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Abstract Stimulant drugs such as amphetamine have, for many decades, been the drugs of choice in the treatment of children with attention-deficit/hyperactivity disorder. However, little is known about their therapeutic mechanisms or about the consequences of their long-term exposure. In the present study we investigated whether repeated exposure of a low dose of amphetamine (0.5mg/kg) to juvenile rats could induce long-term morphological alterations in the prefrontal cortex. In addition, to assess possible behavioural consequences of prolonged exposure to this drug, we examined whether changes in the motor response to various dopamine agonists occurred after this treatment. We found that this dose of amphetamine promotes plasma concentrations of amphetamine sulphate in juvenile rats to levels corresponding to the clinical range used for children with attention-deficit/hyperactivity disorder. Amphetamine (0.5mg/kg; s.c.) was administered twice daily during postnatal days 22-34, and then the brains of the animals were evaluated 2weeks later. This treatment produced an increase in dendritic length and branches of pyramidal neurons of the medial prefrontal cortex, but not in the nucleus accumbens. These changes were associated with an increase in the expression of calcium/calmodulin-dependent protein kinase II, a highly abundant signalling protein in the postsynaptic densities of excitatory synapses. Interestingly, amphetamine pre-treatment did not alter the motor response to various dopamine agonists, including amphetamine. These data suggest that clinical doses of stimulant drugs may be acting as a trophic support at the glutamatergic synapses, thereby enhancing dopamine-glutamate interactions in the prefrontal cortex

Accumbens. --- Agonists. --- Amphetamine. --- Animal. --- Animals. --- Behavioural consequences. --- Brain. --- Children. --- Choice. --- Consequences. --- Cortex. --- Density. --- Disorder. --- Dopamine. --- Drug. --- Drugs. --- Exposure. --- Expression. --- Increase. --- Interaction. --- Interactions. --- Juvenile rats. --- Level. --- Long-term. --- Mechanisms. --- Medial prefrontal cortex. --- Neurons. --- Nucleus accumbens. --- Nucleus-accumbens. --- Nucleus. --- Organization. --- Pattern. --- Plasma. --- Prefrontal cortex. --- Protein. --- Rat. --- Rats. --- Response. --- Stimulant. --- Synapses. --- Treatment.

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Prenatal stress (PS) can produce profound and long-lasting perturbations of individual adaptive capacities, which in turn can result in an increased proneness to behavioural disorders. Indeed, in PS rats there is evidence of impaired social play behaviour, disturbances in a variety of circadian rhythms, enhanced anxiety and increased hypothalamic-pituitary-adrenal (HPA) axis reactivity. This study was designed to experimentally investigate the degree of reversibility of PS-induced disturbances of social play and HPA reactivity by assessing the effect of the enrichment of the physical environment on PS rats during periadolescence. PS subjects showed a reduced expression of social play behaviour and a prolonged corticosterone secretion in response to restraint stress, but both these effects were markedly reversed following environmental enrichment. Interestingly, the enrichment procedure increased social behaviour but had no effect on corticosterone secretion in nonstressed animals, indicating a differential impact of the postnatal environment as a function of prenatal background. As a whole, results clearly indicate that rats prenatally exposed to stress can benefit during periadolescence from the modulatory effects of an enriched environment. Moreover, they confirm that PS may well represent a suitable animal model for the design and testing of new therapeutic strategies for behavioural disorders produced by early insults

Adolescence. --- Adult-rats. --- Animal model. --- Animal-model. --- Animal. --- Animals. --- Anxiety. --- Behaviour. --- Behavioural disorder. --- Circadian rhythm. --- Circadian rhythms. --- Circadian-rhythm. --- Circadian-rhythms. --- Circadian. --- Consequences. --- Corticosterone secretion. --- Corticosterone,distributed pregnancy,therapeutic strategy. --- Corticosterone. --- Design. --- Disorder. --- Enriched environment. --- Enriched. --- Enrichment. --- Environment. --- Environmental enrichment. --- Exposure. --- Expression. --- Function. --- Hpa axis. --- Hypothalamic-pituitary-adrenal. --- Juvenile rats. --- Maternal separation. --- Messenger-rna. --- Mice. --- Model. --- Open-field behavior. --- Physical. --- Play behaviour. --- Play. --- Prenatal stress. --- Prenatal. --- Rat. --- Rats. --- Reactivity. --- Response. --- Restraint stress. --- Restraint. --- Rhythm. --- Rhythms. --- Secretion. --- Social behaviour. --- Social interactions. --- Social play. --- Social. --- Strategies. --- Strategy. --- Stress.