Behavioral and neurochemical effects of Δ9-tetrahydrocannabinol in rats

Bhattacharyya, A.K.; Aulakh, Charanjit S.; Ghosh, P; Rubaai, A.

doi:10.1016/0028-3908(80)90170-7

Cited by 21 publications

(5 citation statements)

References 22 publications

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“…Another behavior measured, sprawling, increased significantly in THC-SS rabbits given THC, in comparison to THC-SR rabbits given the drug. Although this response is not observed in a nondrugged rabbit, it is frequently found after a THC-induced convulsion in an adult THC-SS rabbit (Consroe & Fish, 1980a).…”

Section: Discussionmentioning

confidence: 95%

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The ontogeny of delta‐9‐tetrahydrocannabinol responsiveness in the rabbit

Fish

Consroe

1983

Developmental Psychobiology

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An autosomal recessive condition (thc/thc) in our closed colony of New Zealand White rabbits (Uaz:NZW-thc) results in nonfatal, behavioral convulsions following intravenous (i.v.) injections of delta-9-tetrahydrocannabinol (THC) and other psychoactive cannabinoids of marijuana. The ontogeny of the convulsive response was evaluated in potential THC-seizure-susceptible (SS) rabbits from postnatal Days (PN) 15-548. Ages of nonsusceptibility (PN 15-23), partial susceptibility (PN 24-38), and complete susceptibility (PN 39-548) were found. Also, open-field activity was determined in PN 14-25 THC-SS and THC-seizure-resistant (SR) rabbits. Administration of THC during the seizure-insensitive period resulted in genotype-dependent alternations in photocell activity and sprawling.

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Section: Discussionmentioning

confidence: 95%

“…Those weighmg more than 1 kg were injected with .I ml/ kg. The dose of THC selected was twice the threshold dose required for eliciting convulsions (Consroe & Fish, 1980a). After injection, the rabbits were placed into unfamiliar nest boxes (27.9 cm X 53 cm X 25.4 cm high) and observed for 5 min.…”

Section: Methodsmentioning

confidence: 99%

The ontogeny of delta‐9‐tetrahydrocannabinol responsiveness in the rabbit

Fish

Consroe

1983

Developmental Psychobiology

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“…Drug treatment was then started. The details of the procedures are same as in our previous reports [Bhattacharyya et al, 1979[Bhattacharyya et al, , 1980Bhattacharyya and Pradhan, 1979 a,b].…”

Section: Behavioral Methodsmentioning

confidence: 99%

Correlation of behavioral and neurochemical effects of d‐ and l‐amphetamines

Aulakh¹,

Bhattacharyya²,

Rubaai³

1982

Drug Development Research

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In an attempt to correlate the behavioral and neurochemical effects of d-and I-amphetamines, the time courses of the effects of the two isomers (1 mg/kg; base, i.p.) were studied on spontaneous motor activity (SMA) and stereotyped behavior (ST) as well as on the concentrations of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) in discrete brain areas, such as the caudate nucleus (CN), pons-medulla (PM), and diencephalonmidbrain (DM) in rats. In addition, the dose-response relationship for d-isomer (0.5-2 mg/ kg, i.p.) and I-isomer (1-4 mg/kg, i.p.) was also studied on SMA and ST. SMA increased with the dose up to 1.5 mg/kg for d-isomer and up to 3 mg/kg for I-isomer and then decreased, whereas ST increased with the dose for both the isomers. At 1 mg/kg dose, SMA reached its peak during the fourth postdrug 20-minute period for both d-and I-isomers, whereas ST reached its peak during third to fifth 20-minute periods for d-isomer and during the third period for the I-isomer. The d-isomer significantly increased the DA levels in the CN and DM at 30 minutes postdrug, which reached their maximum at 60 minutes, whereas NE levels in the PM had no significant change at 30 minutes, but were significantly reduced in the DM at 30 minutes and in both PM and DM at 60 minutes postdrug; 5-HT levels in the PM and DM showed no significant change. Compared to d-amphetamine, the I-isomer at 30 and 60 minutes postdrug caused more or less similar changes in the NE levels in the DM and PM, whereas it produced less increase in the DA levels in the CN and DM and significant decrease in 5-HT levels in the DM and PM. It appears that the difference in the behavioral effects induced by the two isomers of amphetamine may be due to the difference in their effects on dopaminergic and serotonergic systems.

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“…However, following a 90 day dosing of THC in Sprague-Dawley rats, no significant change in dopamine receptor or dopamine levels were observed in the caudate nucleus, hypothalamus, septum or hippocampus (Ali et al 1989). Bhattacharyya et al (1980) reported a triphasic dopaminergic response to THC in which the drug led to an initial decrease in caudate nucleus and midbrain dopamine, followed by an increase in dopamine and then a return to baseline. Aulakh et al (1980) found a complicated temporal relationship between THC and dopamine.…”

Section: Thc and Dopamine Synthesismentioning

confidence: 99%

Dopaminergic mechanisms underlying psychosis

Bloomfield¹,

Howes²

2020

Psychotic Disorders

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The theory that dopaminergic mechanisms play a role in psychosis has evolved since the mid-twentieth century. This followed research which found that the clinical potency of antipsychotics was directly related to their affinity for dopamine receptors and drugs that cause dopamine release caused psychotic symptoms. Molecular imaging studies have found consistent evidence that elevated striatal dopamine synthesis capacity is associated with psychotic symptoms including in people with schizophrenia, people at risk of psychosis and first-degree relatives of people with schizophrenia. Importantly, dopamine elevation has been positively correlated with severity of psychotic symptoms. There is also evidence that dopamine dysfunction may be a transdiagnostic feature of psychosis. The dopamine system plays a key role in cognition, including reward prediction error signaling and salience processing. Dopaminergic dysfunction has been hypothesized to give rise to psychosis through aberrant salience processing. Since stressful experiences are highly salient for an organism’s survival, the dopamine system plays a key role in the brain’s response to stressors. Chronic stressors occurring during development can induce long-term changes in dopamine function and may thus provide a pathway through which environmental risk factors for psychosis alter neurobiology to give rise to psychosis. At least some genetic risk factors for psychosis also converge on the dopamine system. These findings have given rise to a “dual hit” model of dopaminergic dysfunction involving genetic vulnerability and responses to environmental stressors.

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Behavioral and neurochemical effects of Δ9-tetrahydrocannabinol in rats

Cited by 21 publications

References 22 publications

The ontogeny of delta‐9‐tetrahydrocannabinol responsiveness in the rabbit

The ontogeny of delta‐9‐tetrahydrocannabinol responsiveness in the rabbit

Correlation of behavioral and neurochemical effects of d‐ and l‐amphetamines

Dopaminergic mechanisms underlying psychosis

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