Exposure to Marijuana Smoke Impairs Memory Retrieval in Mice

Niyuhire, Floride; Varvel, Stephen A.; Martin, Billy R.; Lichtman, Aron H.

doi:10.1124/jpet.107.119594

Cited by 68 publications

(52 citation statements)

References 29 publications

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“…This finding is consistent with studies using relatively high doses of THC (2.5-10 mg/kg), which typically report tolerance (Cha et al, 2006Niyuhire et al, 2007), although exceptions exist (Nava et al, 2001). Rats also develop tolerance to the disruptive effects of THC or full cannabinoid agonists in a delayed nonmatch to sample task after 35 days of repeated administration (Hampson et al, 2003) and to elevated error rates in operant behaviors (Delatte et al, 2002).…”

Section: Discussionsupporting

confidence: 78%

Role of Cannabinoid Receptor Type 1 Desensitization in Greater Tetrahydrocannabinol Impairment of Memory in Adolescent Rats

Moore

Greenleaf²,

Acheson³

et al. 2010

J Pharmacol Exp Ther

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Adolescence is a well defined developmental period during which marijuana use is common. However, little is known about the response to marijuana in adolescents compared with adults. We have shown previously that adolescent rats are more impaired than adults by ⌬ 9 -tetrahydrocannabinol (THC), the main psychoactive compound in marijuana, in a spatial learning task, but the mechanism responsible for this differential impairment is not understood. We determined the role of THC tolerance and cannabinoid receptor type 1 (CB1) regulation in THC-induced spatial learning impairment in adolescent and adult rats. We measured the development of tolerance to THC-induced learning impairment in adolescent (postnatal days 30 -35) and adult (postnatal days 70 -75) rats. We pretreated them for 5 days with 10 mg/kg THC, and then evaluated the effects of vehicle or THC treatment on learning during training in the Morris water maze. We also determined CB1 number and functional coupling in the hippocampus of adolescents and adults. Finally, we measured the time course of hippocampal CB1 desensitization in adolescents and adults during treatment with 10 mg/kg THC or vehicle. Our results indicate that adults, but not adolescents, become tolerant to the effects of THC during water maze training after 5 days of pretreatment. CB1s in adolescent hippocampus are less functionally coupled to G proteins and desensitize more slowly in response to THC treatment than those of adults. THC may impair learning in adolescents more than in adults because of delayed activation of cellular homeostatic adaptive mechanisms underlying cannabinoid tolerance in the hippocampus.

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Section: Discussionsupporting

confidence: 78%

Role of Cannabinoid Receptor Type 1 Desensitization in Greater Tetrahydrocannabinol Impairment of Memory in Adolescent Rats

Moore

Greenleaf²,

Acheson³

et al. 2010

J Pharmacol Exp Ther

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“…The poor memory performance found in mice treated with THC supports previous reports indicating that acute injections of THC disrupt spatial working or short-term memory in the Morris water maze. [11][12][13]24 FAAH −/− Mice Show Enhanced Sensitivity to JZL184-Induced Water Maze Performance Deficits Compared to FAAH +/+ Mice. In the first experiment, the dual FAAH and MAGL inhibitor JZL195 or THC elicited similar magnitudes of acquisition performance in both genotypes.…”

Section: ■ Results and Discussionmentioning

confidence: 99%

“…11,58 Subjects first received a single 5 min acclimation session in which no platform was present, followed by 10 days of training in a fixed-platform task (four trials per day, 10 min between each trial). Repeated acquisition training consisted of five consecutive 2-min trials, in which a new platform location was determined each day but remained constant for that day.…”

Section: ■ Methodsmentioning

confidence: 99%

Dual Fatty Acid Amide Hydrolase and Monoacylglycerol Lipase Blockade Produces THC-Like Morris Water Maze Deficits in Mice

Wise

Long

Abdullah

et al. 2012

ACS Chem. Neurosci.

