Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were lesioned bilaterally in the globus pallidus (GP) with anodal current or 6-OHDA, and were observed in various motor tests 10 min daily for 3 weeks. Body weight, home cage water and food intakes were recorded daily under two different food accessibility conditions. The lesions produced adipsia, aphagia, loss of body weight and motor impairments which could not be reversed by either l-dopa or bromocriptine. Animals could be made to recover, however, by making food easily accessible and palatable. The results do not support a "metabolic" role for the GP but support the idea that aphagia, adipsia and mortality is due to motoric impairments produced by the lesion.
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PMID:Effect of l-dopa or bromocriptine on feeding and motor behavior of rats with lesions in the globus pallidus. 643 68

Both intracerebroventricular (i.c.v.) IL-1beta and exposure to inescapable tail shock (IS) activate acute phase responses (APRs) that include increases in core body temperature (CBT), increases in hypothalamic-pituitary-adrenal activity, decreases in carrier proteins such as corticosterone binding globulin (CBG), aphagia and adipsia. A variety of data suggested that stressors produce APRs by inducing brain IL-1beta. The current series of studies further explored this possibility by determining whether the functional IL-1beta antagonist, alpha-melanocyte-stimulating hormone (alpha-MSH(1-13)), would block IS-induced APRs. Immediately following i.c.v. alpha-MSH(1-13) administration, rats were exposed to a single session of 100, 5 s, 1.6 mA ISs, or control treatment (home cage control). alpha-MSH(1-13) blocked IS-induced increased CBT, increased plasma corticosterone (CORT), decreased CBG, aphagia and adipsia 24 h after IS. The inhibitory effects of alpha-MSH(1-13) were shown not to be a consequence of alpha-MSH(1-13) producing its actions 24 h after its administration because alpha-MSH(1-13) given 24 h before IS did not block IS-induced increased CBT and CORT during IS. Additionally, alpha-MSH(1-13), given 24 h before IS, had no effect on increased CBT, increased CORT, decreased CBG, adipsia, or aphagia 24 h after IS. These data provide support for a specific mode of action for i.c.v. alpha-MSH(1-13), namely blockade of APRs with no impact on acute hyperthermia or increased levels of CORT produced during IS.
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PMID:The long term acute phase-like responses that follow acute stressor exposure are blocked by alpha-melanocyte stimulating hormone. 981 38