Sussex Addiction Research and Intervention Centre (SARIC)

Seminars

We are pleased to announce the following speakers:

Thursday, 17 October 2019, 14:00-15:00 - School of Psychology Colloquia, The Meeting House, University of Sussex

Prof Kent BerridgeProfessor Kent Berridge

James Olds Distinguished University Professor of Psychology and Neuroscience Department of Psychology;
University of Michigan, USA

Liking and Wanting in the brain

Liking and wanting usually go together for pleasant rewards, but turn out to have separable brain mechanisms.

Addictions may arise from this liking/wanting separation. ‘Liking’ is generated by a surprisingly frail and tiny network of hedonic hotspots in brain limbic structures. ‘Wanting' for the same pleasures has a much more robust and larger brain network involving dopamine systems. Surprisingly, the ‘wanting’ system also may have a paradoxical relation to fear. The relation between liking, wanting, and fear systems has further implications for understanding clinical disorders beyond addiction, including depression and schizophrenia

Host: Professor Aldo Badiani

For more information about the research conducted by Professor Kent Berridge please click here


Thursday, 12 September 2019, 14:00-15:00 - School of Psychology Colloquia, Pevensey 1 - 2D11, University of Sussex

Professor Paul VezinaProfessor Paul Vezina

Department of Psychiatry and Behavioral Neuroscience;
The Univerisity of Chicago, USA

Sensitization, uncertainty, and drug taking

I will present some of our work showing how sensitization promotes drug taking and how changes in dopamine-glutamate signaling in the ventral forebrain mediate this effect. I will also describe our recent work exploring behavioral and neurochemical commonalities between the effects of drug sensitization and those produced by repeated intermittent exposure to conditions of uncertainty, as experienced in games of chance.

Our goal is to understand how altered activity in the neurotransmitter circuits of the basal ganglia contributes, with its psychological complements, to both drug and behavioral addictions such as gambling disorder.

Host: Professor Aldo Badiani

For more information about the research conducted by Professor Paul Vezina please click here


Thursday, 16 May 2019, 14:00-15:00 - School of Psychology Colloquia, Pevensey 1 - 1A6, University of Sussex

Dr Karen BachiDr. Keren Bachi

Department of Psychiatry
Department of Environmental Medicine and Public Health
The Addiction Institute of Mount Sinai
Icahn School of Medicine at Mount Sinai, New York, USA

Psychosocial pathways in addiction: brain structure, function, and putative underlying neuroimmune mechanisms.

Impairments in social cognition and functioning are recognized as core illness features associated with atypical brain function in multiple neuropsychiatric illnesses.

Increasingly, impairments in social information processing have also been implicated as core symptoms of drug addiction, whereby the brain regions engaged by social cognition in healthy individuals (e.g., prefrontal cortex, superior temporal sulcus, temporoparietal junction, amygdala, hippocampus, anterior cingulate cortex, and the temporal poles) are implicated in the pathophysiology of drug addiction. Hence, addiction impacts the very same circuits that enable self-monitoring and complex social functioning. Individuals with substance use disorder frequently experience social stress (e.g., childhood maltreatment) which may shape neural and physiological responses to social interactions and exacerbate illness risk.

However, to date, studies of the neural correlates of social cognition in addiction are limited, and specifically literature about the brain function underlying social information processing in individuals with cocaine use disorder remains in its infancy. Knowledge regarding the neural underpinnings of social cognition/function in this population can help to facilitate treatment efficacy and recovery.

This presentation will summarize multimodal imaging and behavioral findings, including childhood trauma effects on gray matter in orbitofrontal cortex of cocaine addicted individuals and observed associations with psychological comorbidity.

Our findings further demonstrate aberrant neural correlates of mentalizing (social inference) and social navigation as associated with severity of drug dependence and social functioning in this population.

I will also discuss how via activation of sympathetic stress systems and the hypothalamic-pituitary-adrenal axis, immune dysregulation may provide a psychobiological link between chronic social stress, deficits in mentalizing and social processing and drug addiction.

