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Biomedical subjects

C Kornetsky

Publications and source records attributed to C Kornetsky.

At least 73 records · Page 4Linked to original sources
PubMed1984

Tripelennamine: enhancement of brain-stimulation reward.

Thresholds for reinforcing electrical stimulation to the medial forebrain bundle were determined in rats by means of a rate-free psychophysical method. The acute administration of tripelennamine lowered the threshold for rewarding brain stimulation in a dose-dependent manner. These results suggest that the abuse liability of tripelennamine may be related to its ability to sensitize the central neural pathway that mediates reward.

Animals↗
PubMed1984

Effects of antipsychotic drugs on brain-stimulation detection: preliminary observations.

The effects of two antipsychotic drugs, haloperidol and clozapine, on the detection of electrical brain stimulation were investigated. Rats were trained to make an instrumental response to a brain stimulation cue delivered via an electrode implanted in one of several forebrain or midbrain loci. A response to this stimulation was reinforced by the delivery of a rewarding electrical stimulus via a second electrode implanted in the hypothalamus. By varying the current intensity of the cue stimulus, a detection threshold was determined in each subject both prior to and after administration of various doses of haloperidol or clozapine. Compared to changes on vehicle control days, both drugs produced a dose-related elevation of the detection thresholds. Although haloperidol was more potent than clozapine in most subjects, the minimal effective doses of haloperidol for affecting detection from forebrain loci were lower than for affecting detection from midbrain loci. A reverse differential sensitivity was observed after clozapine administration. Concurrent effects of these two drugs on latency to respond, as well as on both task defined strength of responding and ability to inhibit responding not only indicated the specificity of threshold elevations, but provided additional behavioral information concerning the actions of the two antipsychotic agents. It is proposed that the method employed in this experiment is suitable for measuring the effects of drugs on the discriminative or perceptual properties of electrical brain stimulation and may indicate central sites of drug action.

Animals↗
PubMed1984

Effects of concomitant pentazocine and tripelennamine on brain-stimulation reward.

Reinforcing thresholds for self-stimulation behavior to the medial forebrain bundle were determined in rats by means of a rate-free psychophysical method. The acute administration of either pentazocine or tripelennamine caused a small but significant lowering of the reward threshold. Combined administration of an ineffective dose of tripelennamine with various doses of pentazocine resulted in a potentiation of this lowering effect. These results suggest that the widespread abuse of the combination of pentazocine and tripelennamine may be due to a pharmacologic potentiation rather than just a summation of their two effects.

Animals↗
PubMed1983

Detection thresholds for electrical stimulation of forebrain and midbrain loci in the rat.

Current intensity thresholds for the detection of electrical brain stimulation were determined from a variety of forebrain and midbrain sites in rats. In a discrete trial, instrumental paradigm, the detection stimulus delivered via one electrode acted as a cue for the availability of response contingent rewarding brain stimulation delivered via a second electrode in the posterolateral hypothalamus. The current intensity of the detection stimulus (20 Hz) was varied according to a modification of the psychophysical method of constant stimuli, while the intensity of contingent rewarding stimulation (160 Hz) was fixed at a highly reinforcing level. Detection thresholds measured from forebrain sites were significantly lower than thresholds from midbrain sites. This difference in detection thresholds was not related to any variability between subjects in site or parameters of the rewarding stimulus used to maintain behavior. Lower detection thresholds from forebrain loci may be due to greater sensitivity to electrical stimuli at the detection site or of the pathways from those sites to areas mediating perception or conditioning.

Animals↗
PubMed1983

The effects of levonantradol on rewarding brain stimulation thresholds in the rat.

Rats were implanted bilaterally with electrodes aimed at the medial forebrain bundle (MFB) and trained to deliver intracranial stimulation. Reward thresholds were determined using a modification of the psychophysical method of limits. Levonantradol, a cannabinoid with reported analgesic activity, was tested at doses between 0.0125 to 0.3 mg/kg. Significant elevations of reward thresholds were observed at 0.2 and 0.3 mg/kg. Since none of the doses tested lowered the reward threshold, an effect believed to be predictive of abuse, these results suggest that levonantradol has little or no abuse liability.

Analgesics↗
PubMed1983

Naloxone lowers brain-stimulation escape thresholds.

Rats were trained to escape from aversive electrical brain stimulation to the mesencephalic reticular formation (MRF). The threshold for this escape behavior was determined by a modification of the psychophysical method of limits. The administration of naloxone (4-16 mg/kg, IP) produced a decrease in escape threshold from MRF stimulation. These findings implicate the involvement of the MRF in the modulation of pain and suggest that threshold changes to stimulation at this level of the nociceptive neuro-axis may represent a change in a motivational-attentional dimension of pain.

Animals↗
PubMed1983

Skin-testing with neurotransmitters in schizophrenic patients.

Pilot data are presented on a methodology to study a profile of simultaneous reactivity to intradermally injected norepinephrine, dopamine, serotonin, and histamine. The subject groups were young and old schizophrenics on medication and young control volunteers. Skin reactivity in terms of vasoconstriction, vasodilation, and whealing was measured over the course of 3 hours after the injections. Although interpretation of the results is limited by several sources of confounding error and the small number of subjects, the data suggest that skin-test profiles are sensitive enough to yield significant differences between the groups, particularly in the area of vasoconstriction. Further, abnormal skin reactivity may mirror the hypothesized alterations in CNS neurotransmitter physiology in schizophrenic patients.

Adult↗
PubMed1981

Effects of chronic naloxone treatment on brain-stimulation reward.

Rats were tested on a rate-free psychophysical procedure in order to determine the absolute reinforcement thresholds for self-stimulation behavior. The administration of naloxone (16 mg/kg) for five days failed to alter the reinforcement thresholds on this procedure. To the extent that naloxone is an effective antagonist of endogenous opioids, we conclude that central endorphin systems are not necessary to support self-stimulation behavior.

Animals↗
PubMed1980

Effects of d-amphetamine and naloxone on brain stimulation reward.

Self-stimulation thresholds were determined in rats by means of a modification of the psychophysical method of limits. Reinforcement values were determined after the administration of d-amphetamine alone, naloxone alone, and naloxone administered concurrently with d-amphetamine. d-Amphetamine yielded dose-related decreases in the threshold (0.25--2.00 mg/kg IP), while naloxone alone (2.0--16 mg/kg IP) caused no consistent changes. For each animal, a dose of d-amphetamine that substantially lowered the threshold was then selected to be administered with varying doses of naloxone. The threshold-lowering effect of d-amphetamine was blocked by naloxone at doses as low as 2.0 or 4.0 mg/kg. This finding suggests the possible involvement of an opiate receptor in the mediation of the enhancement by d-amphetamine of brain stimulation reward.

Animals↗