1988
DOI: 10.1016/0006-8993(88)90749-4
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The effects of Δ9-tetrahydrocannabinol on potassium-evoked release of dopamine in the rat caudate nucleus: an in vivo electrochemical and in vivo microdialysis study

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Cited by 123 publications
(23 citation statements)
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“…Striatal dopamine hyperactivity has long been implicated in mediating information-processing abnormalities seen in schizophrenia (see Braff and Geyer (1990) for a review) and, recently, implicated in disrupting negative priming (Amitai et al, 2013). As noted above, THC increases levels of dopamine in the rat striatum (Ton et al, 1988) and though administration of THC may not reliably increase striatal dopamine transmission in healthy control participants, it has been shown to do so in patients with psychosis and unaffected first-degree relatives (Kuepper et al, 2013). Adolescents may similarly be more sensitive to the dopaminergic effects of cannabis in the striatum.…”
Section: Discussionmentioning
confidence: 93%
See 1 more Smart Citation
“…Striatal dopamine hyperactivity has long been implicated in mediating information-processing abnormalities seen in schizophrenia (see Braff and Geyer (1990) for a review) and, recently, implicated in disrupting negative priming (Amitai et al, 2013). As noted above, THC increases levels of dopamine in the rat striatum (Ton et al, 1988) and though administration of THC may not reliably increase striatal dopamine transmission in healthy control participants, it has been shown to do so in patients with psychosis and unaffected first-degree relatives (Kuepper et al, 2013). Adolescents may similarly be more sensitive to the dopaminergic effects of cannabis in the striatum.…”
Section: Discussionmentioning
confidence: 93%
“…Specifically, Bloomfield et al (2014) found that among chronic users of cannabis prone to positive psychosislike effects in response to cannabis, frequency of use correlated significantly with reduced dopamine synthesis capacity in the striatum. THC has been shown to increase striatal dopamine transmission in rats (Ton et al, 1988) and humans (Bossong et al, 2009). However, as Bloomfield et al (2014) suggest, chronic use of cannabis in humans (assuming no other risk factors are present) may lead to a downregulation of dopaminergic activity in the striatum.…”
Section: Discussionmentioning
confidence: 97%
“…In vivo microdialysis shows that acute THC increases dopamine efflux in the prefrontal cortex (PFC)41, striatum42 and nucleus accumbens (NAc)43. Only one study did not find THC–induced increases in dopamine efflux44, which may have been related to route of administration since that study used a THC gavage whereas the other studies used intravenous injection which produces a rapid increase in THC which reaches the brain promptly compared to gavage which favours sequestration in lipid compartments due to the very high lipid solubility of THC45.…”
Section: Acute Thc and Presynaptic Dopamine In Animalsmentioning
confidence: 99%
“…In this context, it might be the case that KOR activity plays a role in the modulation of THC's rewarding effects and thus the reported change in place avoidance induced by the blocking of KOR reflects changes in reward and not in THC's aversive effects. Such a possibility is supported by the fact that THC increases dopamine release at the nucleus accumbens (Jianping et al 1990; Tanda et al 1997; Ton et al 1988) and increases dynorphin production and release (Houser et al 2000; Mason et al 1999; Welch and Eads 1999) which in turn inhibits mesolimbic dopamine (Manzanares et al 1991; Margolis et al 2006; Spanagel et al 1992). Blocking KOR activity would increase DA and THC's rewarding effects.…”
Section: Discussionmentioning
confidence: 99%