Host: Professor Aldo Badiani

For more information about the research conducted by Dr Keren Bachi please click here


Thursday, 9 May 2019, 14:00-15:00 - School of Psychology Colloquia, The Meeting House, University of Sussex

Dr Lee HogarthDr. Lee Hogarth

Department of Psychology
University of Exter, UK

Drug addiction is a disorder of excessive goal-directed choice in negative affective states, not habit or compulsion

Addiction may be driven by excessive valuation of the drug as the goal of intentional choice (especially in negative affect states), or a habit driven by strong stimulus-response associations, or a compulsion driven by discounting (neglecting) costs imposed on drug-seeking.

The human studies described in this talk favour the excessive goal-directed choice account and contradict the habit and compulsion accounts. Contradicting habit theory, a series of human outcome-devaluation studies failed to demonstrate a predilection for habit learning in treatment-seeking addicts or students with greater dependence symptoms. Contradicting compulsivity theory, sensitivity to costs imposed on drug-seeking is comparable across levels of dependence symptom severity.

By contrast, dependence symptom severity in clinical and sub-clinical samples is reliably associated with greater goal-directed choice of the drug over alternative rewards (as demonstrated in outcome devaluation procedures). Furthermore, negative mood and stress states augment goal-directed drug choice, and individuals who report psychiatric symptoms and substance use to cope with negative affect are more sensitive to these induction effects.

Finally, substance use to cope with negative affect statistically mediates the relationship between psychiatric symptoms and substance dependence severity. Together, these studies suggest that drug dependence is not driven by habit or compulsion, but by excessive valuation of the drug as the goal of voluntary choice, especially during negative affective states in those with psychiatric comorbidity. Implications for optimising addiction treatment are discussed.

Host: Professor Dora Duka

For more information about the research conducted by Dr Lee Hogarth please click here


Tuesday, 7 May 2019, 13:00-14:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

Prof Keith HumpreysProfessor Keith Humphreys

Professor and Section Director for Mental Health Policy

Department of Psychiatry and Behavioral Sciences
Standford University, USA

Brains, Drugs, and Public Policy

The regulation of alcohol, tobacco, opioids, and other addictive drugs is fundamentally political but can be informed by research findings, certainly including those from neuroscience.

Neuroscience has made enormous progress in describing the impact of addictive drug consumption on the brain, including its decision-making apparatus.

However, the lead causes of addiction at the population level in the past 150 years emerge from outside the brain, namely in a substance saturated environment which human beings are poorly equipped by evolution to negotiate. This implies that public health and safety regarding drug can best be maximized by applying the lessons of neuroscience and related fields to policies regarding drug availability and the treatment of addiction.

That said, all policies around drugs let societies choose what type of drug problem they want to have; no policy will eliminate the problem either in absolute terms or with the perspectives of all observers.

Dr Humphreys will illustrate these points both with reference to the scientific literature and to his experiencing advising the U.S. and U.K. governments.

Host: Dr Silvana De Pirro and Professor Aldo Badiani

For more information about the research conducted by Professor Keith Humphreys please click here


Monday, 24 September 2018, 13:00-14:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

Jeff DalleyProfessor Jeff Dalley

Department of Psychiatry and Psychology
Behavioural and Clinical Neuroscience Institute
University of Cambridge, UK

Predisposition to addiction - Clues from longitudinal MRI and translational neuroscience

Addiction to various classes of abused drug (stimulants, alcohol, opioids) mysteriously afflicts some but not all individuals.

Notwithstanding the evident complexity and idiosyncratic nature of addiction many now accept that distinctive neurobehavioural endophenotypes make unique contributions to the various stages of addiction – from initiation and recreational drug use to increasing levels of consumption involving repeated bouts of intoxication, withdrawal and relapse. Although research in experimental animals has increased our understanding of addiction beyond ‘simple’ reinforcement mechanisms, debate still surrounds the validity and translation of such findings (mainly in rodents) to real-world addiction in humans.

This talk reflects on: (i) the so-called translational divide in addiction research, in particular the strengths and weaknesses of categorizing putatively causal traits (anxiety, impulsivity, incentive conditioning, novel seeking and preference) to aspects of addiction; (ii) the inference of ‘addiction’ in experimental animals, and (iii) how progress in this field has been advanced by the translational methodologies of MRI and PET.

