The Future of Addiction and Recovery Healing Arts

2018 ◽  
Author(s):  
Shahla J. Modir ◽  
George E. Muñoz
Keyword(s):  
Addiction Treatment ◽  
Basolateral Amygdala ◽  
Dorsal Striatum ◽  
Brain Regions ◽  
Outcome Data ◽  
Neural Imaging ◽  
Transcranial Magnetic Brain Stimulation ◽  
The Future ◽  
Healing Arts

This chapter peers into the future of addiction treatment. It begins with an exploration of repetitive transcranial magnetic brain stimulation or rTMS as a treatment for SUD. The evidence and clinical data is reviewed. Findings include outcome data on the use of rTMS. Furthermore, important brain regions central to the development of SUD are examined: the ventral tegmental area and ventral striatum appear to play a central role in the binge/intoxication stage, the extended amygdala in the withdrawal/negative affect stage, and the orbitofrontal cortex-dorsal striatum, prefrontal cortex, basolateral amygdala, hippocampus, and insula in craving. The role of genomics and gene-wide associations to deliver future personalized addiction treatments is discussed as is advanced functional neural imaging. Technology for patients and consumers, including relapse prevention apps and bidirectional biometric reading is mentioned. Breakthroughs in addiction immunology, both generalized and substance specific, are discussed as potential points of future study and interventions.

scholarly journals Neural Underpinnings of Obesity: The Role of Oxidative Stress and Inflammation in the Brain

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1018
Author(s):  
Caitlyn A. Mullins ◽  
Ritchel B. Gannaban ◽  
Md Shahjalal Khan ◽  
Harsh Shah ◽  
Md Abu B. Siddik ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Homeostasis ◽  
Dorsal Striatum ◽  
Brain Regions ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Obesity Prevalence ◽  
Beneficial Effects ◽  
The Brain

Obesity prevalence is increasing at an unprecedented rate throughout the world, and is a strong risk factor for metabolic, cardiovascular, and neurological/neurodegenerative disorders. While low-grade systemic inflammation triggered primarily by adipose tissue dysfunction is closely linked to obesity, inflammation is also observed in the brain or the central nervous system (CNS). Considering that the hypothalamus, a classical homeostatic center, and other higher cortical areas (e.g. prefrontal cortex, dorsal striatum, hippocampus, etc.) also actively participate in regulating energy homeostasis by engaging in inhibitory control, reward calculation, and memory retrieval, understanding the role of CNS oxidative stress and inflammation in obesity and their underlying mechanisms would greatly help develop novel therapeutic interventions to correct obesity and related comorbidities. Here we review accumulating evidence for the association between ER stress and mitochondrial dysfunction, the main culprits responsible for oxidative stress and inflammation in various brain regions, and energy imbalance that leads to the development of obesity. Potential beneficial effects of natural antioxidant and anti-inflammatory compounds on CNS health and obesity are also discussed.

The Neural Substrates of In-Group Bias

2008 ◽  
Vol 19 (11) ◽  
pp. 1131-1139 ◽  
Author(s):  
Jay J. Van Bavel ◽  
Dominic J. Packer ◽  
William A. Cunningham
Keyword(s):  
Orbitofrontal Cortex ◽  
Dorsal Striatum ◽  
Mixed Race ◽  
Neural Substrates ◽  
Brain Regions ◽  
Functional Magnetic Resonance ◽  
Intergroup Perception ◽  
Amygdala Activity ◽  
Group Members

Classic minimal-group studies found that people arbitrarily assigned to a novel group quickly display a range of perceptual, affective, and behavioral in-group biases. We randomly assigned participants to a mixed-race team and used functional magnetic resonance imaging to identify brain regions involved in processing novel in-group and out-group members independently of preexisting attitudes, stereotypes, or familiarity. Whereas previous research on intergroup perception found amygdala activity—typically interpreted as negativity—in response to stigmatized social groups, we found greater activity in the amygdala, fusiform gyri, orbitofrontal cortex, and dorsal striatum when participants viewed novel in-group faces than when they viewed novel out-group faces. Moreover, activity in orbitofrontal cortex mediated the in-group bias in self-reported liking for the faces. These in-group biases in neural activity were not moderated by race or by whether participants explicitly attended to team membership or race, a finding suggesting that they may occur automatically. This study helps clarify the role of neural substrates involved in perceptual and affective in-group biases.

