The Role of Galanin System in Modulating Depression, Anxiety, and Addiction-Like Behaviors After Chronic Restraint Stress.
The role of galanin system in modulating depression, anxiety, and addiction-like behaviors after chronic restraint stress.
Neuroscience. 2013 Apr 29;
Zhao X, Seese RR, Yun K, Peng T, Wang Z
There is high comorbidity between stress-related psychiatric disorders and addiction, suggesting they may share one or more common neurobiological mechanisms. Because of its roles in both depressive and addictive behaviors, the galanin system is a strong candidate for such a mechanism. In this study, we tested if galanin and its receptors are involved in stress-associated behaviors and drug addiction. Mice were exposed to 21 days of chronic restraint stress (CRS); subsequently, mRNA levels of galanin, galanin receptors, and the rate-limiting enzymes for synthesis of monoamine autoreceptors were measured in the nucleus accumbens by qRT-PCR. Moreover, we tested the effects of this stress on morphine-induced addictive behaviors. We found that CRS induced anxiety and depression-like behaviors, impaired the formation and facilitated the extinction process in morphine-induced conditioned place preference (CPP), and also blocked morphine-induced behavioral sensitization. These behavioral results were accompanied by a CRS-dependent increase in the mRNA expression of galanin, galanin receptor 1 (GalR1), tyrosine hydroxylase (TH), tryptophan hydroxylase 2, and 5-HT1B receptor. Interestingly, treatment with a commonly used antidepressant, fluoxetine, normalized the CRS-induced behavioral changes based on reversing the higher expression of galanin and TH while increasing the expression of GalR2 and ?2A-adrenceptor. These results indicate that activating the galanin system, with corresponding changes to noradrenergic systems, following chronic stress may modulate stress-associated behaviors and opiate addiction. Our findings suggest that galanin and galanin receptors are worthy of further exploration as potential therapeutic targets to treat stress-related disorders and drug addiction. HubMed – addiction
Cognitive Function During Nicotine Withdrawal: Implications for Nicotine Dependence Treatment.
Neuropharmacology. 2013 Apr 29;
Ashare RL, Falcone M, Lerman C
Nicotine withdrawal is associated with deficits in neurocognitive function including sustained attention, working memory, and response inhibition. Several convergent lines of evidence suggest that these deficits may represent a core dependence phenotype and a target for treatment development efforts. A better understanding of the mechanisms underlying withdrawal-related cognitive deficits may lead to improve nicotine dependence treatment. We begin with an overview of the neurocognitive effects of withdrawal in rodent and human models, followed by discussion of the neurobehavioral mechanisms that are thought to underlie these effects. We then review individual differences in withdrawal-related neurocognitive effects including genetics, gender, and psychiatric comorbidity. We conclude with a discussion of the implications of this research for developing improved therapies, both pharmacotherapy and behavioral treatments, that target cognitive symptoms of nicotine withdrawal. HubMed – addiction
Rapid, Transient Synaptic Plasticity in Addiction.
Neuropharmacology. 2013 Apr 29;
Gipson CD, Kupchik YM, Kalivas PW
Chronic use of addictive drugs produces enduring neuroadaptations in the corticostriatal glutamatergic brain circuitry. The nucleus accumbens (NAc), which integrates cortical information and regulates goal-directed behavior, undergoes long-term morphological and electrophysiological changes that may underlie the increased susceptibility for relapse in drug-experienced individuals even after long periods of withdrawal. Additionally, it has recently been shown that exposure to cues associated with drug use elicits rapid and transient morphological and electrophysiological changes in glutamatergic synapses in the NAc. This review highlights these dynamic drug-induced changes in this pathway that are specific to a drug seeking neuropathology, as well as how these changes impair normal information processing and thereby contribute to the uncontrollable motivation to relapse. Future directions for relapse prevention and pharmacotherapeutic targeting of the rapid, transient synaptic plasticity in relapse are discussed. — 132 words — HubMed – addiction