Relapse to drug use during abstinence is a defining feature of addiction. To date, however, results from studies using rat relapse/reinstatement models have yet to result in FDA-approved medications for relapse prevention. To address this translational gap, we and others have developed rat models of relapse after voluntary abstinence from drug self-administration. One of these models is the electric barrier conflict model. Here, we introduce the model, and then review studies on behavioral and neuropharmacological mechanisms of cue-induced relapse and incubation of drug seeking (time-dependent increase in drug seeking during abstinence) after electric barrier-induced abstinence. We also briefly discuss future directions and potential clinical implications. One major conclusion of our review is that the brain mechanisms controlling drug relapse after electrical barrier-induced voluntary abstinence are likely distinct from those controlling relapse after homecage forced abstinence.
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http://dx.doi.org/10.1016/j.conb.2024.102856 | DOI Listing |
Biochemistry (Mosc)
November 2024
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, 117485, Russia.
Disturbances in the Hedgehog (Hh) signaling play an important role in dysmorphogenesis of bone tissue and central nervous system during prenatal alcohol exposure, which underlies development of fetal alcohol syndrome. The involvement of Hh proteins in the mechanisms of alcohol intake in adults remains obscure. We investigated the role of the Hh cascade in voluntary ethanol drinking and development of anxiety-like behavior (ALB) during early abstinence and assessed changes in the expression of Hh pathway components in different brain regions of male Wistar rats in a model of voluntary alcohol drinking using the intermittent access to 20% ethanol in a two-bottle choice procedure.
View Article and Find Full Text PDFeNeuro
December 2024
Department of Neuroscience, Tufts School of Medicine, Tufts University, Boston, Massachusetts 02111
Although most adults in the United States will drink alcohol in their life, only ∼6% will go on to develop an alcohol use disorder (AUD). While a great deal of work has furthered our understanding of the cycle of addiction, it remains unclear why certain people transition to disordered drinking. Altered activity in regions implicated in AUDs, like the basolateral amygdala (BLA), has been suggested to play a role in the pathophysiology of AUDs, but how these networks contribute to alcohol misuse remains unclear.
View Article and Find Full Text PDFPLoS One
November 2024
Rakai Health Sciences Program, Kalisizo, Uganda.
Neurobiol Aging
January 2025
Department of Biology, The Pennsylvania State University, University Park, PA 16802, USA; Department of Biomedical Engineering, The Pennsylvania State University, University Park, PA 16802, USA; Departments of Neurosurgery Penn State College of Medicine, University Park, PA 16802, USA; Penn State Neuroscience Institute, University Park, PA 16802, USA. Electronic address:
Both alcohol use disorder (AUD) and cognitive decline include disruption in the balance of excitation and inhibition in the cortex, but the potential role of alcohol use on excitation and inhibition on the aging brain is unclear. We examined the effect of moderate voluntary binge alcohol consumption on the aged, pre-disease neuronal environment by measuring intrinsic excitability and spontaneous neurotransmission on prefrontal cortical pyramidal (excitatory, glutamatergic) and non-pyramidal (inhibitory, GABAergic) neurons following a prolonged period of abstinence from alcohol in mice. Results highlight that binge alcohol consumption has lasting impacts on the electrophysiological properties of prefrontal cortical neurons.
View Article and Find Full Text PDFAddiction
February 2025
Department of Sociology and Anthropology, North Carolina State University, Raleigh, NC, USA.
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