1,721,135 research outputs found
Differential Role of CB1 and Opioid Receptors in the Reinstatement of Heroin-Seeking Behaviour and Cannabinoid Intake Following Extinction
No full textStress-induced sleep deprivation modifies corticotropin releasing factor (CRF) levels and CRF binding in rat brain and pituitary
No full textElectroencephalographic (EEG) studies have shown that corticotropin-releasing factor (CRF) administration induces EEG activation, decreases sleep time both in rats and humans and modifies the sleep pattern in sleep deprived rats. In the present study we have investigated whether CRF neuronal activity could be altered in a situation of disrupted sleep-wake cycle. Sleep deprivation (SD) was induced by keeping the rat for 72 h on a small platform (7 cm) surrounded by water. Immediately after the SD period rats were killed and CRF levels and CRF receptor binding were evaluated in different brain areas. A marked increase in CRF levels was present in the striatum (+224%), limbic areas (+144%) and pituitary (+42%) whereas the hypothalamic CRF content was reduced (-57%). A significant decrease in CRF binding was found in the striatum (-33%) and pituitary (-38%) of sleep deprived rats. These results indicate that CRF neuronal activity is stimulated by SD, suggesting that CRF might play an important role in the physiological regulation of the sleep-wake cycle and that an altered CRF neuronal activity might be involved in behavioral modifications related to sleep disturbances. (C) 1997 The Italian Pharmacological Society
Reinstatement of opioid-seeking by cannabinoids in animal models of relapse to drug abuse
No full textSleep-deprivation decreases mu and delta opioid receptor-binding in the rat limbic system
No full textSleep deprivation induced by the platform technique is considered to be a heavy stressful situation in rats. At the end of the sleep deprivation period (72 h) the rat displayed particular behavior characterized by wakefulness, a high degree of motor and exploratory activity, increased alertness and reactivity to environmental stimuli. Our previous results indicated that this behavior was antagonized by the administration of the opioid receptor antagonist naloxone and increased by opioid agonists. In this paper we show that concomitantly with this behavior, a decreased B(max) of mu and delta-opioid receptors is present in the limbic system of these animals. These data suggest an active role of limbic-mu and delta-receptors in the generation of arousal and insomnia related to sleep deprivation induced stress
Endocannabinoid regulation of relapse mechanisms
No full textAddiction involves a complex neuropharmacologic behavioural cycle, in which positive reinforcement exerted by the drug and the negative state of withdrawal drive the user to extremes to obtain the drug. Comprehensive studies have established that relapse is the most common outcome of recovery programs treating addictive behaviours. Several types of anticraving medication are available nowadays, such as naltrexone for the treatment of alcoholism, bupropion for nicotine, methadone or buprenorphine for heroin. This review focuses on recent behavioural data providing a rationale for an endocannabinoid mechanism underlying reinstatement of compulsive drug seeking. Studies supporting the contention that reinstatement of extinguished drug self-administration behaviour may be generated by cannabinoid CB I receptor agonists and attenuated, if not blocked. by CB I receptor antagonists, are here reviewed. In support to these findings, conditioned place preference studies substantiate the involvement of the endocannabinoid system in recidivism mechanisms by demonstrating that motivation to relapse can be triggered by CB I receptor activation while blockade of such receptors may prevent reinstatement of place conditioning induced by either drug primings or drug-associated cues. Finally biochemical studies evaluating changes in endocannabinoid levels, CB I receptor density and CB I mRNA expression during re-exposure to drug following extinction are also examined. Taken together, the evidence available has important implications in the understanding and treatment of relapsing episodes in patients undergoing detoxification
CHRONIC MIANSERIN AFFECTS CORTICOTROPIN RELEASING FACTOR LEVELS IN THE RAT LIMBIC SYSTEMBRAIN
No full textScopolamine and MK801-induced working memory deficits in rats are not reversed by CBD-rich cannabis extracts
No full textSmoking marijuana causes working and short-term memory deficits, an effect that is mediated by cannabinoid receptor (CBI) activation in the brain. While this may be due to the main psychoactive constituent Delta(9)-tetrahydrocannabinol (Delta(9)-THC), plantextracts also contain other cannabinoid and terpenoid compounds with unknown properties. Towards this end, we have recently shown that high concentrations of plant extracts rich in cannabidiol (CBD) can reverse working memory deficits induced by Delta(9)-THC which is a remaining contaminant of this extract [Fadda P, Robinson L, Fratta W. Pertwee RG, Riedel G. Differential effects of THC- and CBD-rich cannabis-ex tracts on working memory in rats. Neuropahrmacology 2004:47:1170-9]. Since this effect was dose-dependent and indicative of memory enhancing qualities of the CBD-rich extract, this prompted a wider investigation into the effects of CBD on other forms of amnesia in order to determine the mechanism of action and to reveal its potency against anticholinergic and antiglutamatergic agents.
We employed a spatial delayed matching to position task in the open-field water maze. Both scopolamine (0.2 mg/kg i.p.) and dizocilpine (MK801: 0.1 mg/kg i.p.) impaired working memory at delays of 30 s and 4 h. Two doses of CBD-rich extracts (5 and 10 mg/kg), which did not affect working memory when given alone, were unable to reverse these deficits when co-administered with scopolamine or MK801.
These data suggest that reversal of working memory deficits by CBD-rich extracts are specific to the cannabinoid system and do not compensate for acutely induced cholinergic or glutamatergic receptor hypoactivity. (c) 2005 Elsevier B.V. All rights reserved
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