Research article summary (published 30 May 2008):

Cocaine decreases the expression of PSA-NCAM protein and attenuates long-term potentiation via glucocorticoid receptors in the rat dentate gyrus.

Full Abstract

The present study investigated a potential role for glucocorticoid (GR) and mineralocorticoid (MR) receptors in the detrimental effects of single cocaine (COC) administration on both the number of polysialylated neural cell adhesion molecule (PSA-NCAM)-positive neurons and the induction of long-term potentiation (LTP) in the rat dentate gyrus (DG). The effects of COC (15 mg/kg i.p.) on the number of PSA-NCAM-positive neurons and the induction of LTP observed 2 days after COC administration were abolished either by depleting circulating corticosterone after administration of metyrapone (100 mg/kg s.c. given 3 h before COC) or by pharmacologically blocking GRs using mifepristone (RU 38486, 10 mg/kg s.c. given 1 h before COC). Administration of the MR blocker spironolactone (50 mg/kg s.c. given 1 h before COC) did not alter the effects of COC on the number of PSA-NCAM-positive neurons or LTP induction. Results have also shown that COC does not change the rate of cell proliferation, as measured by the presence of Ki-67 and the incorporation of bromodeoxyuridine (100 mg/kg i.p. given 2 h after COC) into the newly born cells in the DG 2 days after COC administration. Finally, we observed that GRs colocalized with some, but not all, PSA-NCAM-positive neurons, whereas MRs showed no colocalization with neurons positive for PSA-NCAM in the DG. These data indicate that a single dose of COC may arrest hippocampal susceptibility to plastic changes and lead to functional impairments through the alteration of hippocampal structure and the formation of memory traces.

Author information

Author/s: Mackowiak, Marzena (M); Grzegorzewska, Malgorzata (M); Budziszewska, Boguslawa (B); Chocyk, Agnieszka (A); Hess, Grzegorz (G); Wedzony, Krzysztof (K);

Affiliation: Laboratory of Pharmacology and Brain Biostructure, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343 Kraków, Poland. mackow(-atsign-)if-pan.krakow.pl

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: The European journal of neuroscience (Eur J Neurosci), published in France. (Language: eng)

Reference: 2008-Jun; vol 27 (issue 11) : pp 2928-37

Dates: Created 2008/06/30; Completed 2008/08/20;

PMID: 18588533, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals Bromodeoxyuridine Cell Count Cell Proliferation - drug effects Cocaine - pharmacology Cocaine-Related Disorders - metabolism; physiopathology Corticosterone - antagonists & inhibitors; blood Dentate Gyrus - drug effects; metabolism Dopamine Uptake Inhibitors - pharmacology Down-Regulation - drug effects; physiology Ki-67 Antigen - metabolism Long-Term Potentiation - drug effects; physiology Male

Male Memory - drug effects; physiology Memory Disorders - chemically induced; metabolism; physiopathology Metyrapone - analogs & derivatives; pharmacology Mifepristone - pharmacology Neural Cell Adhesion Molecule L1 - metabolism Neurons - drug effects; metabolism Rats Rats, Wistar Receptors, Glucocorticoid - agonists; antagonists & inhibitors; metabolism Receptors, Mineralocorticoid - antagonists & inhibitors; metabolism Sialic Acids - metabolism Spironolactone - pharmacology

Associated Chemicals: Dopamine Uptake Inhibitors (0) ; Ki-67 Antigen (0) ; Neural Cell Adhesion Molecule L1 (0) ; Receptors, Glucocorticoid (0) ; Receptors, Mineralocorticoid (0) ; Sialic Acids (0) ; polysialyl neural cell adhesion molecule (0) ; metyrapol (17159-42-1) ; Corticosterone (50-22-6) ; Cocaine (50-36-2) ; Spironolactone (52-01-7) ; Metyrapone (54-36-4) ; Bromodeoxyuridine (59-14-3) ; Mifepristone (84371-65-3)

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