NDLI: Prenatal exposure to a cannabinoid agonist produces memory deficits linked to dysfunction in hippocampal long-term potentiation and glutamate release

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Prenatal exposure to a cannabinoid agonist produces memory deficits linked to dysfunction in hippocampal long-term potentiation and glutamate release

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Prenatal exposure to a cannabinoid agonist produces memory deficits linked to dysfunction in hippocampal long-term potentiation and glutamate release

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ferraro, Luca Cagiano, Raffaele Fà, Mauro Antonelli, Tiziana Tattoli, Maria Cuomo, Vincenzo Gessa, Gian Luigi Mereu, Giampaolo Ghiglieri, Veronica Tanganelli, Sergio
Description	Author Affiliation: Mereu G ( Department of Experimental Biology, University of Cagliari, Cittadella Universitaria di Monserrato, 09042 Monserrato, Italy.);
Abstract	To investigate the possible long-term consequences of gestational exposure to cannabinoids on cognitive functions, pregnant rats were administered with the CB1 receptor agonist WIN 55,212-2 (WIN), at a dose (0.5 mgkg) that causes neither malformations nor overt signs of toxicity. Prenatal WIN exposure induced a disruption of memory retention in 40- and 80-day-old offspring subjected to a passive avoidance task. A hyperactive behavior at the ages of 12 and 40 days was also found. The memory impairment caused by the gestational exposure to WIN was correlated with alterations of hippocampal long-term potentiation (LTP) and glutamate release. LTP induced in CA3-CA1 synapses decayed faster in brain slices of rats born from WIN-treated dams, whereas posttetanic and short-term potentiation were similar to the control group. In line with LTP shortening, in vivo microdialysis showed a significant decrease in basal and K(+)-evoked extracellular glutamate levels in the hippocampus of juvenile and adult rats born from WIN-treated dams. A similar reduction in glutamate outflow was also observed in primary cell cultures of hippocampus obtained from pups born from mothers exposed to WIN. The decrease in hippocampal glutamate outflow appears to be the cause of LTP disruption, which in turn might underlie, at least in part, the long-lasting impairment of cognitive functions caused by the gestational exposure to this cannabinoid agonist. These findings could provide an explanation of cognitive alterations observed in children born from women who use marijuana during pregnancy.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	8
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Hippocampus Drug Effects Memory Prenatal Exposure Delayed Effects Receptors, Drug Agonists Animals Avoidance Learning Physiology Benzoxazines Cells, Cultured Electrophysiology Glutamic Acid Physiopathology Long-Term Potentiation Marijuana Smoking Adverse Effects Microdialysis Morpholines Administration & Dosage Toxicity Motor Activity Naphthalenes Pregnancy Rats, Wistar Receptors, Cannabinoid Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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