scholarly journals Context-induced relapse to drug seeking: a review

2008 ◽  
Vol 363 (1507) ◽  
pp. 3233-3243 ◽  
Author(s):  
Hans S Crombag ◽  
Jennifer M Bossert ◽  
Eisuke Koya ◽  
Yavin Shaham
Keyword(s):  
Basolateral Amygdala ◽  
Dorsal Hippocampus ◽  
Dorsal Striatum ◽  
Self Administration ◽  
Occasion Setting ◽  
Drug Seeking ◽  
Psychological Mechanisms ◽  
History Of ◽  
Study Context

In humans, exposure to environmental contexts previously associated with drug intake often provokes relapse to drug use, but the mechanisms mediating this relapse are unknown. Based on early studies by Bouton & Bolles on context-induced ‘renewal’ of learned behaviours, we developed a procedure to study context-induced relapse to drug seeking. In this procedure, rats are first trained to self-administer drug in one context. Next, drug-reinforced lever responding is extinguished in a different (non-drug) context. Subsequently, context-induced reinstatement of drug seeking is assessed by re-exposing rats to the drug-associated context. Using variations of this procedure, we and others reported reliable context-induced reinstatement in rats with a history of heroin, cocaine, heroin–cocaine combination, alcohol and nicotine self-administration. Here, we first discuss potential psychological mechanisms of context-induced reinstatement, including excitatory and inhibitory Pavlovian conditioning, and occasion setting. We then summarize results from pharmacological and neuroanatomical studies on the role of several neurotransmitter systems (dopamine, glutamate, serotonin and opioids) and brain areas (ventral tegmental area, accumbens shell, dorsal striatum, basolateral amygdala, prefrontal cortex, dorsal hippocampus and lateral hypothalamus) in context-induced reinstatement. We conclude by discussing the clinical implications of rat studies on context-induced reinstatement of drug seeking.

scholarly journals Disruption of Cigarette Smoking Addiction After Dorsal Striatum Damage

2021 ◽  
Vol 15 ◽  
Author(s):  
Chuya Jing ◽  
Changxin Jing ◽  
Liangcheng Zheng ◽  
Ganji Hong ◽  
Jingjing Zheng ◽  
...  
Keyword(s):  
Brain Damage ◽  
Parietal Lobe ◽  
Dorsal Striatum ◽  
Internal Capsule ◽  
Brain Regions ◽  
Addictive Behavior ◽  
Smoking Addiction ◽  
Midbrain Dopamine ◽  
Study Participants

Studies have shown that addictive behavior is associated with many brain regions, such as the insula, globus pallidus, amygdala, nucleus accumbens, and midbrain dopamine system, but only a few studies have explored the role of the dorsal striatum in addictive behavior. In June 2020, we started contacting 608 patients who were hospitalized between January 2017 and December 2019, and we recruited 11 smoking addicts with dorsal striatum damage and 20 controls with brain damage that did not involve the dorsal striatum (the damaged areas included the frontal lobe, temporal lobe, parietal lobe, brain stem, thalamus, internal capsule, and so on). All study participants had brain damage due to acute cerebral infarction. Disruption of smoking addiction was found to be significantly associated with the dorsal striatum (Phi = 0.794770, P = 0.000015). Our findings suggested that patients in the dorsal striatum group were more likely to discontinue smoking than those in the non-dorsal striatum group. The characteristics of this interruption is that smoking can be quit more easily and quickly without recurrence and that the impulse to smoke is reduced. These results suggest that the dorsal striatum is a key area for addiction to smoking.

scholarly journals Altered theta / beta frequency synchrony links abnormal anxiety-related behavior to synaptic inhibition in Neuroligin-2 knockout mice

2019 ◽  
Author(s):  
Hugo Cruces-Solis ◽  
Olga Babaev ◽  
Heba Ali ◽  
Carolina Piletti Chatain ◽  
Vasyl Mykytiuk ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Basolateral Amygdala ◽  
Brain Regions ◽  
Synaptic Inhibition ◽  
Bed Nucleus ◽  
Adhesion Protein ◽  
Inhibitory Synaptic Transmission ◽  
Theta Frequency ◽  
Beta Frequency

