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Chunk #1 — Introduction

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GABAergic gene expression in postmortem hippocampus from alcoholics and cocaine addicts; corresponding findings in alcohol-naïve P and NP rats.
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There has been increasing interest in the role of the hippocampus in addiction, a disorder that involves changes in neuronal circuits involved in saliency/reward, motivation/drive, memory/conditioning and control/disinhibition [3], [4]. The hippocampus is implicated in long and short term episodic memory thereby playing a role in the processing of contextual cues within the memory/conditioning neuronal circuit that is considered to be important in drug reinforcement behaviors in animals and craving and relapse in humans [4]. Imaging studies in humans have shown that cue-elicited craving activates the hippocampus [3]. Addictive drugs impair neurogenesis in the adult hippocampus and there is increasing evidence to show that this may be associated with impairments of learning and memory [4]–[6]. Suppression of adult hippocampal neurogenesis has been shown to increase cocaine self-administration in rats [7]. Moreover, the hippocampus is part of the default mode network, a set of brain regions that exhibit resting state synchronized low frequency oscillations. The default mode network is impaired in addiction and it has been suggested that the altered resting state functional connectivity may underlie the heightened sensitivity to drug