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The Gill Center for Biomolecular Science

Gill Seminars

Previous Speakers

Upcoming Speakers

September 30, 2015
George F. Koob, Ph.D. Director

National Institute on Alcohol Abuse and Alcoholism, Washington, DC, USA

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium during the 2015 Gill Symposium

Title: Neuroplasticity in the brain stress systems in addiction

Abstract: Addiction to alcohol and drugs has been conceptualized as a chronically relapsing disorder of compulsive drug seeking and taking that progresses through three stages: binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation. Multiple sources of reinforcement contribute to the motivation to compulsively seek drugs including core elements of positive reinforcement (binge/intoxication stage) and negative reinforcement (withdrawal/negative affect stage) and conditioned reinforcement (preoccupation-anticipation stage). The construct of negative reinforcement can be defined here as drug taking that alleviates a negative emotional state created by drug abstinence. The negative emotional state that drives such negative reinforcement is hypothesized to derive from dysregulation of key neurochemical circuits that form the brain stress systems within the extended amygdala, basal ganglia and frontal cortex. Specific neuroplasticity in these circuits includes not only recruitment of the classic hormonal stress axis mediated by corticotropin-releasing factor (CRF) in the hypothalamus, but also extrahypothalamic CRF in the extended amygdala and frontal cortex. Recruitment of dynorphin-k opioid aversive systems in the ventral striatum and extended amygdala represents another dynamic neuroplasticity of the brain stress systems. In animal models, acute withdrawal from all major drugs of abuse increases reward thresholds, increases anxiety-like responses, and increases extracellular levels of CRF in the central nucleus of the amygdala. CRF receptor antagonists block anxiety-like responses associated with withdrawal, the increases in reward thresholds produced by withdrawal from drugs of abuse, and compulsive-like drug taking during extended access. Excessive drug taking also engages activation of CRF in the medial prefrontal cortex and is accompanied by deficits in executive function that may facilitate the transition to compulsive-like responding and relapse. Excessive activation of the nucleus accumbens via the release of mesocorticolimbic dopamine or activation of opioid receptors has long been hypothesized to subsequently activate the dynorphin-k opioid system, which in turn can decrease dopaminergic activity in the mesocorticolimbic dopamine system. Antagonism of the k opioid system can also block anxiety-like effects and reward deficits associated with withdrawal from drugs of abuse and can block the development of compulsive-like responding during extended access to drugs of abuse, suggesting another powerful brain stress/anti-reward system that contributes to compulsive drug seeking. Thus, compelling evidence exists to argue that plasticity in the brain stress systems, a heretofore largely neglected component of dependence and addiction, is triggered by acute excessive drug intake, is sensitized during repeated withdrawal, persists into protracted abstinence, and contributes to the development and persistence of addiction. The neuroplasticity of the brain stress systems in addiction not only provides understanding of the neurobiology of negative reinforcement mechanisms in addiction, but also provides key insights into how the brain processes negative emotions.

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September 30, 2015
Garret D. Stuber, Ph.D.

University of North Carolina, at Chapel Hill

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium during the 2015 Gill Symposium

Title: Dissecting the neural circuits that mediate motivated behavior

Abstract: In order to survive and effectively navigate an ever-changing and unpredictable environment,
organisms must readily adapt their behavior to seek out needed resources, while simultaneously
avoiding life-threatening situations. These opposing processes are controlled by neural circuitry that
is readily engaged by both environmental and physiological factors to promote behavioral output. The
work of my lab studies the precise neural circuits that control both reward and aversive-related behavioral responses. By utilizing optogenetic and other circuit mapping tools, we aim to delineate the precise functional synaptic connections between molecularly distinct neuronal populations that are critical for the generation of these critical behavioral states. A holistic understanding of the interconnected neural circuit elements that mediate diverse motivational behaviors will likely provide important insight into a variety of complex neurological and neuropsychiatric illnesses such as drug and alcohol addiction, anxiety,
depression, and eating disorders.

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September 30, 2015
Mary Kay Lobo, Ph.D.

University of Maryland School of Medicine

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium during the 2015 Gill Symposium

Title: Pending

Abstract: Pending

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September 30, 2015
Larry (Loren) Parsons, Ph.D.

The Scripps Research Institute

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium during the 2015 Gill Symposium

Title: Pending

Abstract: Pending.

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September 30, 2015
Marina E. Wolf, Ph.D.

Rosalind Franklin University of Medicine and Science

Seminar will take place in the Indiana Memorial Union, Whittenberger Auditorium during the 2015 Gill Symposium

Title: Pending

Abstract: Pending

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November 2, 2015
A. Vania Apkarian, Ph.D.

Northwestern University School of Medicine

Seminar will be held in Psychology, Room 101 at 4:00 p.m.

Title: Transition to chronic pain: Predictors and consequences

Abstract: 1) I will review accumulating evidence regarding brain reorganization with chronic pain. Both human brain imaging studies as well as animal model studies specifically interrogating the role of supraspinal plasticity will be emphasized. The primary take home message is that the grey matter of the neocortex dynamically changes with chronic pain and this reorganization is pain type specific.

2) It is common clinical knowledge that although a very large patient population presents with similar injuries that give rise to pain, only a small minority of them develop chronic pain. Thus the critical question in the field of pain research is: what characteristics differentiate between those that develop chronic pain and the ones who properly recover from their injury into health. I will review the results from the only existing longitudinal brain-imaging based study, where brain anatomical and functional properties were studied as subjects transitioned from acute to chronic pain. One hundred and twenty sub-acute back pain patients (SBP, no back pain for at least one year and persistence of back pain for 4-12 weeks of an intensity of 5/10) were recruited and followed over one year, where repeated brain imaging and pain questionnaire outcomes were collected. Sixty-eight subjects completed the study. Different subgroups of these subjects were analyzed at various phases of the study to examine 1) brain grey matter reorganization and related functional properties, 2) brain white matter properties as predictors of pain chronification, 3) changes in brain activity reflecting back pain in the transition to chronic pain, 4) relationship between smoking and chronic pain. The primary result of these analyses is the important observation that very simple brain parameters accurately predict who will develop chronic pain and who will not. Both anatomical and functional properties seem critical.
 If time permits I will present an overall mechanistic model of the transition to chronic pain that summarizes the results presented in both lectures.

Overall we envision four distinct phases for transition from acute to chronic pain:

  1. Predisposition
  2. Injury or inciting event
  3. Transition
  4. Maintenance

Mechanisms underlying each of these phases are distinct. Phase 2 is primarily determined by nociceptive processes, while phase 1 seems mainly brain dependent,  for chronic back pain.

Reference papers:
Corticostriatal functional connectivity predicts transition to chronic back pain.
Baliki MN, Petre B, Torbey S, Herrmann KM, Huang L, Schnitzer TJ, Fields HL, Apkarian AV.
Nat Neurosci. 2012 Jul 1;15(8):1117-9.

A dynamic network perspective of chronic pain.
Farmer MA, Baliki MN, Apkarian AV.
Neurosci Lett. 2012 Jun 29;520(2):197-203.

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April 4, 2016
David A. Lewis, M.D.

University of Pittsburgh

Seminar will be held in Psychology, Room 101 at 4:00 p.m.

Title: Pending

Abstract: Pending

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April 18, 2016
Rodney Samaco, Ph.D.

Baylor College of Medicine

Seminar will be held in Psychology, Room 101 at 4:00 p.m.

Title: Pending

Abstract: Pending

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