Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present experiments were performed to determine whether the age-related loss of striatal D2 receptors could be localized to a kainic acid-sensitive neuronal population. This neurotoxin selectively destroys intrinsic neurons. Thus, if kainic acid reduced striatal D2 receptor concentrations such that age differences in this parameter were no longer observed, it would be a good indication that the D2 receptors lost through aging are also sensitive to kainic acid. Mature (6 months) and senescent (24 months) rats were stereotaxically, unilaterally injected with 3 micrograms/0.5 microliter kainic acid into the right striatum. Seven days later striatal D2 receptors were assessed with [3H]-spiperone in one group of mature and senescent rats. A second group of mature and senescent unilaterally lesioned rats was anesthetized and perfused. Brains were dissected and processed for striatal cell counts using cresyl violet staining, tyrosine hydroxylase and met-enkephalin using immunocytochemistry, and acetylcholinesterase using histochemistry. Age-related differences in D2-receptor concentrations were observed in intact, but not lesioned, striata. Kainic acid was less effective in reducing D2-receptor concentrations in senescent animals, suggesting that some proportion of the receptors was already lost prior to lesioning. Kainic acid also reduced total neuronal numbers, as well as Met-Enk and AChE positive staining, to approximately the same extent in mature and senescent rats. No age differences were seen in any of the other parameters following kainic acid administration.
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PMID:The deleterious effects of aging and kainic acid may be selective for similar striatal neuronal populations. 168 53

The cerebellum, probably owing to its traditional concept limited to motor control, is less well studied in immunoregulation. To obtain more comprehension and knowledge on cerebellar functions, we investigated effect of cerebellar fastigial nucleus (FN), an output nucleus of the spinocerebellum, on lymphocyte functions, and explored central and peripheral pathways involved in the effect. Kainic acid (KA) was microinjected into bilateral FN of rats (0.4 microg KA in 0.4 microl saline for each side) to destroy neurons of the nuclei. On days 8, 16 and 32 following the FN lesions, methyl-thiazole-tetrazolium (MTT) assay and flow cytometry were used to measure proliferation of concanavalin A (Con A)-induced lymphocytes and cytotoxicity of natural killer (NK) cells against YAC-1 cells, respectively. Meanwhile, glutamate and monoamine neurotransmitters, including norepinephrine (NE), dopamine (DA) and 5-hydroxytryptamine (5-HT), in the hypothalamus and the spleen were determined by means of high-performance liquid chromatography (HPLC) assay. Adrenocorticotropic hormone (ACTH) and cortisol in the plasma were also detected respectively by radioimmunoassay and chemiluminescent immunoassay after the FN lesions. We found that the Con A-induced lymphocyte proliferation and the NK cell cytotoxicity were both significantly enhanced on days 8, 16 and 32 following the effective lesions of the bilateral FN in comparison with those of matching control rats microinjected with saline in their FN. Contents of glutamate and NE, not DA and 5-HT, in the hypothalamus, and concentration of NE, not DA, in the spleen were all remarkably reduced on the 16th day following the FN lesions, when both the T lymphocyte proliferation and the NK cell cytotoxicity were dramatically increased. However, levels of ACTH and cortisol in the plasma had no notable differences between FN lesion rats and FN saline ones when the enhanced T and NK cell functions occurred. These findings reveal that the cerebellar FN participates in the modulation of lymphocyte functions and that the hypothalamus and sympathetic nerves innervating lymphoid organs are involved in this neuroimmunomodulation. Thus, a possible central and peripheral pathway for the spinocerebellum to regulate lymphocyte functions is suggested, i.e. cerebellum-hypothalamus-sympathetic nerves-lymphocytes, while the functional axis of hypothalamus-pituitary-adrenal gland may not contribute to mediation of the spinocerebellar immunomodulation.
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PMID:Effect of lesions of cerebellar fastigial nuclei on lymphocyte functions of rats. 1571 Apr 91