Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.3 (phospholipase C)
 18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The stress-related neuropeptide corticotropin-releasing factor (CRF) and the serotonin system are both critically involved in the pathophysiology of mental disorders, including anxiety and depression. To understand the potential link between them, we investigated the impact of CRF on 5-HT functions in pyramidal neurons of the prefrontal cortex (PFC), a brain region that is crucial for the control of emotion and cognition. One prominent function of serotonin in PFC is to regulate GABAergic inhibitory transmission, as indicated by a 5-HT-induced large, desensitizing (approximately 4 min) enhancement of the amplitude and frequency of spontaneous IPSCs (sIPSCs). In PFC slices exposed to CRF treatment, the regulation of sIPSCs by 5-HT was significantly prolonged (8-10 min), and this effect of CRF was blocked by treatment with the competitive CRF receptor antagonist alpha-helical CRF9-41 and with the CRF-R1-specific antagonist astressin. Inhibiting phospholipase C or protein kinase C (PKC) abolished the prolongation by CRF of the effects of 5-HT on sIPSCs. In PFC slices prepared from animals previously exposed to acute stress (forced swim or elevated platform), the regulation of sIPSCs by 5-HT was significantly prolonged, mimicking the effect of CRF treatment. The stress-induced prolongation of the effects of 5-HT on sIPSCs was diminished by alpha-helical CRF9-41 treatment, mimicked by direct activation of PKC, and reversed by short-term treatment with drugs that have anxiolytic efficacy. These results show that in response to stressful stimuli, CRF alters the serotonergic regulation of GABA transmission through a mechanism that is dependent on PKC. The interaction between CRF and 5-HT may play an important role in psychiatric disorders, in which both are highly implicated.
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PMID:Corticotropin-releasing factor and acute stress prolongs serotonergic regulation of GABA transmission in prefrontal cortical pyramidal neurons. 1516 92

In order to understand the role of sympatho-adrenomedullary (SAM) system in mediating stress effect on non-specific immune responses in fishes, the splenic macrophage phagocytic and respiratory burst activities of normal and chemically sympathectomized Channa punctatus under restraint stress were studied. Chemical sympathectomy abrogated the differential effects of acute stress on diverse functions of macrophages. The SAM regulation of macrophage activities was substantiated by in vitro experiments with catecholamines, the end product of SAM system. Further, for the first time in fishes, different adrenoceptors and their precise second messenger system regulating diverse functions of macrophages by catecholamines were demonstrated. Norepinephrine (NE)/epinephrine (E) decreased the phagocytosis through beta-adrenergic receptor as only propranolol, the beta-adrenergic receptor antagonist, blocked the suppressive effect of NE/E. However, dopamine (DA) regulates phagocytosis solely via the dopaminergic receptor. The DA effect was mimicked by DA receptor agonists, apomorphine and bromocryptine. Adenylate cyclase system linked to beta-adrenoceptor/dopaminergic receptor seems to be involved in mediating the effect of catecholamine on phagocytosis since db cAMP inhibited the phagocytosis in a dose-dependent manner. In case of superoxide production, only phenoxybenzamine, an alpha-adrenergic receptor antagonist, was seen effective in blocking the stimulatory effect of NE/E. Further, Ca2+ as second messenger system coupled to alpha1-adrenergic receptor was shown to mediate this effect since phospholipase C (PLC) inhibitor, U73122 and intracellular calcium chelating agent, BAPTA-AM downregulated the NE/E-induced superoxide production. The role of calcium in modulation of superoxide production was also emphasized using calcium ionophore A23187.
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PMID:Role of adrenoceptor-coupled second messenger system in sympatho-adrenomedullary modulation of splenic macrophage functions in live fish Channa punctatus. 1757 46