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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 58 (1978), S. 189-195 
    ISSN: 1432-2072
    Keywords: Dextroamphetamine ; Methylphenidate ; Growth hormone ; Cortisol ; Euphoria ; Arousal
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract These studies examine the interface between central neurochemical events, psychologic state, and neuroendocrine activity. Fifty-nine healthy young men received dextroamphetamine (10 or 20 mg), methylphenidate (10 or 20 mg), or placebo. Psychologic state and serum concentrations of growth hormone, cortisol, and amphetamine were monitored for 2 h following drug ingestion. There was considerable variance in both the endocrine and psychologic responses to these drugs. In general, both dextroamphetamine (20 mg) and methylphenidate (20 mg) stimulated growth hormone release, while only dextroamphetamine stimulated cortisol release. The variance in psychologic response precluded statistically significant differences among the drug groups; however, dextroamphetamine and methylphenidate appeared about equally effective in eliciting euphoria. Growth hormone response following these drugs correlated selectively with increases in euphoria, while cortisol response correlated somewhat selectively with increases in arousal. Serum amphetamine concentration correlated only with degree of growth hormone response and degree of elation. These findings suggest that a common or linked central mechanism underlies both the growth hormone response and euphoria elicited by these drugs, and that a different mechanism underlies the cortisol and arousal responses. More importantly, these findings suggest another way in which psychopharmacologic agents can be used to elucidate the neurophysiology of both pathologic and normative psychologic states.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 63 (1979), S. 273-280 
    ISSN: 1432-2072
    Keywords: Dopamine ; Lateral inhibition ; Attention ; Schizophrenia ; Model for schizophrenia ; Schizophrenic symptoms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A hypothesis is briefly discussed proposing that schizophrenic symptoms are due to a breakdown in a mechanism by which conscious attention is limited and directed. It is shown that this mechanism can be modelled in terms of a simple nerve network in which every channel inhibits all the others. Failure of this inhibition would cause the defect hypothesised to occur in schizophrenia. It is shown that if dopamine is given a central role as transmitter in such a network then the various predictions about the biochemistry of schizophrenia that follow are not only consistent with the evidence for the ‘dopamine theory’ of schizophrenia, but also with much of the evidence held to be contrary to that theory. While not purporting to be an experimentally validated description of schizophrenia, this model goes beyond the single amine theories of schizophrenia and links dysfunctions in amine systems with specific behavioural control mechanisms. Given the current state of knowledge, such models can make only limited predictions about the biochemistry of schizophrenia. However, an attempt to link behavioural and biochemical systems in this way will be crucial for the development of viable animal models of schizophrenia.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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