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[P1.70]: Mutual dependence and integration of neuronal precursors into a common autonomic circuit in the vertebrate head
Author(s) -
Chen R.,
TakanoMaruyama M.,
Gaufo G.O.
Publication year - 2008
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2008.09.120
Subject(s) - citation , chen , library science , computer science , history , genealogy , artificial intelligence , biology , paleontology
controversial. In particular, the implications of possible long-term consequences of in utero exposure to cannabis derivatives on brain circuitry are poorly understood. In this study the synthetic CB1 agonistWIN 55,212-2 (WIN)was administered daily to pregnant rats from gestational day 5 to 20 (0.5 mg/kg). This dose is equivalent to a moderate or low exposure to marijuana in humans and has no overt toxic effects. The treatment with WIN did not affect gestational and reproduction parameters and WIN-exposed pups did not show any sign of malformations or malnutrition. The offspring were sacrificed at 40 and 80 days-old. Behaviorally, prenatal treatment with WIN initially altered pup performance in homing behavior and produced a decrease in the rate of separation-induced ultrasonic vocalizations. Behavioral deficits that resulted were long-lasting, since prenatal WIN exposure caused a disruption of memory retention in young and adult offspring subjected either to a passive or an active avoidance task. Morphologically, compared to age-matched controls, an analysis of dendritic branching of Golgi-impregnated hippocampal granule cells of the dentate gyrus in prenatal WIN-exposed rats showed a significant increase in the amount of dendritic arbor and in the complexity of the dendritic trees at both ages. These findings suggest that mild to moderate exposure to cannabinoids during crucial periods of brain development can cause dysmorphic maturation of the granule cells associated with exuberant dendritic growth and/or the failure of these neurons to undergo normalmaturational dendritic pruning. Such subtlemorphological alterations and commensurate changes in brain circuitrywould be, in turn, a factor underlying the behavioral deficits observed both in juvenile and adult rats. The findings suggest that even mild prenatal exposure to a cannabinoid agonist may result in longterm deleterious consequences with respect to structure and function.