AbstractInhibitory synaptic transmission plays a key role in the circuits underlying anxiety behaviors, but the network mechanisms by which disruptions in synaptic inhibition contribute to pathological anxiety processing remain largely unknown. Here we addressed this question in mice lacking the inhibitory synapse-specific adhesion protein Neuroligin-2 (Nlgn2), which display widespread reduction in inhibitory synaptic transmission as well as a pronounced anxiety phenotype. To investigate how the lack of synaptic inhibition alters the communication between key brain regions in anxiety processing, we recorded local field potentials (LFPs) simultaneously from a network of brain regions involved in anxiety processing, including the basolateral amygdala (BLA), centromedial amygdala, bed nucleus of the stria terminalis, prefrontal cortex and ventral hippocampus (vHPC). We found that LFP power in the vHPC was profoundly increased while vHPC-directed theta frequency synchrony was disrupted in Nlgn2 KO mice under anxiogenic conditions. Instead, deletion of Nlgn2 increased beta frequency synchrony across the anxiety network, and the theta / beta synchrony ratio strongly predicted anxiety behaviors in an open field paradigm. Local deletion of Nlgn2 in the vHPC and BLA revealed that they encode distinct aspects of the anxiety phenotype of the Nlgn2 KO mice, with vHPC linked to anxiety induced freezing and BLA linked to reduction in exploratory activity. Together, our data demonstrate that alterations in long-range functional connectivity link synaptic inhibition to abnormal anxiety behaviors, and that Nlgn2 KO mice represent an interesting model to study the role of inhibitory synaptic transmission in the circuits underlying anxiety disorders.

Central, but not basolateral, amygdala involvement in the anxiolytic-like effects of midazolam in rats in the elevated plus maze

2010 ◽  
Vol 26 (4) ◽  
pp. 543-554 ◽  
Author(s):  
Milene C Carvalho ◽  
Caio M Moreira ◽  
Janaína M Zanoveli ◽  
Marcus L Brandão
Keyword(s):  
Basolateral Amygdala ◽  
Elevated Plus Maze ◽  
Dorsal Hippocampus ◽  
Dorsal Striatum ◽  
Input And Output ◽  
Plus Maze ◽  
Main Input ◽  
Fear And Anxiety ◽  
Behavior Of Rats

The role of the amygdala in the mediation of fear and anxiety has been extensively investigated. However, how the amygdala functions during the organization of the anxiety-like behaviors generated in the elevated plus maze (EPM) is still under investigation. The basolateral (BLA) and the central (CeA) nuclei are the main input and output stations of the amygdala. In the present study, we ethopharmacologically analyzed the behavior of rats subjected to the EPM and the tissue content of the monoamines dopamine (DA) and serotonin (5-HT) and their metabolites in the nucleus accumbens (NAc), dorsal hippocampus (DH), and dorsal striatum (DS) of animals injected with saline or midazolam (20 and 30 nmol/0.2 µL) into the BLA or CeA. Injections of midazolam into the CeA, but not BLA, caused clear anxiolytic-like effects in the EPM. These treatments did not cause significant changes in 5-HT or DA contents in the NAc, DH, or DS of animals tested in the EPM. The data suggest that the anxiolytic-like effects of midazolam in the EPM also appear to rely on GABA-benzodiazepine mechanisms in the CeA, but not BLA, and do not appear to depend on 5-HT and DA mechanisms prevalent in limbic structures.

Challenges of Fear Conditioning Research in the Age of RDoC

2017 ◽  
Vol 225 (3) ◽  
pp. 189-199 ◽  
Author(s):  
Tina B. Lonsdorf ◽  
Jan Richter
Keyword(s):  
Fear Conditioning ◽  
Clinical Diagnosis ◽  
Research Domain Criteria ◽  
Major Focus ◽  
The Future ◽  
Definition Of ◽  
Methodological Considerations ◽  
Research Domain

Abstract. As the criticism of the definition of the phenotype (i.e., clinical diagnosis) represents the major focus of the Research Domain Criteria (RDoC) initiative, it is somewhat surprising that discussions have not yet focused more on specific conceptual and procedural considerations of the suggested RDoC constructs, sub-constructs, and associated paradigms. We argue that we need more precise thinking as well as a conceptual and methodological discussion of RDoC domains and constructs, their interrelationships as well as their experimental operationalization and nomenclature. The present work is intended to start such a debate using fear conditioning as an example. Thereby, we aim to provide thought-provoking impulses on the role of fear conditioning in the age of RDoC as well as conceptual and methodological considerations and suggestions to guide RDoC-based fear conditioning research in the future.

The Role of Tradeoff Salience and Connectedness to the Future Self

2011 ◽  
Author(s):  
Daniel Bartels ◽  
Oleg Urminsky ◽  
Shane Frederick
Keyword(s):  
The Future ◽  
Future Self
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