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Effect of treatment with the neuroactive peptide posatirelin on microanatomical changes of frontal cortex anf hippocampus caused by lesions of the locus ceruleus
No full textEFFECTS OF A METHANOLIC EXTRACT AND A HYPERFORIN-ENRICHED CO2 EXTRACT OF YPERICUM PERFORATUM ON ALCOHOL INTAKE IN RATS.
No full textInhibition of cell dehydration-induced drinking by tachykinins: evaluation of possible renal effects accounting for the long-lasting inhibition.
No full textCentral injection of the tachykinins (TKs) neurokinin A (NKA), eledoisin (ELE), and kassinin (KASS) produced long-lasting inhibition (up to 6 h) of drinking induced by subcutaneous hypertonic NaCl, while substance P (SP) and physalaemin (PHYS) evoked short-lasting effects. The hypothesis that water retention or increased Na+ excretion by the kidney (induced by TKs) may reduce the need for water ingestion was tested. The results obtained both in urine collection experiments and in nephrectomized rats showed that the duration of the effect of NKA, ELE, and KASS is not due to water retention or increased Na+ excretion by the kidney. The effect of NKA, but not that of ELE and KASS, was shortened by nephrectomy, even though NKA did not modify urine volume or Na+ excretion. Indomethacin pretreatment, like nephrectomy, reduced the duration of the NKA effect, suggesting that renal prostaglandins are involved in it. On the other hand, the long-lasting effect of the three TKs cannot be easily explained in terms of slow metabolic degradation, particularly for NKA. Alternatively, it might be hypothesized that these TKs produce a modification of osmoreceptor function lasting well beyond the life of the peptide, and/or that they produce Na+ loss through emunctories different from the kidney
3-[2-[4-(4-Fluorobenzoyl)piperidin-1-yl]ethyl]-5,6,7,8-tetrahydro-4(3H)quinazolinones: serotonin 5-HT2A receptor antagonists endowed with potent, central action
No full textHyperphagic effect of novel compounds with high affinity for imidazoline I2 binding sites
No full textPrevious studies have suggested that imidazoline I(2) receptors play a role in feeding control in rats. The effect of subcutaneous (s.c.) injections of four novel imidazoline I(2) ligands, 2-naphthalen-2yl-4,5-dihydro-1H-imidazole hydrochloride (benazoline), 2-styryl-4,5-dihydro-1H-imidazole oxalate (tracizoline), o-nitro-tracizoline and o-methyl-tracizoline (metrazoline) on food intake during the light phase was now evaluated in freely feeding male Wistar rats. Their effect was compared to that of idazoxan, a high-affinity ligand at imidazoline I(2) binding sites, but also a potent alpha(2)-adrenoceptor antagonist. Compared to idazoxan, metrazoline exhibits a higher pK(i) for imidazoline I(2) binding sites in rat liver, while the other compounds have a slightly lower pK(i); on the other hand, the novel compounds have much lower affinity than idazoxan at alpha(2)-adrenoceptors. Idazoxan stimulated drinking at a dose as low as 1 mg/kg, and evoked feeding at a higher dose (30 mg/kg). The selective alpha(2)-adrenoceptor antagonist 2-methoxy-idazoxan (RX821002), with negligible affinity at imidazoline I(2) binding sites, significantly increased drinking but failed to stimulate feeding at doses of 10-50 mg/kg. Metrazoline induced hyperphagia and water drinking at doses of 50 mg/kg or higher. Its dipsogenic effect was secondary to the hyperphagic effect, since it was not observed in rats without access to food. Benazoline significantly increased feeding only in response to 30 mg/kg, but its effect was less pronounced than that of metrazoline. Tracizoline and o-nitro-tracizoline were inactive. Following injection into the lateral cerebroventricle at doses up to 100 microgram/rat, and into the third or fourth brain ventricle at doses up to 50 microgram/rat, neither idazoxan nor metrazoline induced hyperphagia. The present results support the idea that imidazoline I(2) ligands influence feeding in rats, and suggest that their site of action is not in the central nervous system. The finding that idazoxan elicits a more potent hyperphagic effect than metrazoline and benazoline, although its affinity for imidazoline I(2) binding sites is lower than that of metrazoline and similar to that of benazoline, raises the question whether its hyperphagic effect might also be due to interaction with other receptors