Host: Dr. Ilse Pienaar

For more information about the research conducted by Professor Jeff Dalley please click here


Friday, 7 September 2018, 14:00-15:00 - John Maynard Smith (JMS) Building, room 4D13 University of Sussex

dr_steve_mahlerDr. Steve Mahler

Assistant Professor
Department of Neurobiology and Behaviour
University of California, Irvine, USA

The DREADDed Weed: Chemogenetic Dissection of Dopamine Function after Adolescent Cannabinoid Exposure

Adolescence is a critical window of maturation for reward-related brain circuits, which is in part orchestrated by endocannabinoid (ECB) signaling.
Exogenous perturbation of cannabinoid transmission with drugs like cannabis during adolescence may therefore have consequences on mesolimbic reward circuit development, and persistently alter motivated behavior into adulthood. ECB signaling regulates ventral tegmental area (VTA) dopamine (DA) projections to forebrain regions like nucleus accumbens (NAc) and dorsal medial prefrontal cortex (dmPFC), yet it remains unclear how exogenous cannabinoid receptor stimulation during adolescence alters DA circuits, and DA-dependent behaviors.

Here, I discuss our recent dissections of DA system function in adult tyrosine hydroxylase: Cre (TH:Cre) rats following adolescent dosing with a rewarding cannabinoid drug, and find several long-lasting alterations in DA stimulated endocannabinoid transmission, neural activity in reward circuits, and motivated behavior.

Our results reveal that adolescence is a critical window of development during which even small doses of cannabinoids drugs can persistently alter mesolimbic DA circuit neural and endocannabinoid activity, causing potentiated reward-seeking behaviors that could increase vulnerability to later-life addiction or other psychiatric disorders.

Host: Dr. Eisuke Koya

For more information about the research conducted in the Mahler Lab please click here


Thursday, 26 July 2018, 13:00-14:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

Professor_Wolfgang_SommerProfessor Wolfgang Sommer

Professor for Psychiatry at the University of Heidelberg,
Chair of the Department of Addiction Medicine,
Deputy director of the Institute for Psychopharmacology,
Central Institute for Mental Health in Mannheim, Germany

Losing control: alcohol, glutamate and the prefrontal cortex

The medial prefrontal cortex (mPFC) is critically involved in cognitive flexibility and top down control over behavior in both in humans and animals. How these mPFC functions are organized and implemented on the neural level is so far unknown.

Importantly, mPFC function is progressively compromised by chronic or excessive alcohol consumption. A potential pathomechanism underlying the alterations in neuronal function is dysregulation of glutamatergic neurotransmission.

Among these alcohol-induced changes is a long-lasting deficit of metabotropic glutamate receptor 2 (mGluR2) in mPFC neurons of both humans and rodents. This deficit comprises a common pathological mechanism for excessive alcohol cue reactivity and impaired cognitive flexibility as demonstrated in rat models of cue-induced alcohol seeking and attentional set shifting, respectively.

To further understand how the mPFC exert control over behavior, we have developed methods for tracing and manipulating the activity state of the glutamatergic neurons.

We found that distinct sets of neurons in the mPFC play a key role in alcohol seeking. To further investigate the dynamics of local networks within mPFC and their relation to the expression of alcohol seeking behaviors we are currently setting up microendoscopic calcium imaging of neuronal activity in freely moving rats.

According to Hebb’s concept of neuronal ensembles, specific sets of neurons may interact in the storage and processing of memories, and this principle has recently been demonstrated for the pursuit of several drug or natural rewards. Initial results will be discussed in the context of ensemble concept and for their potential ramifications to alcohol use disorders.

Host: Professor Dora Duka


Wednesday, 30 May 2018, 17:30-18:30 - Fulton B Lecture Theatre, University of Sussex

Rudi Fortson QCRudi Fortson QC

Visiting Professor of Law
Queen Mary University, UK
Indipendent practing Barrister
Sussex Prior Fault Team

Drugs and Harm Reduction: Has the UK lost its Crown?

The UK, which was once a pioneer and leader in the field of drug harm-reduction, is now falling behind other countries.

The Misuse of Drugs Act 1971, which has often been criticised as an instrument of prohibition, was designed to be regulatory and sufficiently flexible to respond to harmful effects of drug use that are sufficient to constitute a social problem.

In the event, the intensity of UK drug laws has increased while the incidence of recreational and problematic drug use remains high. Harm reduction initiatives such as onsite drug checking, supervised drug consumption facilities, and the prescription or licensing of cannabis for medicinal purposes, encounter significant legal problems.

