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Biomedical subjects

W H Bridger

Publications and source records attributed to W H Bridger.

At least 37 records · Page 2Linked to original sources
PubMed1981

Inescapable shock alters mescaline's disruption of active avoidance acquisition.

Rats were tested on a two-way avoidance acquisition with or without inescapable shock given 24 h prior to training. Mescaline given to nonshock rats disrupted acquisition in a dose-dependent fashion and tolerance developed to this disruption. Mescaline given to shock rats had no effect on acquisition even though levels of acquisition were the same for both shock and nonshock rats without drug. Moreover, subchronic treatment (5 days facilitated acquisition. These experiments demonstrate an interaction between shock, which presumably is a stressor, and mescaline. The data are consistent with the observation that when animals are exposed to presumptive stressors (e.g., shock, handling) hallucinogens can facilitate behavior, while in other situations, hallucinogens disrupt behavior.

Animals↗
PubMed1981

L-Tryptophan's effects on mouse killing, feeding, drinking, locomotion, and brain serotonin.

Injections of the serotonin precursor l-tryptophan (25, 50, and 100 mg/kg IP), inhibited mouse killing behavior in rats, as indicated by a dose dependent increase in latencies to attack and kill mice. Tests in 24 hr food deprived rats revealed that feeding behavior was also significantly decreased by about 30% by tryptophan injections (50--100 mg/kg IP). Concomitant with the behavioral changes were increased levels of brain serotonin and its metabolite 5-hydroxyindoleacetic acid. Drinking, latencies to sniff mice, and ability to locomote on a rotating rod were not affected by l-tryptophan injections, although spontaneous activity in an open field was reliably reduced by 33% with a dose of 100 mg/kg. Thus, while the degree of selectivity for tryptophan's effects on behavior remains open to question, these findings are consistent with hypotheses of an inhibitory role for central serotonergic systems, particularly in mouse killing and feeding behaviors.

Aggression↗
PubMed1980

Effects of prematurity and early intervention on responsivity to tactual stimuli: a comparison of preterm and full-term infants.

Cardiac and behavioral responses to a tactual stimulus were evaluated during the first sleep cycle for 3 groups of infants: 30 full terms, 30 nonintervened preterms, and 30 intervened preterms. Prior to testing, the latter group had received a regimen of multimodal sensory stimulation, which emphasized the tactual and vestibular modalities. The results showed that the intervention altered the preterms' sensory functioning mainly during active sleep. In this state, the full terms and the intervened preterms exhibited a significant cardiac acceleration to the stimulus, while the nonintervened preterms failed to do so. Similarly, the behavioral response of the intervened preterm more closely approximated that of the full terms. During quiet sleep the intervention did not affect either the cardiac or the behavioral response. In this sleep state, the full terms' cardiac response was that of monophasic acceleration, whereas both groups of preterms exhibited a biphasic response with a smaller initial acceleration which was followed by a deceleration below baseline. Behaviorally, the preterms responded less frequently and gave smaller responses than the full terms. Thus there were marked differences between preterms and full terms, and the intervention seemed to narrow this gap to some extent.

Female↗
PubMed1979

Manipulations of dietary tryptophan: effects on mouse killing and brain serotonin in the rat.

Maintaining rats on a tryptophan-free diet for 4--6 days induced mouse killing in non-killer rats, and significantly facilitated killing in killer rats, as indicated by shorter latencies to kill the mice. The killing responses were similar in topography to the natural killing responses. These changes in killing behavior did not appear to be due to generalized changes in irritability. The increased killing after maintenance on a tryptophan-free diet was accompanied by a 26% reduction in brain serotonin (5-HT) and a 29% reduction in brain 5-hydroxyindoleacetic acid (5-HIAA). When the tryptophan-free diet was supplemented with L-tryptophan (0.5 or 2%), brain 5-HT and 5-HIAA were increased above control levels, and the rat's killing response appeared normal both in terms of latency and topography, similar to that seen in control chow fed animals. While rats consumed less of the tryptophan-free and tryptophan supplemented diets, control subjects deprived of chow such that they lost as much weight as rats fed the tryptophan-free diet, did not show changes in killing behavior. These results are consistent with the hypothesis that central serotonergic systems exert inhibitory control over mouse killing behavior in rats.

