Kathleen Kantak

Director: Laboratory of Behavioral Neuroscience

Dr. Kantak began as an Assistant Professor in the Department of Psychology at Boston University in 1982 and founded the Laboratory of Behavioral Neuroscience. She rose through the ranks to Full Professor, with tenure. She is concurrently affiliated with the Center for Neuroscience, the Interdisciplinary Graduate and Undergraduate Programs in Neuroscience, the Bimolecular Pharmacology Graduate Training Program, and the Transformative Training Program in Addiction Science at Boston University. She also holds an appointment as Lecturer at Harvard Medical School, Department of Psychiatry (Psychobiology) in conjunction with the Division of Behavioral Biology at the New England Primate Research Center. Dr. Kantak has received grant funding from the National Institute on Drug Abuse since 1987 to study various aspects of drug addiction, including medication development and other treatment modalities.

Her current research focuses on cognitive aspects of addiction-related behavior. Her overall goal is to conduct translational research using trans-species behavioral models of cognition and drug abuse and to interface her work with that of neurobiologists to understand mechanisms and with that of clinicians to improve drug addiction treatment outcomes.

Using intravenous drug self-administration procedures in rats, Dr. Kantak has investigated how multiple memory systems regulate drug-seeking and drug-taking behavior as well as how drug exposure influences the neurocognitive functioning of multiple memory systems. In addition, she spearheaded the effort to develop animal protocols that model exposure therapy targeting drug-related cues in clinical populations. She incorporates cognitive-enhancing pharmacotherapy and brief interventions with environmental enrichment or targeted cognitive training to improve extinction learning for relapse prevention. Within the context of these studies, she and her collaborators elaborate the neurosubstrates and neuroplasticity changes associated with these therapeutic strategies as well as translate these approaches to nonhuman primates and human subjects. In another line of research, Dr. Kantak evaluates frontostriatal and medial temporal lobe neurocognitive deficits in rats with an Attention Deficit/Hyperactivity Disorder phenotype. Focusing on the adolescent developmental period, she evaluates the response of rats with an ADHD phenotype to stimulant and non-stimulant medications, particularly in terms of comorbidity between ADHD and later vulnerability to drug addiction.

Selected Publications

• Kantak KM, Nic Dhonnchadha BÁ (2011) Pharmacological Enhancement of Drug Cue Extinction Learning: Translational Challenges. In: Addiction Reviews 2010, George Uhl editor, Ann NY Acad Sci. 1216: 122-137.
• Harvey RC, Sen S, Deaciuc A, Dwoskin LP, Kantak KM (2011). Methylphenidate treatment in adolescent rats with an attention deficit/hyperactivity disorder phenotype: Cocaine addiction vulnerability and dopamine transporter function. Neuropsychopharmacology, 36: 837-847.
• Nic Dhonnchadha BÁ, Lovascio B, Shrestha N, Kirkman C, Lin A, Leite-Morris KA, Man HY, Kaplan GB, Kantak KM (2012) Changes in expression of c-Fos protein following cocaine-cue extinction learning. Behav Brain Res. 234:100-106.
• Achat-Mendes C, Nic Dhonnchadha BA, Platt DM, Kantak KM, Spealman RD (2012). Glycine transporter-1 inhibition preceding extinction training inhibits reacquisition of cocaine seeking. Neuropsychopharmacology. 37: 2837-2845.
• Nic Dhonnchadha BA, Lin A, Leite-Morris KA, Kaplan GB, Man HY, Kantak KM (2013). Alterations in expression and phosphorylation of GluA1 receptors following cocaine-cue extinction learning. Behav Brain Res, 238: 119-123.
• Somkuwar SS, Darna M, Kantak KM, Dwoskin LP (2013). Adolescence methylphenidate treatment in a rodent model of attention deficit/hyperactivity disorder: Dopamine transporter function and cellular distribution in adulthood. Biochemical Pharmacology, 86: 309-316.
• Somkuwar SS*, Jordan CJ*, Kantak KM, Dwoskin LP (2013). Adolescent atomoxetine treatment in a rodent model of ADHD: Effects on cocaine self-administration and dopamine transporters in frontostriatal regions. Neuropsychopharmacology, in press.
  * co-first authors