Sussex Addiction Research and Intervention Centre (SARIC)

Seminars

We are pleased to announce the following speakers:

Monday, 4 December 2017, 13:0-14:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

Catherine Le MoinDr. Catherine Le Moine

Neuropsychopharmacology of addiction
Research Director, INCIA (Aquitaine Institute for Cognitive and Integrative Neuroscience)
University of Bordeaux, France

Affective memories associated with withdrawal in opiate dependence: From cellular imaging to in vivo recordings

Host: Dr. Eisuke Koya


Wednesday, 8 November 2017, 18:30-20:00 - Brighton and Sussex Medical School, Chowen Lecture Theatre, University of Sussex

Aldo BadianiProfessor Aldo Badiani

Professor of Psychology and Addiction Medicine
Director, SARIC
School of Psychology
University of Sussex, Brighton, UK

Your Brain on Drugs: Not the Same Everywhere

Addictive drugs such as cocaine, heroin, or alcohol are often thought to be the same in their ability to produce ‘pleasure’ by activating the ‘reward’ circuitry of the brain.

In this lecture, I will show that different classes of drugs produce unique neurobiological effects and distinctive internal states, which in turn are exquisitely sensitive to the environment surrounding drug use.

This is a free, open lecture – everyone is welcome, but numbers are limited so please reserve your place.


Monday, 24 April 2017, 13:00-14:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

RitaZ_GoldsteinProfessor Rita Z. Goldstein

Chief, Neuropsychoimaging of Addiction and Related Conditions (NARC)
Research Program and Brain Imaging Centre (BIC)
Department of Psychiatry and Department of Neuroscience,
Friedman Brain Institute
Icahn School of Medicine at Mount Sinai, New York, USA

Neuroimaging in drug addiction: an eye towards intervention purposes

Drug addiction is a chronically relapsing disorder characterized by compulsive drug use despite catastrophic personal consequences (e.g., loss of family, job) and even when the substance is no longer perceived as pleasurable.

In this talk, Dr. Goldstein will present results of human neuroimaging studies, utilizing a multimodal approach (neuropsychology, functional magnetic resonance imaging, positron emission tomography, event-related potentials recordings), to explore the neurobiology underlying the core psychological impairments in drug addiction (impulsivity, drive/motivation, insight/awareness) as associated with its clinical symptomatology (intoxication, craving, bingeing, withdrawal).

The focus of this talk is on understanding the role of the dopaminergic mesocorticolimbic circuit, and especially the prefrontal cortex, in higher-order executive dysfunction (e.g., disadvantageous decision-making such as trading a car
for a couple of cocaine hits) in drug addicted individuals.

The theoretical model that guides the presented research is called iRISA (Impaired Response Inhibition and Salience Attribution), postulating that abnormalities in the orbitofrontal cortex and anterior cingulate cortex, as related to dopaminergic dysfunction, contribute to the core clinical symptoms in drug addiction.

Specifically, Dr. Goldstein’s multi-modality program of research is guided by the underlying working hypothesis that drug addicted individuals disproportionately attribute reward value to their drug of choice at the expense of other potentially but no-longer-rewarding stimuli, with a concomitant decrease in the ability to inhibit maladaptive drug use.

In this talk, Dr. Goldstein will also explore whether treatment (as usual) and 6-month abstinence enhance recovery in these brain-behavior compromises in treatment seeking cocaine addicted individuals.

Promising novel fMRI studies, which combine pharmacological (i.e., oral methylphenidate, or RitalinTM) and salient cognitive tasks or functional connectivity during resting-state, will be discussed as examples for using neuroimaging in the empirical guidance for the development of effective neurorehabilitation strategies in cocaine addiction.


Monday, 24 October 2016, 13:00-14:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

Dr. Daniele Caprioli

Dr. Daniele Caprioli

Assistant Professor,
Department of Physiology and Pharmacology,
Sapienza University of Rome, Rome, Italy

Neuronal mechanisms of drug relapse after cessation of prolonged contingency management in a rat model

Despite decades of research on the neurobiological mechanisms of psychostimulant addiction, the only effective treatment for many addicts is contingency management. In this behavioral method, the availability of non-drug rewards (e.g., monetary vouchers), given in exchange for being drug free (verified by drug testing), maintains prolonged abstinence in many psychostimulant addicts.

However, when contingency management is discontinued, most addicts relapse to drug use.The brain mechanisms underlying relapse after cessation of contingency management are unknown and until recently, an animal model of this human condition did not exist.

In the present lecture I will present a new choice-based rat model of relapse, along with its first neurobehavioral characterization, in which Meth craving is observed after prolonged voluntary abstinence. Specifically I will provide evidences that relapse after voluntary abstinence from methamphetamine self-administration is mediated by (1) dorsomedial striatum neuronal ensembles that are comprised of heterogeneous D1- and D2-expressing neurons;
(2) anterior insula to central amygdala projections.


Thursday, 6 October 2016, 15:00-16:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

Markus_Heilig

Professor Markus Heilig

Director at the Center for Social and Affective Neuroscience,
Department of Clinical and Experimental Medicine,
Linköping University, Sweden

Stress-induced relapse to alcohol seeking: Back to the drawing board

Progression into alcohol addiction is characterized by lasting changes in brain function. These result in escalated voluntary alcohol intake, alcohol seeking despite adverse consequences, and increased sensitivity to relapse triggered
by stress.

The neural substrates of these behavioral traits have remained unknown. We have found that a history of alcohol dependence results in DNA-hypermethylation selectively in the medial prefrontal cortex, leading to a persistent reprogramming of the mPFC transcriptome.

We have then identified an epigenetic enzyme, PRDM2, as a key mediator of these expression changes and their behavior consequences.

Our findings indicate that DNA-methylation mediated repression of PRDM2 is involved in multiple aspects of alcohol dependence, including stress-induced relapse, compulsivity-like behavior and escalation of alcohol intake.


Monday, 12 September 2016, 13:00-14:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

Marco_Leyton

Professor Marco Leyton

Department of Psychiatry, Faculty of Medicine,
McGill University, Quebec, Canada

Individual differences in dopamine transmission: A potential vulnerability pathway to addiction

Altered dopamine neurotransmission has long been implicated in the susceptibility to and development of addictions. However, our understanding of how this occurs remains poor, particularly in humans.

Today’s presentation will summarize recent developments using functional neuroimaging and methods for manipulating dopamine transmission.

These studies suggest that, in healthy humans, compulsively abused drugs across multiple pharmacological classes increase extracellular dopamine levels in the striatum. These effects are closely related to the ability of reward-related cues to elicit and sustain approach and desire, weakly related to positive mood tone, and related to euphoria only tenuously if at all.

Individual differences in the magnitude of these dopamine responses have been associated with differences in personality traits, cortical thickness, serotonergic tone, autoreceptor mediated inhibitory feedback, and past drug exposure. Following repeated drug use, the dopamine responses can become progressively larger (sensitized) and conditioned to environmental cues. Both of these effects are seen first within the ventral limbic striatum, and then, as drug exposure increases, in the dorsolateral striatum.

Finally, impulsive individuals at risk for addictions exhibit altered drug-induced dopamine responses. Both increases and decreases have been observed, potentially related to the presence vs. absence of drug related cues. Together, these studies replicate and extend features identified in animal models, and raise the possibility that one biological vulnerability trait for addiction is susceptibility to labile dopaminergic and appetitive responses to reward-related cues.