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Mood Elevators

However, clinical results with compounds enhancing cholinergic function have not been overly convincing (272). In the case of tacriae, however, the beneficial therapeutic iadex was sufficient to justify regulatory approval ia several countries. Psychostimulants such as pemoline, amphetamine, procaine, and methylphenidate have failed to show cognitive enhancing effects ia patients with dementia, except possibly as iadirect consequences of mood elevation. [Pg.239]

Monoamine Oxidase Inhibitors. MAOIs inactivate the enzyme MAO, which is responsible for the oxidative deamination of a variety of endogenous and exogenous substances. Among the endogenous substances are the neurotransmitters, norepinephrine, dopamine, and serotonin. The prototype MAOI is iproniazid [54-92-2] (25), originally tested as an antitubercular dmg and a close chemical relative of the effective antitubercular, isoniazid [54-85-3] (26). Tubercular patients exhibited mood elevation, although no reHef of their tuberculosis, following chronic administration of iproniazid. In... [Pg.465]

Monophasic Preparations Monoxide Mood Disorders Mood Elevators Mood-stabilising Drugs Morbus Alzheimer Morphogens Morpholines Motilin... [Pg.1497]

The precise mechanism through which benzodiazepines and barbiturates produce mood elevation remains to be elucidated. The mood-elevating effect of the benzodiazepines and barbiturates is probably mediated not only by acute increases in the actions of GABA but also by neural connections from... [Pg.121]

Hypomania Abnormal mood elevation that does not meet the criteria for mania. [Pg.1568]

Cerebral blood flow and glucose metabolism Nicotine increases cerebral blood flow (Hara et al. 1993 Yokoi et al. 1993). Functional MRI of smokers who were administered intravenous nicotine shows increases of cerebral blood flow in several areas of the brain. Corresponding to feelings of mood elevation, nicotine activates the nucleus accumbens, amygdala, cingulate cortex, and frontal lobes. This activation is very consistent with functional systems subserving arousal and reinforcement. [Pg.113]

Abuse potential Some patients may use these agents for mood elevations or psychedelic experiences. Cannabinoids, barbiturates, opiates, and alcohol may have additive effects with anticholinergics. [Pg.1300]

In normal subjects the tricyclics only show anticholinergic and sedative activity but have no mood elevating action. In depressed subjects their mood elevating effect has a delay of 2-3 weeks. The reasons for this delay are unknown and could be both pharmacokinetic or pharmacodynamic in natme. [Pg.352]

Iproniazid, originally developed for the treatment of tuberculosis, exhibited mood-elevating properties during clinical trials in tuberculosis patients with depression. The distinguishing biochemical feature between iproniazid and other chemically similar antituberculosis compounds was the ability of the former to inhibit MAO. Thus, a series of hydrazine and non-hydrazine-related... [Pg.391]

The mood-elevating properties of the first monoamine oxidase... [Pg.94]

An emerging group of antidepressant interventions comprises several hormones that have been shown to have mood-elevating or mood-modulating effects (see Halbreich, Chapter 17, in this volume). This group includes mostly cortisol suppressors, thyroid hormones, estrogen, and other steroids. However, more recently several other hormones, such as melatonin and oxytocin, were proclaimed as players in the field, but their place is still to be claimed. [Pg.7]

Effect on CNS Large doses of glucocorticoids cause euphoria, mood elevation, nervousness, restlessness, which are reversible type of actions. They often produce behavioural disturbances inhuman being and also increase intracranial pressure. [Pg.283]

During clinical studies of iproniazid (201) in the treatment of tuberculosis it was found to have a mood-elevating effect. It was later found to be an inhibitor of monoamine oxidase (MAO), the enzyme which oxidatively deaminates such neurotransmitters as noradrenaline and serotonin, and it was tried in the treatment of depression in 1957. Other MAO inhibitors were introduced later, most of them being hydrazine derivatives. Heterocyclic examples include isocarboxazid (202) and nialamide (203). They are toxic and cause dangerous hypertensive crises if food with a high tyramine content is eaten, and on this account their use is limited. [Pg.174]

QUALITATIVE COMMENTS (with 150 mg) Between two and five hours, very peaceful and euphoric mood elevation, similar to mescaline, but without any visual distortion. Mild enhancement of color perception, possibly a function of mood elevation. There was no nausea, no eyes-closed vision. Slept easily that evening. ... [Pg.126]


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See also in sourсe #XX -- [ Pg.131 , Pg.132 ]




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