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The Fragile-X mental retardation protein, the protein absent in Fragile-X syndrome, is synthesized near synapses upon neurotransmitter activation. Humans and mice lacking this protein exhibit abnormal dendritic spine lengths and numbers. Here we investigated Fragile-X protein levels in animals exposed to behavioral paradigms that induce neuronal morphological change. Fragile-X protein immunoreactivity was examined in visual cortices of rats reared in a complex environment for 10 or 20 days, motor cortices of rats trained on motor-skill tasks for 3 or 7 days, and either visual or motor cortices of inactive controls. Rats exposed to a complex environment for 20 days or trained for 7 days on motor-skill tasks exhibited increased Fragile-X protein immunoreactivity in visual or motor cortices, respectively. These results provide the first evidence for a behaviorally induced alteration of Fragile-X protein expression and are compatible with previous findings suggesting synaptic regulation of its expression. These results also strengthen the association of Fragile-X mental retardation protein expression with the alteration of synaptic structure.

The Fragile-X mental retardation protein, the protein absent in Fragile-X syndrome, is synthesized near synapses upon neurotransmitter activation. Humans and mice lacking this protein exhibit abnormal dendritic spine lengths and numbers. Here we investigated Fragile-X protein levels in animals exposed to behavioral paradigms that induce neuronal morphological change. Fragile-X protein immunoreactivity was examined in visual cortices of rats reared in a complex environment for 10 or 20 days, motor cortices of rats trained on motor-skill tasks for 3 or 7 days, and either visual or motor cortices of inactive controls. Rats exposed to a complex environment for 20 days or trained for 7 days on motor-skill tasks exhibited increased Fragile-X protein immunoreactivity in visual or motor cortices, respectively. These results provide the first evidence for a behaviorally induced alteration of Fragile-X protein expression and are compatible with previous findings suggesting synaptic regulation of its expression. These results also strengthen the association of Fragile-X mental retardation protein expression with the alteration of synaptic structure., (Copyright 2000 Academic Press.)

Synaptoneurosomes, a subcellular fraction of resealed presynaptic plus postsynaptic entities, contain polyribosomal aggregates and are capable of protein synthesis. Upon treatment with K(+), which has been shown to cause depolarization, we observed a rapid increase followed by a decrease in the size of polyribosomal complexes. These were shown by sucrose density gradient analysis to represent a shift of part of the total RNA into polyribosomes; accelerated incorporation of amino acids into polypeptides was also demonstrated. Calcium chelators in the medium reduce the steady-state size of polyribosomal complexes, but do not eliminate the response to depolarization, while intracellular calcium chelators have more profound effects, suggesting that there is mobilization of intracellular calcium stores. Thus depolarization-related changes may affect binding and release of translation initiation complexes with messenger RNA found near synaptic junctions.