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The hypothesis that 5-hydroxytryptamine (5-HT) neurons and/or receptors are involved in the mechanism of action of hallucinogens is supported by the fact that intraventricular administration of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) selectively destroys central 5-HT neurons in the brain and potentiates the behavioral effects of lysergic acid diethylamide (LSD), 2,5-dimethoxy-4-methylamphetamine (DOM) and mescaline. The locus in the brain where this potentiation might occur is not known. In the present experiment, the medial forebrain bundle (MFB) was studied because it is the primary tract containing fibers from the cell bodies in the raphe nuclei to forebrain structures receiving 5-HT input. Male rats received 5,7-DHT (6 micrograms/2 microliter) or vehicle injections bilaterally into the MFB; this procedure caused a significant reduction of 5-HT in the cortex, hippocampus and hypothalamus of lesioned rats, but not in the striatum. Regional dopamine and norepinephrine concentrations were not affected by this treatment. The behavioral effects of the hallucinogens were tested in a situation in which the animals pressed a bar under a fixed ratio-40 (FR-40) schedule of food reinforcement. The disruptive effects of LSD on responding were enhanced in the 5,7-DHT-treated animals, while the effects of DOM were diminished; there was no change in the response to mescaline. These data suggest that, while 5-HT neurons are involved in the behavioral effects of hallucinogens, the precise sites and/or mechanisms of action of LSD, DOM and mescaline may differ.
R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
October 2001,
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R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
June 1984,
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R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
September 1976,
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R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
November 1977,
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R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
October 1980,
Behavioral and neural biology,
R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
June 1978,
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R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
January 1991,
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R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
January 1982,
Psychopharmacology,
R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
January 1986,
Behavioral and neural biology,
R L Commissaris, and
D J Mokler, and
W H Lyness, and
K E Moore, and
R H Rech
September 1975,
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