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γ‐aminobutyric acidergic interneuron vulnerability to aging in canine prefrontal cortex
Author(s) -
Pugliese M.,
Carrasco J.L.,
Geloso M.C.,
Mascort J.,
Michetti F.,
Mahy N.
Publication year - 2004
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20223
Subject(s) - calretinin , parvalbumin , gabaergic , interneuron , neuroscience , calbindin , biology , human brain , prefrontal cortex , inhibitory postsynaptic potential , immunohistochemistry , cognition , immunology
The aged dog is considered a promising model for examining molecular and cellular processes involved in a variety of human neurological disorders. By using the canine counterpart of senile dementia of the Alzheimer's type (ccSDAT), we investigated the specific vulnerability of the γ‐aminobutyric acid (GABA) cortical subset of interneurons, characterized by their calcium‐binding protein content, to neuronal death. Dogs representing a large variety of breeds were classified into three groups: young control, aged control, and ccSDAT. In all dogs, the general distribution and cell typology of parvalbumin‐, calretinin‐, and calbindin‐positive neurons were found to be similar to those in the human. As in Alzheimer's disease patients, neurons displaying parvalbumin or calretinin immunoreactivity were resistant and the calbindin‐positive ones depleted. Together with aging, amyloid deposition in its early phase (stage II) participates in this specific neuronal death, but with a lower potency. In conclusion, our data provide evidence that preservation of GABAergic cortical interneurons has to be focused on the early stage of β‐amyloid deposition. We also demonstrate the usefulness of dogs of all breeds for investigating the early phases of human brain aging and Alzheimer's disease. © 2004 Wiley‐Liss, Inc.