Possible mechanism of action for the attenuation of ethanol intake induced by ritanserin in rats
No full textThe 5-HT2 receptor antagonist, ritanserin, reduces alcohol intake in rats and the nucleus accumbens (NAC) has been proposed as a site of action for the drug. Recent microdialysis studies have shown that acute subcutaneous (SC) administration of ritanserin increases extracellular 5-HT levels in the NAC. The present study evaluated, in genetically heterogeneous rats with developed preference for 3% ethanol, whether the attenuation of ethanol intake induced by ritanserin might be related to its effect on the synaptic availability of 5-HT in the NAC. Damaging 5-HTergic neurons by intracerebroventricular infusion of 5,7-dihydroxytryptamine (5,7-DHT) abolished the effect of ritanserin on ethanol consumption. Injections of the 5-HT3 receptor antagonist MDL 72222 into the NAC significantly reduced the inhibitory effect of SC injection of ritanserin, 1 mg/kg, and completely abolished the effect of ritanserin, 0.1 mg/kg. Subcutaneous injections of MDL 72222, 0.3 mg/kg 3 times/day, suppressed the effect of SC ritanserin, 0.1 mg/kg. The present findings, together with those of previous experiments showing that the tryptophan hydroxylase inhibitor p-chlorophenylalanine abolishes the effect of ritanserin, support the hypothesis that its effect on ethanol intake may be due to increased synaptic availability of 5-HT into the NAC
Effect of lesions of the nucleus basalis magnocellularis and of treatment with posatirelin on cholinergic neurotransmission enzymes in the rat cerebral cortex
No full textMicroanatomical and electrophysiological changes of the rat dentate gyrus caused by lesions of the nucleus basalis magnocellularis.
No full textThe effect of unilateral or bilateral lesions of the nucleus basalis magnocellularis (NBM) on the dentate gyrus of the hippocampus were assessed using microanatomical and electrophysiological techniques. NBM is the main cholinergic basal forebrain nucleus that supplies the fronto-parietal cortex. Lesions were induced using the neurotoxin ibotenic acid or a radio-frequency system and did not affect glutamic acid decarboxylase activity both in the frontal cortex and in the hippocampus. At 4 weeks after lesioning, a loss of choline acetyltransferase (ChAT) activity and of ChAT-immunoreactive fibres was observed in the frontal cortex but not in the hippocampus and no changes in the density of granule neurons of the dentate gyrus or in the hippocampal long-term potentiation (LTP) were noticeable. At 8 weeks after lesioning the loss of both ChAT activity and of ChAT-immunoreactive fibres persisted in the frontal cortex of NBM-lesioned rats. Moreover, at this time a significant decrease in the density of granule neurons in the dentate gyrus accompanied by a reduced probability of dentate LTP induction were observed in both ibotenic acid- and radio-frequency-lesioned rats. These findings have shown that although NBM does not send direct cholinergic projections to the hippocampus, lesions of this cholinergic nucleus are accompanied by delayed neurodegenerative changes involving the dentate gyrus. This suggests the occurrence of indirect connections between NBM and the hippocampus, the functional relevance of which should be explored
Effects of kassinin, a tachykinin of the skin of the African frog Kassina senegalensis, on body fluid homeostasis in rats.
No full textIn Wistar rats loaded with SC hypertonic NaCl solution kassinin produces an inhibition of cell-dehydration drinking which lasts several hours. The long duration of the effect does not depend on a renal excretion of sodium but, hypothetically, on a redistribution of electrolytes between the extra- and the intra-cellular compartments of body fluids
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