scholarly journals Effect of Prenatal Cocaine Exposure on D2 Receptors and DAT in Rhesus Macaques

2006 ◽  
Vol 2 ◽  
Author(s):  
Jennifer R Pryweller
Keyword(s):  
Rhesus Macaques ◽  
Brain Regions ◽  
Anterior Cingulate ◽  
Binding Potential ◽  
Future Research ◽  
Cocaine Exposure ◽  
Prenatal Cocaine Exposure ◽  
D3 Receptors ◽  
Prenatal Cocaine ◽  
Pet Scans

Five adult rhesus monkeys with a history of prenatal cocaine exposure (PNCE) and two saline-exposed control animals were used to optimize positron emission tomography (PET) imaging methods and to gather preliminary data on the effects of PNCE on dopamine systems in the adult non-human primate central nervous system. Dynamic PET scans were performed on each monkey to measure the binding kinetics of PET ligands specific for dopamine D2/D3 receptors ([18F]fallypride) and dopamine transporter ([18F]FECNT). PET scans were coregistered to structural T1-weighted MR images to aid in identification of regions with significant dopamine innervation for tracer kinetic analysis. Brain regions of interest (ROI) included caudate, putamen, substantia nigra and anterior cingulate cortex. Kinetic modeling using a cerebellum reference region was implemented in the PMOD software package to determine ligand binding potentials for D2/D3 receptors and dopamine transporters (DAT) in each of the ROIs to test whether fallypride and/or FECNT binding potentials, measures of D2/D3 and DAT levels respectively, were influenced by prenatal cocaine exposure. Preliminary results suggest a trend of reduced D2/D3 binding potential with increased PNCE, but future research is necessary.

scholarly journals Cannabinoids, reward processing, and psychosis

2021 ◽  
Author(s):  
Brandon Gunasekera ◽  
Kelly Diederen ◽  
Sagnik Bhattacharyya
Keyword(s):  
Psychotic Disorders ◽  
Neural Substrates ◽  
Brain Regions ◽  
Reward Processing ◽  
Anterior Cingulate ◽  
Psychotic Symptoms ◽  
Dopamine Synthesis ◽  
Future Research ◽  
Drug Challenge ◽  
Psychotomimetic Effects

Abstract Background Evidence suggests that an overlap exists between the neurobiology of psychotic disorders and the effects of cannabinoids on neurocognitive and neurochemical substrates involved in reward processing. Aims We investigate whether the psychotomimetic effects of delta-9-tetrahydrocannabinol (THC) and the antipsychotic potential of cannabidiol (CBD) are underpinned by their effects on the reward system and dopamine. Methods This narrative review focuses on the overlap between altered dopamine signalling and reward processing induced by cannabinoids, pre-clinically and in humans. A systematic search was conducted of acute cannabinoid drug-challenge studies using neuroimaging in healthy subjects and those with psychosis Results There is evidence of increased striatal presynaptic dopamine synthesis and release in psychosis, as well as abnormal engagement of the striatum during reward processing. Although, acute THC challenges have elicited a modest effect on striatal dopamine, cannabis users generally indicate impaired presynaptic dopaminergic function. Functional MRI studies have identified that a single dose of THC may modulate regions involved in reward and salience processing such as the striatum, midbrain, insular, and anterior cingulate, with some effects correlating with the severity of THC-induced psychotic symptoms. CBD may modulate brain regions involved in reward/salience processing in an opposite direction to that of THC. Conclusions There is evidence to suggest modulation of reward processing and its neural substrates by THC and CBD. Whether such effects underlie the psychotomimetic/antipsychotic effects of these cannabinoids remains unclear. Future research should address these unanswered questions to understand the relationship between endocannabinoid dysfunction, reward processing abnormalities, and psychosis.

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