1,721,204 research outputs found
Molecular mechanisms of cannabinoid addiction
No full textCannabis is the world's most widely used illicit substance, with an estimated number of 119–224 million users worldwide. In recent years we assisted to an increased effort aimed to individuate the brain circuits underlying cannabis addiction and dependence. Similarly to other drugs of abuse, repeated exposure to cannabinoids causes brain neuroadaptations that persist long after drug effects, contribute to the negative affective states during withdrawal, and ultimately facilitate relapse. Recently, considerable progress has been made in understanding the cellular and molecular consequences of prolonged cannabis use, among which is the identification of specific set of transcriptional regulations that develop differently after chronic cannabinoids and in the abstinent brain
Stress-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
Failure of naloxone to modify electroencephalogram interictal epileptiform discharges in patients with primary generalized epilepsy after sleep deprivation
No full textSleep deprivation (SD) is a method widely used to activate EEG epileptiform activity, but the basis of this effect remains unknown. One possibility is that SD shares a common mechanism with physical and psychological stresses that also precipitate seizures. Because endogenous opioids are released during stress, opioids may play a role in enhancing epileptiform EEG patterns after SD. We report the effects of SD on EEG epileptiform activity in a small but highly homogeneous population of 13 epileptic patients with idiopathic (primary) generalized epilepsy (IGE). SD increased EEG interictal epileptiform discharges (IEDs); this activation was not modified by naloxone (NAL). Our results, in contrast to those of previous investigations of localization-related epilepsy, which showed an increase in IEDs after NAL administration, suggest a possible difference in the mechanism whereby SD enhances IEDs in IGE and localization-related epilepsy
CHRONIC MIANSERIN AFFECTS CORTICOTROPIN RELEASING FACTOR LEVELS IN THE RAT LIMBIC SYSTEMBRAIN
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