“
“The neuronal mechanisms underlying
social withdrawal, one of the core negative symptoms of schizophrenia, are not well understood. Recent studies suggest an involvement of the endocannabinoid system in the pathophysiology of schizophrenia and, in particular, of negative symptoms. We used biochemical, pharmacological, and behavioral approaches to investigate the role played by the endocannabinoid system in social withdrawal induced by sub-chronic administration of phencyclidine (PCP). Pharmacological enhancement of endocannabinoid levels via systemic administration of URB597, an inhibitor of endocannabinoid degradation, reversed social withdrawal in PCP-treated rats via stimulation of CB1 receptors, but reduced social interaction in control animals through activation of a cannabinoid/vanilloid-sensitive see more receptor. In addition, the potent CB agonist CP55,940 reversed PCP-induced social withdrawal in a CB1-dependent manner, whereas pharmacological blockade of CB1 receptors by either AM25(1) or SR141716 reduced the time spent in social interaction in control animals. PCP-induced social withdrawal was accompanied by a decrease of anandamide (AEA) levels in the amygdala and prefrontal cortex, and these deficits were reversed by URB597. As CB1 receptors are
URMC-099 clinical trial predominantly expressed on GABAergic interneurons containing the anxiogenic peptide cholecystokinin (CCK), we also examined whether the PCP-induced social withdrawal resulted from deficient CB1-mediated modulation of CCK transmission. The selective CCK2 antagonist LY225910 blocked both PCP- and AM251-induced social withdrawal, but not URB597 effect in control rats. Taken together, these findings indicate that AEA-mediated activation of CB1 receptors is crucial for social interaction, and that PCP-induced social withdrawal results from Molecular motor deficient endocannabinoid transmission.”
“While it is well documented that substance users exhibit attentional
bias toward addiction-related stimuli, the exact mechanism remains unclear.
To differentiate between distinct aspects of attentional allocation in the smoking-cue attentional bias observed in smokers.
Active smokers (AS) and non-smoking controls completed spatial cueing tasks with pairs of smoking and neutral pictorial cues to measure attentional capture, and an attentional blink task with either a smoking or neutral image appearing behind the first target (T1) to measure aspects of attention separate from capture. In addition, we tested groups of sports enthusiasts, and non-enthusiasts in corresponding tasks replacing smoking images with sports-related images to address the possibility that effects found in the smoking study were due simply to greater stimulus familiarity.
Smoking cues reflexively capture smokers’ attention, as AS showed a greater bias toward smoking cues in short stimulus-onset asynchrony (SOA; the time between the onset of two stimuli) trials, but not in trials with a longer SOA.
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