Overexpression of the p75 neurotrophin receptor in the sensori-motor cortex of rats exposed to ethanol during early postnatal life.
Foetal alcohol syndrome is a known cause of mental retardation. It has been suggested that the anatomical and functional alterations observed in the cerebral cortex could be mediated by an interference of ethanol with developmental processes modulated by neurotrophins and/or their receptors. We have studied by immunohistochemistry the expression of the p75 neurotrophin receptor (p75 NTR) in the sensori-motor cortex of P10 and P20 rats exposed to the inhalation of ethanol during the first week of postnatal life. At both the studied ages, the number of p75 NTR immunoreactive neurons was higher in ethanol treated animals compared to controls. The increase of immunoreactive elements was relatively more marked in the motor than in the somatosensory cortex. The involvement of p75 NTR in ethanol-induced apoptosis and neural plasticity is discussed.
Toesca
Amelia
A
Institute of Anatomy, Catholic University, L.go F. Vito 1, 00168, Rome, Italy.
Giannetti
Stefano
S
Granato
Alberto
A
D000818:Animals; D000831:Animals, Newborn; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D000431:Ethanol / Q000494:pharmacology*; D007150:Immunohistochemistry; D009044:Motor Cortex / Q000187:drug effects* / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor / Q000187:drug effects / Q000378:metabolism*; D013003:Somatosensory Cortex / Q000187:drug effects* / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects
D002492:Central Nervous System Depressants; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D000431:Ethanol