Brain reward circuitry:The overlapping neurobiology of trauma and substance use disorders

Mental health symptoms secondary to trauma exposure and substance use disorders(SUDs)co-occur frequently in both clinical and community samples.The possibility of a shared aetiology remains an important question in translational neuroscience.Advancements in genetics,basic science,and neuroimaging have led to an improved understanding of the neural basis of these disorders,their frequent comorbidity and high rates of relapse remain a clinical challenge.This project aimed to conduct a review of the field’s current understanding regarding the neural circuitry underlying posttraumatic stress disorder and SUD.A comprehensive review was conducted of available published literature regarding the shared neurobiology of these disorders,and is summarized in detail,including evidence from both animal and clinical studies.Upon summarizing the relevant literature,this review puts forth a hypothesis related to their shared neurobiology within the context of fear processing and reward cues.It provides an overview of brain reward circuitry and its relation to the neurobiology,symptomology,and phenomenology of trauma and substance use.This review provides clinical insights and implications of the proposed theory,including the potential development of novel pharmacological and therapeutic treatments to address this shared neurobiology.Limitations and extensions of this theory are discussed to provide future directions and insights for this shared phenomena.

Differential Effects of Voluntary Ethanol Consumption on Dopamine Output in the Nucleus Accumbens Shell of Roman High- and Low-Avoidance Rats: A Behavioral and Brain Microdialysis Study

The Roman high(RHA) and low-Avoidance (RLA) rats were selectively bred for rapid vs poor acquisition of two-way active avoidance behavior. These lines differ in numerous behavioral traits, with RLA rats being more fearful/anxious than RHA rats, and the latter being novelty-seekers and showing larger intake of, and preference for, addictive substances including ethanol (ETH). Moreover, several differences in central dopaminergic, serotonergic, and GABAergic functions have been reported in these two lines. Since those neural systems are involved in the regulation of ETH consumption, it was considered of interest to investigate: 1) the differences in ETH intake and preference between RHA and RLA rats, 2) the effects of ETH on DA release in the shell of the nucleus accumbens (AcbSh) using brain microdialysis. ETH solutions of increasing concentrations (2% - 10%) were presented on alternate days in a free choice with water. To examine ETH intake and preference stability, animals were subsequently switched to daily presentations of 10% ETH for 10 consecutive days. RHA rats consumed significantly larger amounts of ETH and displayed higher ETH preference than did RLA rats throughout the acquisition and maintenance phases. Following chronic exposure to ETH the animals were habituated to a restricted access to ETH schedule (2% ETH, 2 h per day × 4 days) before surgical implantation of a dialysis probe in the AcbSh. Under these experimental conditions, voluntary ETH intake (2%, 1 h, p.o.) produced a significant increase in accumbal DA output in RHA rats but not in their RLA counterparts. Finally, the i.p. administration of ETH (0.25 g/kg) to na?ve Roman rats produced a significant increment in accumbal DA output only in RHA rats. These results indicate that the mesolimbic dopaminergic system of RHA rats is more responsive to the effects of ETH than that of RLA rats.

High on food： the interaction between the neural circuits for feeding and for reward

Hunger, mostly initiated by a deficiency in energy, induces food seeking and intake. However, the drive toward food is not only regulated by physiological needs, but is motivated by the pleasure derived from ingestion of food, in particular palatable foods. Therefore, feeding is viewed as an adaptive motivated behavior that involves integrated communication between homeostatic feeding circuits and reward circuits. The initiation and termination of a feeding episode are instructed by a variety of neuronal signals, and maladaptive plasticity in almost any component of the network may lead to the development of pathological eating disorders. In this review we will summarize the latest understanding of how the feeding circuits and reward circuits in the brain interact. We will emphasize communication between the hypothalamus and the mesolimbic dopamine system and highlight complexities, discrepancies, open questions and future directions for the field.