Aggression↗
PubMed1979

A comparison of the effects of acute and subacute administration of beta-phenylethylamine and d-amphetamine on mouse killing behavior of rats.

beta-Phenylethylamine (PEA) is an endogenous amine that in some instances acts biochemically and behaviorally like amphetamine. In the present experiments, the effects of PEA on mouse killing by rats were compared and constrasted with the effects of d-amphetamine on this behavior. When given acutely to experienced mouse killing rats, PEA (16 and 32 mg/kg) inhibited killing in a direct dose dependent manner. This is similar to the dose dependent inhibition of killing by amphetamine reported previously. However, d-amphetamine but not PEA showed physiologic tolerance following 8 days of twice daily administration. Cross tolerance between the two drugs only occurred when d-amphetamine was administered subacutely. It was concluded that PEA and d-amphetamine have sililar acute effects but differed when given subacutely since PEA did not show tolerance and there was not bidirectional cross-tolerance. These data suggest that these drugs have different pharmacologic actions when given repeatedly. One possible difference may be the duration of action.

Aggression↗
PubMed1978

Effects of para-chlorophenylalanine and 5-hydroxytryptophan on mouse killing behavior in killer rats.

The effects of para-chlorophenylalanine (PCPA) on mouse killing behavior were examined in natural killer rats. Forty-eight hr after injection, this serotonin synthesis inhibitor, at relatively low doses of 75 and 150 mg/kg, facilitated mouse killing, as indicated by a decrease in latency to attack the mouse. This effect was revealed in a test of satiation, in which five successive mice were presented to the rat, and also in a novel cage situation. Other than the shorter latencies to attack and kill mice, the killing response was similar in topography to the natural kill. The increase in killing after PCPA injection was associated with a reliable reduction in brain serotonin and in 5-hydroxyindoleacetic acid, and the time courses of the behavioral and biochemical changes were generally similar. In contrast to PCPA, injection of the serotonin precursor 5-hydroxytryptophan (5-HTP, 100 mg/kg) reliably lengthened attack and kill latencies in killer rats. In rats pretreated with PCPA, 5-HTP not only reversed this drug's facilitation of killing, but completely blocked killing in 67% of the rats tested. These results strengthen the hypothesis that brain serotonergic neurons are involved in the inhibition of mouse killing.

5-Hydroxytryptophan↗
PubMed1977

Facilitation and disruption by mescaline and 3,4-dimethoxyphenylethylamine of shock avoidance in rats.

The effects of mescaline hydrochloride (4.95-79.2 mg/kg i.p.) and its non-hallucinogenic analogue 3,4-dimethoxyphenylethylamine hydrochloride (DMPEA) (12.5-100 mg/kg i.p.) on shock avoidance in a shuttlebox were studied in male Long-Evans rats trained to high (above 88%, good performers) or low (below 6%, poor performers) stable base-line avoidance rates. In good performers, mescaline and DMPEA caused a dose-dependent decrease in avoidance rate (ED 50's 44.6 and 39.2 mg/kg, respectively) without affecting presession (5-min adaptation period) or intertrial shuttlebox crossings. In poor performers, mescaline caused a dose-dependent increase in avoidance rate (ED 50 = 24.8 mg/kg) and intertrial crossings, without affecting presession crossings. The results suggest that mescaline, but not DMPEA, has dual facilitative and disruptive effects on avoidance behavior at similar dose ranges. The facilitative, but not the disruptive, effect may be related to changes in motor activity.

Animals↗
PubMed1977

Cross-modal transfer in human infants.

This study investigated cross-modal transfer in infants by their proclivity to respond differentially to novel and familiar stimuli after familiarization in a different sensory modality. Across a variety of stimulus shapes, 1-year-old infants significantly and reliably looked more at and reached more for the novel than the familiar stimulus subsequent to information input from tactual stimulation. Furthermore, for the first time, it is demonstrated that not only do infants gain information about the shape of objects from their oral experience with them but this information can be made available to the visual modality.

Discrimination, Psychological↗
PubMed1975

Does increasing stress change the behavioral action of mescaline from disruption to facilitation?

This experiment is related to the hypothesis of Bridger and of Wray that hallucinogens have facilitatory effects on animal behavior when stress is part of the experiment and have disruptive effects otherwise. Male Long-Evans rats were trained to high (above 89%), stable base line rates of shuttlebox avoidance, then given each of four treatments at 6-day intervals after returning to base line avoidance rates: 1. saline (1 ml i.p.), 2. saline+stressor, 3. mescaline hydrochloride (36.6 mg/kg i.p.), 4. mescaline (39.6 mg/kg i.p.)+stressor. Stress treatment was 1.0 mA footshock (1 sec duration) every 20-30 sec for 15 min between injection and session. Sessions (100 trials) began 20 min after injection. Treatments 1 and 2 had no effect on avoidance rate. Treatments 3 and 4 significantly decreased avoidance rate, with the latter causing significantly more decrease than the former. None of the treatments affected presession (5 min adaptation period) or intertrial crossings of the shuttlebox or latency on escape trials. These results suggest that exposure to a stressor, per se, is not the crucial factor causing hallucinogens to have facilitatory effects on animal behavior.

Adaptation, Psychological↗