Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma tachykinin levels are known to be altered with sexual acyclicity and loss of reproductive function. Ovulatory dysfunction, as seen in postmenopausal women, is also often encountered in hypothyroid patients. To know the involvement of different tachykinin genes in hypothyroidism-associated reproductive disorders, we performed DD-PCR with the pituitary RNA of control and hypothyroid rats to see the differentially expressed gene profile. Subsequently, we selected a few clones, tachykinin being one of them. Since its expression was up regulated in hypothyroidism as it does in the sexually acyclic females, we wanted to correlate these two phenomena with hypothyroidism associated reproductive disorders. We observed differential expression of tac2 along with other tk genes and their receptors in rat pituitary and ovary, which suggests that hypothyroidism affects the expression of these genes in these tissues. The experiments were repeated in ovarian tissue obtained at surgery from hypothyroid human patients, which showed similar expression pattern of TAC3 (equivalent to rat tac2) and their receptors as in rat ovary. Significant reduction of tac2 expression in reproductively less active rat ovary suggests the association of tac2 with reproductive senescence. Our results suggest that decline in reproductive function in hypothyroidism is associated with altered expression level of tac2 and its receptors. Further investigation in this area could elucidate the possible mechanism of tachykinins' involvement in loss of sexual cyclicity and other reproductive disorders associated with hypothyroidism.
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PMID:Tachykinin family genes and their receptors are differentially expressed in the hypothyroid ovary and pituitary. 1776 64

The effects of neonatal thyroid deficiency or hyperthyroidism on the development of neurones containing certain neuropeptides was examined in the brains of rats killed at two weeks of age. Five brain areas were dissected and extracted for radioimmunoassay measurement of vasoactive intestinal polypeptide (VIP), somatostatin, cholecystokinin octapeptide (CCK), substance P and neurotensin, whilst corresponding immunocytochemical data were obtained from a quantitative morphological analysis of cell bodies in the cingulate cortex. The two methods of analysis did not always agree, but in hypothyroidism both the concentration of VIP and the number of cells containing VIP-like immunoreactivity were significantly decreased in the anterior and posterior cingulate cortex. In contrast to these effects on the late maturing VIP neurones, the earlier developing somatostatin system was relatively unaffected, whilst neuropeptides localized in cortical fibres rather than cell bodies (such as substance P and neurotensin) were found by radioimmunoassay to be elevated. Hyperthyroidism had less marked effects than neonatal thyroidectomy, although the concentration of CCK (but not the number of immunostained cells) was significantly increased in the cingulate cortex. Radioimmunoassay results from three subcortical areas showed a decrease in VIP concentration in the hypothyroid hypothalamus, and in hyperthyroidism significant elevations of VIP in the basal ganglia, somatostatin in the hypothalamus and CCK in the hippocampus. It appears that in the brain areas studied thyroid disorders result in dis-synchronous shifts in the developmental patterns of the different neuropeptides, and that the effects of thyroid hormone on peptides as on other transmitters are critically dependent on the developmental profile of the system in question.
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PMID:Effects of changes in neonatal thyroid status on the development of neuropeptide systems in the rat brain. 2487 27


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