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Séminaire - Kuei Y. TsengCannabis and Prefrontal Maturation during Adolescence

Abstract :

Cannabis abuse during adolescence increases the risk of developing psychosis and prefrontal cortex (PFC)-dependent cognitive deficits later in life. The CB1 cannabinoid receptor has long been known to mediate the psychoactive effects of cannabis, yet the mechanisms underlying such vulnerability remain unknown. Here, I will discuss data from my lab and others showing that long-lasting deficits in prefrontal functions can occur following repeated exposure to cannabinoids during adolescence. We recently found conclusive evidence that early and mid-adolescence are unique developmental periods during which the cannabinoid system interacts with PFC maturation. Data indicate that too much CB1 receptor stimulation during adolescence can arrest the development and maturation of PFC functional capacity.

Together, these findings are directly applicable not only to natural cannabinoids, but also to the new generation of synthetic, easily-obtainable, and more potent CB1 receptor agonists (e.g., JWH-018, CP47,497) currently available legally and illegally all over the world. prefrontal cortex (PFC)-dependent cognitive deficits later in life. The CB1 cannabinoid receptor has long been known to mediate the psychoactive effects of cannabis, yet the mechanisms underlying such vulnerability remain unknown. Here, I will discuss data from my lab and others showing that long-lasting deficits in prefrontal functions can occur following repeated exposure to cannabinoids during adolescence.

We recently found conclusive evidence that early and mid-adolescence are unique developmental periods during which the cannabinoid system interacts with PFC maturation. Data indicate that too much CB1 receptor stimulation during adolescence can arrest the development and maturation of PFC functional capacity. Together, these findings are directly applicable not only to natural cannabinoids, but also to the new generation of synthetic, easily-obtainable, and more potent CB1 receptor agonists (e.g., JWH-018, CP47,497) currently available legally and illegally all over the world.

Selected publications

Caballero A, Tseng KY (2016) GABAergic inhibitory function as a limiting factor for prefrontal development during adolescence. Trends in Neurosciences (Epub May 24) IF: 13.6

Cass DK/Flores-Barrera E/Thomases DR, Vital W, Caballero A, Tseng KY (2014) Cannabinoid CB1R stimulation during adolescence impairs the maturation of GABA function in the adult rat prefrontal cortex. Molecular Psychiatry 19(5): 536-43. IF: 15.15

Flores-Barrera E/Thomases DR, Heng LJ, Cass DK, Caballero A, Tseng KY (2014) Late adolescent expression of GluN2B transmission in the prefrontal cortex is input-specific and requires postsynaptic PKA and D1 dopamine receptor signaling. Biological Psychiatry 75(6): 508-16. IF: 9.25

Thomases DR, Cass DK, Meyer JD, Tseng KY (2014) Early adolescent MK-801 exposure impairs the maturation of ventral hippocampal control of basolateral amygdalar drive in the adult prefrontal cortex. The Journal of Neuroscience 34(27): 9059-66. IF: 6.8


Cass DK, Thomases DR, Caballero A, Tseng KY (2013) Developmental disruption of GABA function in the medial prefrontal cortex by non-contingent cocaine experience during early adolescence. Biological Psychiatry 74(7): 490-501. IF: 9.25, Comment in: Enduring effects of adolescent drug exposure (Biological Psychiatry Oct-2013)


Thomases DR, Cass DK, Tseng KY (2013) Periadolescent exposure to the NMDA receptor antagonist MK-801 impairs the functional maturation of local GABAergic circuits in the adult prefrontal cortex. The Journal Neuroscience 33(1): 26-34. IF: 7.12

Caballero A, Flores-Barrera E, Cass DK, Tseng KY (2014) Differential regulation of parvalbumin and calretinin interneurons in the prefrontal cortex during adolescence. Brain Structure & Function 219: 395-406. [Epub 02/12/13]. IF: 7.84


Lew S, Tseng KY (2014) Dopamine modulation of GABAergic function enables network stability and input selectivity for sustaining working memory in a computational model of the prefrontal cortex. Neuropsychopharmacology 39(13): 3067-76. IF: 7.8

Scientific focus :

Short bio

EDUCATION Medical Education and Graduate Schools 1991 - 1997 MD, University of Buenos Aires School of Medicine, Buenos Aires, Argentina 1998 - 2002 PhD, Department of Physiology & Biophysics (Physiology & Neuroscience), University of Buenos Aires School of Medicine, Argentina Thesis qualification: Outstanding (with distinction); Advisor: Dr. MG Murer Postdoctoral Training 2001 - 2006 Center for Neuropharmacology & Neuroscience, Albany Medical College, NY, USA; Advisor: Dr. P O’Donnell

TEACHING My teaching duties are directed to students of the Chicago Medical School, the School of Graduate & Postdoctoral Studies, the Scholl College of Podiatric Medicine and the College of Health Professions.

RESEARCH & SCHOLARSHIP Understanding how a given synaptic function matures and changes during critical periods of postnatal development to aging is crucial for gaining insights on how a disease state emerges in the brain and becomes irreversibly abnormal when untreated. Projects 1. Synaptic mechanisms underlying the functional maturation of cortical circuits during adolescence 2. Cortico-subcortical dynamics underlying the onset of impulsive and disinhibited behaviors 3. Non-dopaminergic adaptations underlying the pathophysiology of Parkinson’s disease

PUBLICATION LIST • Peer-reviewed Articles: 61 (+5 manuscripts submitted or in preparation) • 4 Books (edited) and 11 Book Chapters • h index: 31 (Publish or Perish search engine, April 2016)