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Using extracellular recording we studied changes in the reactivity of rat hippocampal slices to an agonist of the 5-HT7 receptor, 5-carboxamidotryptamine (5-CT; 0.025-1 µM), induced by an earlier treatment of animals with corticosterone. Spontaneous bursting activity was recorded in ex vivo slices incubated in the presence of 2-[4-(2-methoxyphenyl)-1piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide (WAY 100635; 2 µM), an antagonist of the 5-HT1A receptor, in the medium devoid of Mg2+ ions. Saturation binding assays were performed using [3H]-(2R)-1-[(3-hydroxyphenyl)sulfonyl]-2-[2-(4-methyl-1-piperidinyl)ethyl]pyrrolidine hydrochloride (SB 269970), a specific antagonist of the 5-HT7 receptor. Repetitive, but not single, corticosterone administration lasting 7 and 21 days, resulted in an enhancement of the effect related to the 5-HT7 receptor activation without changes in its binding properties. In a separate set of experiments rats were treated with corticosterone for 3 weeks and additionally with imipramine, beginning on the eighth day of corticosterone administration. In the corticosterone plus imipramine group the excitatory effect of 5-CT was weaker than in the corticosterone group, indicating that corticosterone-induced functional modifications in the reactivity of the 5-HT7 receptor were reversed and further weakened by imipramine treatment. This effect was accompanied by a reduction in the density of [3H]-SB 269970 binding sites. Thus, imipramine treatment counteracts the corticosterone-induced increase in the reactivity of the hippocampal circuitry to the activation of the 5-HT7 receptor.
Morphological adaptations of Daphnia filtration apparatus in response to unsuitable food conditions are examined and set against earlier published data. To maximize food gathering under limiting food conditions, Daphnia can respond morphologically by plastic changes in the size and structure of its filter apparatus. Under low food quantity and/or poor quality, the area of Daphnia filter screen increases and the mesh size decreases.
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Mirtazapine (MIR)is an antidepressant which enhances noradrenergic and serotonergic 5-HT1A neurotransmission via antagomism of central alpha2 - adrenergic autoreceptors and heteroreceptors.The drugs does not inhibit noradrenaline and serotonin reuptake but blocks the 5-HT2 and 5-HT3 receptors and has high affinity only for central and peripheral histamine H1 receptors.The present study was aimed at determining whether repeated MIR treatment induced adaptive changes in the alpha1 - adrenergic receptors,similar to those reported by us early for tricyclic antidepressants,The experiments were carried out on male mice and rats.MIR was administered at a dose of 10 mg/kg once or repeatedly (twice daily for 14 days).The obtained results showed that MIR administrated repeatedly potentiated the methoxamine-induced exploratory hyperactivity in rats and clonidine- induced aggressiveness in mice,those effects being mediated by alpha1 - adrenergic receptors. MIR given repeatedly (but not acutely)increased the binding (Bmax )of [3H ]prazosin to alpha1 - adrenergic receptors in cerebral cortex,however,the ability of the alpha1 - adrenoceptor agonist phenylephrine to compete for the these sites was not significantly changed.The above results indicate that repeated MIR administration increases the responsiveness of alpha1 - adrenergic system (behavioural and biochemical changes),as tricyclics do.However, the question whether the increased functional responsiveness found in the present study is important for the clinical antidepressant efficacy,remains open.
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