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PubMed · 4710185

Restricting licit supply.

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L F Tice. 1973. Restricting licit supply.. https://pubmed.ncbi.nlm.nih.gov/4710185/

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Saw palmetto is an indirectly acting sympathomimetic in the rat-isolated prostate gland.

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4-methyl benzylamine stimulates food consumption and counteracts the hypophagic effects of amphetamine acting on brain Shaker-like Kv1.1 channels.

1.--4-methyl benzylamine (4-MBZ; 28 microg, 231 nmol) elicits a hyperphagic response in starved mice in contrast to the hypophagia induced by the parent compound benzylamine (BZ; 33 microg, 231 nmol) or by amphetamine (AMPH, 2 mug). 2.--In mice starved for only 4 h, and therefore with little stimulation to eat, the maximal increase in food consumption induced by intracerebroventricular (i.c.v.)-injected 4-MBZ was 190% over that of the controls (ED(50) 8.3+/-2.7 microg mouse(-1); 68+/-22 nmol mouse(-1)), whereas after i.p. administration, these values were 160% and approximately 129 mg kg(-1), respectively. 3.--The hyperphagic effect of 4-MBZ was reduced by more than 60% in mice pretreated with antisense oligodeoxyribonucleotide (aODN(1)) previously found to selectively inhibit (over 50%) the expression of Shaker-like Kv1.1 channels. 4.--In mice highly stimulated to eat after 12-h fasting, 4-MBZ (28 microg) significantly reduced (to about 70%) the hypophagic response by AMPH (2 microg) or BZ (33 microg). Conversely, these two compounds reduced (respectively, by 69 and 44%) the hyperphagic response of 4-MBZ in 4-h fasting mice. 5.--4-MBZ (28 microg) also reduced the hypermotility and the stimulation of inspection activity elicited by AMPH in mice and the release of DA stimulated by AMPH (2 microg) from the nucleus accumbens of rats. We hypothesize that 4-MBZ elicits hyperphagic effects probably by opening Shaker-like Kv1.1 subtypes in the brain, whereas AMPH and BZ are hypophagic by blocking these channels.

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Characterization of the rapid-onset type of behavioral sensitization to amphetamine in mice: role of drug-environment conditioning.

A rapid-onset type of behavioral sensitization (ROBS) has been demonstrated in rats treated with a single 'priming' injection of amphetamine (AMP). In that species, however, this phenomenon was restricted to AMP-induced stereotyped behavior (SB), not occurring for the locomotor-stimulant effect (LSE) of AMP and not reflecting environment-specific sensitization. In the present study, the ROBS was characterized in the mouse. Mice received a single 'priming' intraperitoneal injection of 5.0 mg/kg AMP which was paired or not with environment. At different intervals (3, 4 or 5 h) subgroups were tested for AMP (1.5 or 5.0 mg/kg)-induced SB or AMP (1.5 mg/kg)-induced open-field LSE. Results showed that: (1) in the absence of drug-environment association, a priming injection of AMP increased the SB induced by a 1.5 mg/kg AMP challenge injection given 3 h (but not 4 or 5 h) later; (2) when the dose of AMP challenge injection was increased to 5.0 mg/kg, an enhancement of SB was verified at all the intervals tested (3, 4, and 5 h); (3) when animals were tested in an open field, the priming injection of AMP produced an increase in the LSE of a 1.5 mg/kg AMP challenge injection, given 4 h later; (4) drug-environment association increased both SB and locomotion after a saline challenge injection and potentiated the rapid-onset sensitization of both behaviors in AMP-challenged mice. Collectively, these results demonstrate that the ROBS phenomenon also occurs in mice, is extended to AMP-induced LSE, and is markedly potentiated by (but does not depend on) environmental conditioning.

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