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Neurobiological effects

Table 7.4 Comparative Neurobiological Effects of MDMA Administration in Rats and Humans... Table 7.4 Comparative Neurobiological Effects of MDMA Administration in Rats and Humans...
Posttraumatic stress disorder (PTSD) refers to a pattern of anxiety, distress, and avoidance following an event experienced as threatening and/or intensely distressing. This disorder has been reported to have behavioral (Zaidi and Foy, 1994) and neurobiological effects into adulthood (Charney and Bremner, 1999). Much of the developmental research on the condition derives from retrospective studies of adults. The many possible biases inherent in such research preclude the generation of firm conclusions on the developmental course of the condition. An important process in the study of PTSD will be to identify the developmental path of the disorder in the context of the prevalence of anxiety disorders in childhood (Costellot et ah, 1996 Pynoos et ah, 1999). [Pg.140]

Simerly RB (1995) Hormonal regulation of limbic and hypothalamic pathways. In Micevych PE, Hammer RP (Eds), Neurobiological Effects of Sex Steroid Hormones, pp. 85-114. Cambridge University Press, New York. [Pg.519]

Hull, E. M. 1995. Dopaminergic influences on male rat sexual behavior. In Neurobiological effects of sex steroid hormones (Ed. by P.E. Micevych R. Hammer), pp 234-253. Cambridge Cambridge University Press. [Pg.341]

A related development is the tremendous expansion of neuroscience. Thyroid hormones occupy a central place in brain development. It seems pertinent to bring the neurobiological effects of thyroid hormone disorder to the attention of the neuroscience community, especially as hypothyroidism affects nerve cell growth and connectivity, neurotransmitter levels, membrane functions, and other areas of neurobiology. [Pg.384]

Benedetti F, Mayberg HS, Wager TD et al (2005) Neurobiological mechanisms of the placebo effect. J Neurosci 25 10390-10402... [Pg.983]

These insights into the structure of sleep and the neurobiological processes underlying it have yielded several targets for therapeutic intervention and provided novel methods by which to assess the differential effects of hypnotics on sleep-relevant neural circuits. [Pg.1136]

French ED, Dillon K, Wu X Cannabinoids excite dopamine neurons in the ventral tegmentum and substantia nigra. Neuroreport 8 649—632, 1997 Fujinaga M, Maze M Neurobiology of nitrous oxide-induced antinociceptive effects. Mol Neurobiol 25 167-189, 2002... [Pg.306]

Nortriptyline. Nortriptyhne, a tricychc antidepressant, has been shown in double-blind, placebo-controlled randomized trials to be superior to placebo for smoking cessation (Prochazka et al. 1998). Nortriptyline appears to have efficacy comparable to that of bupropion for smoking cessation (Hall et al. 2002). The efficacy of this agent may be improved with more intensive behavioral therapies (Hall et al. 1998). Nortriptyline s mechanism of action is thought to relate to its noradrenergic and serotonergic reuptake blockade, because these two neurotransmitters have been implicated in the neurobiology of nicotine dependence. Side effects of nortiptyline are typical of tricyclic antidepressants and include dry mouth, blurred vision, constipation, and orthostatic hypotension. Nortriptyline appears to have some utility for smokers with a past history of major depression, and it can be recommended as a second-... [Pg.325]

Finally, there is little or no clinical evidence that morphine causes psychological dependence or drug-seeking behaviour, tolerance or problematic respiratory depression in patients. These events simply do not occur when opioids are used to control pain. The reason is likely to be that the actions of morphine and the context of its use in a person in pain are neurobiologically quite different from the effects of opioids in street use. These actions of opioids are described in more detail in Chapter 23. [Pg.259]

A second objective is to produce behavioural changes in animals that are analogous to depression so that the model can be used to discover its neurobiological cause(s). This is a far more demanding problem and its success rests on satisfying at least three criteria (see Willner 1984) face validity (i.e. the behaviour looks like depression), construct validity (i.e. the causes and consequences of the behavioural change are the same as in depression) and predictive validity (i.e. the behaviour is reliably prevented only by drugs which have antidepressant effects in humans). [Pg.429]

These observations suggest differential mechanisms for the aggression-heightening effects of amphetamine as distinct from the disruptive actions on social and aggressive behavior. The neurobiological mechanisms for... [Pg.84]

Kasper, Siegfried and Bruce S. McEwen, Neurobiological and Clinical Effects of the Antidepressant Tianeptine , CNS Drugs 22, no. 1 (2008) 15-26... [Pg.205]

Lara-Lemus A., Drucker-Colin R., Mendez-Franco J., Palomero-Rivero M., Perez de la Mora M. (1998). Biochemical effects induced by REM sleep deprivation in naive and in D-amphetamine treated rats. Neurobiology 6(1), 13-22. [Pg.215]


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