Addiction
Displaying results 1-42 of 42
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Impairment of Synaptic Plasticity by Cannabis,
9-THC, and Synthetic Cannabinoids
- Alexander F. Hoffman,
- Eun-Kyung Hwang,
- and Carl R. Lupica
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Synaptic Targets of
- Alexander F. Hoffman,
- and Carl R. Lupica
Marijuana contains the psychoactive molecule
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Some patients do not respond to naltrexone, a μ-opioid receptor antagonist used to treat alcohol addiction. An SNP in the μ-opioid receptor gene may be useful for predicting naltrexone response.
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Nicotinic acetylcholine receptor subunits that are highly expressed in the medial habenula and/or interpeduncular nucleus play a critical role in nicotine withdrawal.
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Nicotine intake and nicotine seeking are reduced by blocking glutamatergic neurotransmission and by facilitating GABA neurotransmission. Medications that target these pathways are being evaluated in human smokers.
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Neurobiological mechanisms that underlie drug addiction have been identified across the entire addiction cycle. Although the details vary across drugs of abuse and stages of the cycle, the mesocorticolimbic pathway plays a key role.
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Even after a long period of abstinence from cocaine, synaptic changes induced by drug use may lead to relapse. Changes on excitatory afferents onto dopamine neurons in the ventral tegmental area occur after first exposure.
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Several symptoms of addictive behavior (e.g., escalation of drug use and neurocognitive deficits) occur in laboratory animals. Animal studies can thus be used to study the neural and genetic basis for drug addiction.
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The bed nucleus of the stria terminalis (the BNST) is a key middle management region of the extended amygdala. Alcohol-induced dysregulation of N-methyl-D-aspartate (NMDA) receptors in the BNST may disrupt key neural circuitries.
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Repeated cocaine exposure produces stable gene expression changes (e.g., in brain-derived neurotrophic factor [BDNF]) in discrete brain regions. Many of these changes coincide with drug-seeking behavior.
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Nearly 80% of nicotine users stop smoking once treated with varenicline (Chantix). Its success suggests that compounds modulating the cholinergic system may serve as promising drugs for smoking cessation treatment.
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Drugs like cocaine activate the transcription factor CREB within neurons of the nucleus accumbens. This causes an increase in CREB-regulated dynorphin, which may contribute to a drug withdrawal state and thus continued drug use.
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During cocaine withdrawal, AMPA receptor levels in nucleus accumbens synapses increase. But the time course of up-regulation and the type of AMPA receptor affected depend on the cocaine regimen.
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The effectiveness of opioid medications to reduce opioid choice is determined by the state of opioid dependence and withdrawal in the subject. Currently, no nonopioid medications safely and reliably reduce opioid choice.
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The α4β2* nicotinic acetylcholine receptors (nAChRs) mediate behaviors related to nicotine addiction. Other α and β subunits can be incorporated into nAChRs and may modulate these behaviors.
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Nicotine exposure during adolescence alters acetylcholine and glutamate receptor signaling in the prefrontal cortex, one of the last brain areas to mature. This may help explain altered cognitive function and attention performance in adolescents who smoke.
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The Central Amygdala and Alcohol: Role of
-Aminobutyric Acid, Glutamate, and Neuropeptides
- Marisa Roberto,
- Nicholas W. Gilpin,
- and George R. Siggins
Alcohol has strong and persistent effects on synaptic transmission in the central amygdala. Most notably, it potentiates the GABAergic system.
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Optogenetics allows for pathway-specific manipulation of neural circuitry over a range of timescales. It can be effectively combined with slice electrophysiology and in vivo behavioral paradigms.
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Molecular signals induced during the early phases of drug usage may produce long-lasting neuronal alterations. For example, cocaine may enhance expression of transcription factor
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Opiate addiction involves dopamine-dependent and dopamine-independent mechanisms. The ventral tegmental area (VTA) appears to be crucial for the selection of these pathways.
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Opiate drugs exert their primary addictive effects on the μ opioid receptor. But glutamate receptors (e.g., NMDA), which are involved in most types of memory formation, are also critical for opiate reward.
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Opiate drugs induce longer-lasting neuronal adaptations in two brain regions rich in catecholamine neurons. These changes contribute to opiate dependence and addiction.
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The most effective drugs to treat alcohol, opioid, and nicotine addiction involve receptor stimulation, with the goal of obviating drug withdrawal. Effective treatments for psychostimulant addiction remain elusive.
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