catalepsy/kanapė

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Modulation by female sex hormones of the cannabinoid-induced catalepsy and analgesia in ovariectomized mice.

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Cannabinoids are psychoactive compounds with many pharmacological properties such as analgesia, sedation and catalepsy most of which are mediated by cannabinoid CB1 receptors. In the present study, we evaluated whether the ovarian sex hormones are involved in the cannabinoid-induced catalepsy and

Effect of restraint stress on cannabis-induced catalepsy in rats.

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The effect of restraint stress (1, 2 and 4 hr) on cannabis-induced catalepsy, was investigated in rats. Restraint stress produced a time-related-potentiation of the cataleptic effect of a sub-cataleptic dose of cannabis. Stress (4 hr)-induced potentiation of cannabis catalepsy was attenuated after

CB1 cannabinoid receptor-mediated anandamide signaling mechanisms of the inferior colliculus modulate the haloperidol-induced catalepsy.

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The inferior colliculus (IC), a midbrain structure that processes acoustic information of aversive nature, is distinguished from other auditory nuclei in the brainstem by its connections with structures of the motor system. Previous evidence relating the IC to motor behavior shows that glutamatergic

Effects of cannabinoid receptor stimulation and blockade on catalepsy produced by dopamine receptor antagonists.

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The ability of cannabinoid receptor stimulation or blockade to alter catalepsy produced by dopamine D1 and D2 receptor antagonists was studied in rats. The cannabinoid receptor antagonist SR 141716A (N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-me thyl-1H-

Enhancement by chlordiazepoxide of catalepsy induced in rats by intravenous or intrapallidal injections of enantiomeric cannabinoids.

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The cataleptic response of rats to (-)-delta-9-tetrahydrocannabinol (delta-9-THC), measured using a bar test, was enhanced by subcutaneous pretreatment with chlordiazepoxide (10 mg/kg). Significant potentiation was observed when the cannabinoid was administered peripherally (0.1-1.0 mg/kg i.v.) and

Pharmacological and pharmacokinetic characterization of the cannabinoid receptor 2 agonist, GW405833, utilizing rodent models of acute and chronic pain, anxiety, ataxia and catalepsy.

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To date, two cannabinoid receptors have been identified, CB1 and CB2. Activation of these receptors with non-selective cannabinoid receptor agonists reduces pain sensitivity in animals and humans. However, activation of CB1 receptors is also associated with central side effects, including ataxia and

Effects of Cannabis sativa extract on haloperidol-induced catalepsy and oxidative stress in the mice.

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Haloperidol is a classic antipsychotic drug known for its propensity to cause extrapyramidal symptoms due to blockade of dopamine D2 receptors in the striatum. Interest in medicinal uses of cannabis is growing. Cannabis sativa has been suggested as a possible adjunctive in treatment of Parkinson's

Change in hypothermia and catalepsy induced by cannabinoids or morphine in mice tolerant to these substances.

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delta 8-Tetrahydrocannabinol (THC)- and 8 beta, 9 beta-epoxyhexahydrocannabinol (EHHC)-tolerant mice were tolerant to the hypothermia produced by morphine while 8 alpha, 9 alpha-EHHC-tolerant mice were not. Morphine-tolerant mice acquired partial tolerance to the hypothermic effect of 8 alpha,9

Cannabis-induced catalepsy in mice: role of putative neurotransmitters.

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Evaluation of the in vivo receptor occupancy for the behavioral effects of cannabinoids using a radiolabeled cannabinoid receptor agonist, R-[125/131I]AM2233.

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G-protein coupled receptors exist in both high and low agonist affinity conformations, with tracer levels of agonist radioligands preferentially binding to the former. The goal of the present study was to characterize the in vivo binding of the aminoalkyindole-based, CB1 receptor agonist,

Inhalation exposure to smoke from synthetic "marijuana" produces potent cannabimimetic effects in mice.

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BACKGROUND Use of synthetic "marijuana" has increased in recent years, produced adverse effects and prompted the temporary DEA ban of five specific cannabinoid analogs, including JWH-018. The objectives of the current study include determining the chemical content of the herbal product, Buzz,

Opioid and cannabinoid synergy in a mouse neuropathic pain model.

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Clinical studies have reported that pan-cannabinoid receptor agonists may have efficacy in neuropathic pain states and that this might be enhanced by co-administration with opioids. While cannabinoid-opioid analgesic synergy has been demonstrated in animal models of acute pain, it has not been

Cyclic ovarian hormone modulation of supraspinal Δ9-tetrahydrocannabinol-induced antinociception and cannabinoid receptor binding in the female rat.

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Estrous cycle-related fluctuations in delta-9-tetrahydrocannabinol (THC)-induced antinociception have been observed in the rat. The aim of this study was to determine which major ovarian hormone modulates the antinociceptive effects of i.c.v. THC, and whether hormone modulation of THC's behavioral

The cannabinoid agonists WIN 55,212-2 and CP 55,940 attenuate rotational behavior induced by a dopamine D1 but not a D2 agonist in rats with unilateral lesions of the nigrostriatal pathway.

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The effect of cannabinoid receptor stimulation on rotational behavior induced by a dopamine D1 and a D2 agonist was studied in rats with unilateral 6-hydroxydopamine-induced lesions of the dopaminergic nigrostriatal pathway. The cannabinoid agonists WIN 55,212-2 (2.5 mg/kg) and CP 55,940 (0.1 mg/kg)

Cannabinoid receptor agonist and antagonist effects on motor function in normal and 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP)-treated non-human primates.

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BACKGROUND Although cannabinoid effects on motor function have been extensively studied in rodents, the role of cannabinoids in regulating behavior in primates is relatively unknown. OBJECTIVE We compared the effects of cannabinoid agonists and dopamine antagonists on unconditioned behaviors in

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