Addiction

Summary

Addiction is generally a neuropsychological disorder defining pervasive and intense urge to engage in maladaptive behaviors providing immediate sensory rewards (e.g. consuming drugs, excessively gambling), despite their harmful consequences. Dependence is generally an addiction that can involve withdrawal issues. Addictive disorder is a category of mental disorders defining important intensities of addictions or dependences, which induce functional disabilities. There are no agreed definitions on these terms – see section on 'definitions'. Repetitive drug use alters brain function in ways that perpetuate craving, and weakens (but does not completely negate) self-control. This phenomenon – drugs reshaping brain function – has led to an understanding of addiction as a brain disorder with a complex variety of psychosocial as well as neurobiological (and thus involuntary) factors that are implicated in addiction's development.

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https://en.wikipedia.org/wiki/Addiction

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Reward timing, that is, the delay after which reward is delivered following an action is known to strongly influence reinforcement learning. Here, we asked if reward timing could also modulate how people learn and consolidate new motor skills. In 60 healthy participants, we found that delaying reward delivery by a few seconds influenced motor learning. Indeed, training with a short reward delay (1 s) induced continuous improvements in performance, whereas a long reward delay (6 s) led to initially high learning rates that were followed by an early plateau in the learning curve and a lower performance at the end of training. Participants who learned the skill with a long reward delay also exhibited reduced overnight memory consolidation. Overall, our data show that reward timing affects the dynamics and consolidation of motor learning, a finding that could be exploited in future rehabilitation programs.

CELL PRESS2022

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The identification of neural substrates underlying the long lasting debilitating impact of drug cues is critical for developing novel therapeutic tools. Metabolic coupling has long been considered a key mechanism through which astrocytes and neurons actively interact in response of neuronal activity, but recent findings suggested that disrupting metabolic coupling may represent an innovative approach to prevent memory formation, in particular drug-related memories. Here, we review converging evidence illustrating how memory and addiction share neural circuitry and molecular mechanisms implicating lactate-mediated metabolic coupling between astrocytes and neurons. With several aspects of addiction depending on mnemonic processes elicited by drug experience, disrupting lactate transport involved in the formation of a pathological learning, linking the incentive, and motivational effects of drugs with drug-conditioned stimuli represent a promising approach to encourage abstinence.

Wiley-Blackwell2016

Disrupting astrocyte-neuron lactate transfer persistently reduces conditioned responses to cocaine

Benjamin Boury-Jamot, Benjamin Boutrel, Anthony Carrard, Pierre Magistretti, Jean-Luc Martin

A central problem in the treatment of drug addiction is the high risk of relapse often precipitated by drug-associated cues. The transfer of glycogen-derived lactate from astrocytes to neurons is required for long-term memory. Whereas blockade of drug memory reconsolidation represents a potential therapeutic strategy, the role of astrocyte-neuron lactate transport in long-term conditioning has received little attention. By infusing an inhibitor of glycogen phosphorylase into the basolateral amygdala of rats, we report that disruption of astrocyte-derived lactate not only transiently impaired the acquisition of a cocaine-induced conditioned place preference but also persistently disrupted an established conditioning. The drug memory was rescued by L-Lactate co-administration through a mechanism requiring the synaptic plasticity-related transcription factor Zif268 and extracellular signal-regulated kinase (ERK) signalling pathway but not the brain-derived neurotrophic factor (Bdnf). The long-term amnesia induced by glycogenolysis inhibition and the concomitant decreased expression of phospho-ERK were both restored with L-Lactate co-administration. These findings reveal a critical role for astrocyte-derived lactate in positive memory formation and highlight a novel amygdala-dependent reconsolidation process, whose disruption may offer a novel therapeutic target to reduce the long-lasting conditioned responses to cocaine.

Nature Publishing Group2015