth hormone as assessed by the reverse hemolytic plaque assay. 796 75

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

The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) receives many thin-myelinated Adelta-fiber and unmyelinated C primary afferent fibers and has been implicated in the processing of nociceptive information. Somatostatin (SST) is a neuromodulator in the brain and spinal cord. A number of studies have demonstrated that SST can play a key role in pain modulation at the spinal cord level. However, there is little information available on functional SST receptor expression in the SG neurons of the Vc in mice. This study examined the direct membrane effects of SST and SST receptor type 2 agonist, seglitide (SEG) on the SG neurons of Vc in gramicidin perforated current clamp mode. In addition, SSTR2 mRNA expression was detected on the SG neurons using single cell RT-PCR in juvenile mice. Most SG neurons (37/68, 54%) were hyperpolarized after a bath application of SST. When SST was applied in stages, the second responses (83% of the first response) were less intense than those after the first application suggesting that SSTRs are desensitized by repeated application. The SST-induced hyperpolarizing response was maintained in the presence of TTX (Na(+) channel blocker), AP-5 (NMDA receptor antagonist), CNQX (non-NMDA glutamate receptor antagonist), picrotoxin (GABA(A) receptor antagonist) and strychnine (glycine receptor antagonist), respectively, suggesting that SST has direct effects on the postsynaptic SG neurons. SSTR2 mRNA was detected in 11 out of 28 (39%) SG neurons tested. The SST-induced hyperpolarizing effects were mimicked by SEG, a SSTR2 agonist. These results suggest that functional SSTR2 receptors are expressed on the SG neurons of Vc in juvenile mice and can be a potential target for modulating orofacial pain.
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PMID:Inhibitory effects of somatostatin on the substantia gelatinosa neurons of trigeminal subnucleus caudalis via somatostatin type 2 receptors in juvenile mice. 1978 64