Synaptic plasticity is preserved in the temporal cortex of 20-month-old rats.

Abstract The molecular mechanisms associated with age-related alterations in the plasticity of the cortical neurons in response to chemically-induced seizure are largely unknown. Administration of pentylenetetrazole (PTZ) (50 mg/kg body weight) to rats of various ages evoked tonic-clonic seizures. Using immunoblotting and in situ hybridization analysis we found that 72 h after the onset of seizure, the mRNA for microtubule-associated protein 1B (MAP1B), a marker of synaptic plasticity, was increased in the cortex of 3-month-old rats. The levels of MAP1B mRNA in the cortex of 3-month-old rats returned to control levels by 10 days after PTZ administration. The levels of MAP1B mRNA in the hippocampus and cortex of 20 months at later times (10 days) and returned nearly to basal levels by 20 days following PTZ treatment. Immunohistochemical analysis revealed that MAP1B-like immunoreactivity was confined to layer II and neuronal processes extending into layer I. In contrast, the staining of MAP1B in the temporal cortex of 20-month-old animals was restricted to neuronal cell bodies of layer II. Since synaptic plasticity is associated mainly with neuronal processes we conclude that synaptic plasticity is reduced in the temporal cortex of 20-month-old rats. Remarkably, the induction of MAP1B in neuronal extensions was not impaired in the temporal cortex of older animals following intense neuronal activity. However, the aged rat brain responded more slowly to chemically-induced seizure although the levels of MAP1B induction are not decreased as compared to the levels expressed by 3-month-old rats.