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Acute administration of Δ 9 -tetrahydrocannabinol (THC) or exposure to marijuana smoke impairs short-term spatial memory in water maze tasks through a CB 1 receptor mechanism of action. N-Arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG) are endogenous cannabinoids that are predominantly metabolized by the respective enzymes fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL). Although the MAGL inhibitor JZL184 enhances short-term synaptic plasticity, it has yet to be evaluated in the Morris water maze. Previous research demonstrated that simultaneous, complete blockade of FAAH and MAGL produces full blown THC-like effects. Thus, in the following studies we tested whether dual blockade of FAAH and MAGL would impair learning in a repeated acquisition Morris water maze task. Mice treated with the dual FAAH/MAGL inhibitor JZL195 (20 mg/kg) as well as JZL184-treated FAAH −/− mice displayed robust deficits in Morris water maze performance that were similar in magnitude to THC-treated mice. While 20 or 40 mg/kg impaired water maze performance in FAAH −/− mice, only the high dose of JZL184 disrupted performance in FAAH +/+ mice. The memory impairing effects of JZL184 were blocked by the CB 1 receptor antagonist rimonabant. Neither JZL184 nor JZL195 impaired performance in a cued version of the water maze task, arguing against the notion that sensorimotor or motivational deficits accounted for the impaired acquisition performance. JZL184 increased 2-AG levels in the hippocampus, prefrontal cortex, and cerebellum to a similar degree in FAAH −/− and +/+ mice. FAAH −/− mice, regardless of drug treatment, possessed elevated AEA levels in each brain region assessed. The results of this study reveal that concomitant increases in AEA and 2-AG disrupt short-term spatial memory performance in a manner similar to that of THC. KEYWORDS: Cannabinoid, memory, N-arachidonoylethanolamine (anandamide), 2-arachidonoylglycerol (2-AG), fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL)The endogenous cannabinoid signaling system has been widely studied to understand its role in physiological and pathological processes. To date, two major endogenous cannabinoids, Narachidonoylethanolamine (anandamide, AEA) and 2-arachidonoylglycerol (2-AG), and their distinct biosynthetic and degradative pathways have been extensively investigated. Both AEA and 2-AG are synthesized and released on demand, in response to diverse physiological stimuli, and are rapidly inactivated by hydrolysis after cellular reuptake. AEA 1 is metabolized by fatty acid amide hydrolase (FAAH), whereas monoacylglycerol lipase (MAGL) is the major catabolic enzyme of 2-AG. 2 These endogenous cannabinoids as well as exogenously administered cannabinoids activate two cannabinoid receptors, CB 1 and CB 2 . 3,4 CB 1 receptors are heterogeneously distributed in high concentrations throughout the central nervous system and periphery and are the predominant target for the psychomimetic effects of Δ 9 -tetrahydrocannabi...

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“…In these regards, cannabis exhibits similar properties with other drugs of abuse, namely rewarding effects with initial use. However, like opiates and unlike ethanol, cocaine, amphetamine, and nicotine, acute administration of THC and cannabidiol have been shown to disrupt hippocampus-dependent spatial learning in the Morris water maze and radial arm maze (Lichtman et al 1995;Lichtman and Martin 1996;Da Silva and Takahashi 2002;Cha et al 2007;Niyuhire et al 2007) as well as contextual fear conditioning (Lemos et al 2010;Stern et al 2012). In line with the animal studies, human studies also suggest that acute cannabinoids result in impaired memory (Tinklenberg et al 1970;Ferraro 1980; for review, see Ranganathan and D'Souza 2006).…”

Section: Cannabismentioning

confidence: 86%

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

2016

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It has long been hypothesized that conditioning mechanisms play major roles in addiction. Specifically, the associations between rewarding properties of drugs of abuse and the drug context can contribute to future use and facilitate the transition from initial drug use into drug dependency. On the other hand, the self-medication hypothesis of drug abuse suggests that negative consequences of drug withdrawal result in relapse to drug use as an attempt to alleviate the negative symptoms. In this review, we explored these hypotheses and the involvement of the hippocampus in the development and maintenance of addiction to widely abused drugs such as cocaine, amphetamine, nicotine, alcohol, opiates, and cannabis. Studies suggest that initial exposure to stimulants (i.e., cocaine, nicotine, and amphetamine) and alcohol may enhance hippocampal function and, therefore, the formation of augmented drug-context associations that contribute to the development of addiction. In line with the self-medication hypothesis, withdrawal from stimulants, ethanol, and cannabis results in hippocampus-dependent learning and memory deficits, which suggest that an attempt to alleviate these deficits may contribute to relapse to drug use and maintenance of addiction. Interestingly, opiate withdrawal leads to enhancement of hippocampus-dependent learning and memory. Given that a conditioned aversion to drug context develops during opiate withdrawal, the cognitive enhancement in this case may result in the formation of an augmented association between withdrawalinduced aversion and withdrawal context. Therefore, individuals with opiate addiction may return to opiate use to avoid aversive symptoms triggered by the withdrawal context. Overall, the systematic examination of the role of the hippocampus in drug addiction may help to formulate a better understanding of addiction and underlying neural substrates.Addiction is a major worldwide health problem that results in maladaptive behavioral changes, some that can last a lifetime. This behavioral plasticity, often times maladaptive, must be associated changes in neural plasticity. In fact, it has been noted multiple times that there is a high degree of overlap between the neurobiology of learning and memory and the neurobiology of addiction

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Exposure to Marijuana Smoke Impairs Memory Retrieval in Mice

Cited by 68 publications

References 29 publications

Role of Cannabinoid Receptor Type 1 Desensitization in Greater Tetrahydrocannabinol Impairment of Memory in Adolescent Rats

Role of Cannabinoid Receptor Type 1 Desensitization in Greater Tetrahydrocannabinol Impairment of Memory in Adolescent Rats

Dual Fatty Acid Amide Hydrolase and Monoacylglycerol Lipase Blockade Produces THC-Like Morris Water Maze Deficits in Mice

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

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