However – as this talk will demonstrate - there is increasing goodwill between agencies in the public and private sector to promote and to practice harm-reduction measures in the interests of personal and public health.

These findings suggest that the CeA is involved with assigning increasing value to reward and directing decision-making by generating narrowly focused motivation to seek out reward that may persist in the face of more rewarding alternatives and adverse consequences.

Host: Dr. Hans Crombag

CRC Annual Public Lecture 2018. For more information about the event please click here


Friday, 27 April 2018, 13:00-14:00 - Ashdown House Room 102, University of Sussex

Dr Mike RobinsonDr. Mike Robinson

Assistant Professor of Psychology, Neuroscience and Behaviour
Department of Psychology
Wesleyan University, CT, USA

Optogenetic Activation of the Central Amygdala Generates Individual Differences in Compulsive Reward Seeking Despite Adverse Consequences.

Drug and behavioral addictions are characterized by focused pursuit of a single reward above all others. Excessive motivation to pursue reward leads to persistent addictive-like decisions that often undermine an individual’s best interests, and prevail despite adverse consequences.

The amygdala plays a key role in reward processing and generating motivation. In the following studies, we explored how optogenetic stimulation of the central amygdala (CeA) modulates decision-making and reward choice, causing specific rewards to be almost compulsively preferred in manners that model many of the DSM criteria for addiction.

Rats were trained to choose between a reward paired with CeA laser stimulation or an otherwise unpaired identical or alternative reward. Rats developed a nearly exclusive preference for the CeA laser-paired reward over the unpaired reward. This was true whether the reward was a sucrose pellet or an infusion of cocaine.

For sucrose, this preference persisted even when a much larger sucrose reward was offered as an alternative, or when the preferred reward was paired with an electric footshock. CeA laser stimulation also produced persistent pursuit of a flavored reward paired with conditioned taste aversion. For cocaine, CeA laser stimulation produced an escalation of cocaine intake, and compulsive nibbling of the nose port paired with laser-associated cocaine, as though seeking more. For both cocaine and sucrose, CeA stimulation dramatically increased an animal’s motivation for the laser-paired reward over an otherwise identical unpaired reward. In each case, these effects were not the consequence of any independently rewarding properties of optogenetic activation of the CeA alone.

These findings suggest that the CeA is involved with assigning increasing value to reward and directing decision-making by generating narrowly focused motivation to seek out reward that may persist in the face of more rewarding alternatives and adverse consequences.

Host: Dr. Hans Crombag

For more information about the research conducted in the Robinson Lab (Behavioural Neuroscience of Motivation, Reward & Desire) please click here


Monday, 22 January 2018, 13:00-14:00 - Sussex Neuroscience Seminar Room, CRPC Building 4.03, University of Sussex

Bryan_SingerDr. Bryan F. Singer

Lecturer in Psychology, Life, Health & Chemical Sciences
Faculty of STEM
The Open University, Milton Keynes, UK

Dopamine Transmission, Dendritic Plasticity, and the Attribution of Incentive Value to Salient Reward-Predictive Stimuli

There is considerable individual variation in the degree to which cues exert motivational control over behaviour, and we have been able to model this diversity in rodents. Specifically, we have found that when a lever conditioned stimulus (CS) predicts food reward, outbred rats differ in the exact conditioned response they learn and perform. For some rats, the lever-CS becomes “wanted” – these “sign-tracker” (ST) rats approach the lever and interact with it until the reward is delivered. In contrast, “goal-tracker” (GT) rats orient to the lever-CS, but do not interact with it and instead approach the location of food delivery.

Individual variation in dopamine (DA) neurotransmission and uptake contribute to this variation in the extent to which reward cues acquire motivational value. We are also investigating how this variation in DA transmission impacts dendritic changes associated with learning and memory. Finally, we are developing new tools for detecting variation in cue-evoked motivation in people.

Altogether, we hope to find ways to identify and reduce the motivational power of reward-paired cues in certain individuals, and this may prove to be useful for combatting disorders ranging from food addiction to substance abuse.

Host: Professor Aldo Badiani


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.

An mp3 Audio file of this Lecture is available here


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 seekingcocaine 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.

Host: Professor Dora Duka


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.

Host: Professor Aldo Badiani


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.

Host: Professor Aldo Badiani


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.

Host: Professor Aldo Badiani