Linked Life Data

15700288

Source:http://linkedlifedata.com/resource/pubmed/id/15700288

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-2-21
pubmed:abstractText
Exposure to cocaine in utero can result in cognitive deficits potentially through a disruption in the inhibitory processes of the frontal cortex. One potential mechanism is through alterations in the inhibitory local circuit neurons containing the calcium-binding protein, parvalbumin. Parvalbumin-immunostaining primarily identifies 2 types of local circuit neurons: larger, rounder, axo-somal basket cells and smaller, more-spindle shaped, axo-axonic chandelier cells. Both are thought to have critical impact on the excitatory/inhibitory balance due to the proximal site of projection on pyramidal neurons. Calretinin, another calcium-binding protein, identifies a distinct sub-population of inhibitory local circuits that impinges more distally on the dendritic arbor and serves as a control population for this study. Here, we examine local circuit neurons containing either parvalbumin or calretinin in adolescent male rats (approximately 45 days old) exposed to saline or cocaine (3 mg/kg, intravenous twice a day during embryonic days 10 to 20). Prenatal cocaine exposure caused select changes in the parvalbumin, but not calretinin, containing cells in the frontal cortex. Specifically, prenatal cocaine exposure is associated with a 50% reduction in spindle-shaped parvalbumin-immunoreactive cells potentially indicating a select loss of chandelier cells or a shift to a rounder shape. Additionally, a reduction in the number of dendrites of parvalbumin-immunoreactive cells in rats exposed to cocaine in utero was noted. Other measures of both parvalbumin- and calretinin-immunoreactive cells were unchanged, including total number of cells, distribution by depth, and sizes of cells. These changes to the excitatory/inhibitory balance in the frontal cortex may contribute to the cognitive deficits associated with prenatal cocaine exposure.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0887-4476
pubmed:author
pubmed:issnType
Print
pubmed:volume
56
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-11
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Prenatal exposure to cocaine selectively disrupts the development of parvalbumin containing local circuit neurons in the medial prefrontal cortex of the rat.
pubmed:affiliation
Neuropsychopharmacology Research Unit, Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520-8066, USA. bret.morrow@yale.edu
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.