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

The learned helpless rat is considered to be one of the better animal models of depression. A genetically inbred strain with a high vulnerability to develop helplessness (LH), as well as a highly resistant strain (NLH) have both been developed. Since the brain peptide neuropeptide Y (NPY) is involved in the regulation of a number of behaviors known to be altered in clinical depression as well as in learned helplessness, we measured the relative level of NPY mRNA in the hippocampus and cortex of control Sprague Dawley (SD), LH and NLH rats. We find that NLH rats have approximately a 30-35% decrease in basal hippocampal NPY mRNA compared with SD and LH rats. By contrast, cortical NPY mRNA and hippocampal pre-proenkephalin and somatostatin mRNA levels were not significantly different in the 3 strains. The data suggest that the regulation of NPY gene expression may be involved in the reduced vulnerability of NLH rats to develop learned helplessness.
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PMID:Hippocampal neuropeptide Y mRNA is reduced in a strain of learned helpless resistant rats. 135 57

Plasma glucose level depends on the peripheral intra-islet crosstalk between A cells (glucagon) + B-cells (insulin) and D-cells (somatostatin). Gastrointestinal hormones (secretin, CCK-PZ, gastrin, and serotonin) modulate the glucose- and amino acids-induced secretions of insulin and glucagon, respectively. Serotonin (5-HT) arose from the enterochromaffin cells during postprandial periods excites basal but inhibits excited B-cells. Serotonin excites adrenal glands that release adrenaline (Ad) + dopamine (DA). The former is positively correlated with hyperglycemia, whereas DA antagonizes this effect. Noradrenaline (NA) released from both sympathetic nerves and adrenal glands modulates the Ad release from this latter and excites A-cells. Thus, NA attenuates the hyperglycemic effects triggered by Ad. Dopamine released from both sources, adrenal glands and peripheral sympathetic nerves, antagonizes Ad-induced hyperglycemia plus the NA-triggered glucagon secretion. Both plasma insulin and glucagon cross the blood-brain barrier and excite A5(NA) and C1(Ad) neurons, respectively. C1 (Ad) neurons send excitatory drives to both islet A-cells and adrenal glands. Both central nervous system A5(NA) and C1(Ad) nuclei interchange inhibitory axons. Predominance of the former redounds in hyperinsulinism plus hypoglycemia, whereas the latter axis is responsible for hyperglucagonemia + hyperglycemia. In addition, the dorsal raphe serotonergic and the median raphe serotonergic nuclei interchange excitatory axons with the C1 (Ad) and the A5(NA) neurons, respectively. Hence, the former binomial axis (responsible for uncoping stress) is positively correlated with the hyperglycemic syndrome, whereas the A5(NA) + median raphe serotonergic binomial is correlated with hypoglycemia. Hence, the insulin resistance disorder should be underlain by the overactivity of both axes simultaneously. The above pathophysiological mechanisms are consistent with the successful neuropharmacological manipulations addressed to treat these neuroendocrine syndromes. Finally, one of the showiest findings derived from our research work arises from the unbalance between the DA versus 5-HT circulating parameters demonstrating that absolute predominance of the former is always paralleled by hypoglycemia (endogenous depression syndrome), whereas the opposite profile is registered in mammals affected by hyperglycemia (dysthymic depression and uncoping stress syndromes).
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PMID:Insulin versus glucagon crosstalk: central plus peripheral mechanisms. 2383 33