Abnormal Interactions Of Neurodevelopment With Drugs Of Abuse Trigger Permanent Deficit In The Endocannabinoid System-dependent Brain Natural Ability To Alter And Protect Itself Predictors Of Involuntary Hospitalizations To Acute Psychiatry | 62146
Journal of Addiction Research & Therapy
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Abnormal interactions of neurodevelopment with drugs of abuse trigger permanent deficit in the endocannabinoid system-dependent brain natural ability to alter and protect itself Predictors of involuntary hospitalizations to acute psychiatry
5th International Conference and Exhibition on Addiction Research & Therapy
Cannabis abuse is considered to be the serious, if not the greatest known environmental risk for neuropsychiatric disorders.
Individuals who are exposed to cannabis experience variety of psychoactive effects such as general alteration of conscious
perception, euphoria, problems with social interactions, memory and learning, and occasionally anxiety and paranoia. Our
research indicates that abnormal interactions of neurodevelopment with the environment triggered by drugs of abuse during
neonatal or adolescent periods may permanently impair brain function including the brain natural ability to alter and protect
itself, i.e. endocannabinoid system (eCB)-dependent inherent neuroprotection of circuit integrity and neuroplasticity. The
eCB system represents a major activity-dependent regulatory system in the central nervous system and has been implicated in
multiple brain functions, including synaptic plasticity and the homeostatic regulation of network activity patterns. Noteworthy,
deficiency in eCB signaling found in developmental model for psychosis is associated with abnormalities in prefrontal cortexdependent
fear discrimination learning. We also show that mouse model of adolescent cannabis abuse shows deficits in an
endocannabinoid -mediated signaling and neuroplasticity in adult prefrontal cortex, a brain region encompassing neural circuit
for decision-making. Blockade of the primary gene product responsible for degrading the endogenous endocannabinoid, with
the specific drug ameliorates these deficits. The observed deficit in endocannabinoid-dependent signaling in the brain may
represent a neural maladaptation underlying cortical network instability and abnormal cognitive functioning triggered by
overactive CB1 receptor during adolescence. The validity of these observations to human conditions relies on their criteria and
translating data obtained in mouse to human behavior and physiology. These results suggest that transiently overactive CB1
receptor in the brain during adolescence leads to permanent alterations in the endocannabinoid system dependent signaling
and neuroplasticity. Cannabis abuse during adolescence increases the risk of schizophrenia, which involves developmental
maladaptations in neural circuitry that result in impaired brain functioning. In addition, the endocannabinoid system is altered
in the brains of people with schizophrenia. These findings provide additional insights into the pathological processes related to
increased risk for neuropsychiatric disorders and point towards developing new treatment strategies.
Korzus is an Assistant Professor in Neuroscience and Psychology at University of California Riverside. He completed his Ph.D. in Molecular Biology and Biochemistry at the University of Georgia-Athens. He completed a postdoctoral fellowship at Howard Hughes Medical Institute at University of California San Diego and is the recipient of numerous Medical Research Awards. Currently, he is a P.I. of the National Mental Health Institute’s research program “Prefrontal circuit and function in memory accuracy” and the holder of NARSAD Award.