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Abstract
Homocysteine (HCY) is a sulphur-containing amino acid, which has been linked to neurodegenerative
diseases such as Alzheimer's disease, and is widely reported to enhance vulnerability
of neurons to oxidative, excitotoxic and apoptotic injury via perturbed calcium homeostasis,
activation of N-methyl-D-aspartate (NMDA) and metabotropic glutamate (mGlu) receptors.
The present study was undertaken to investigate the effects of HCY on long-term potentiation
(LTP) and synaptic transmission after chronic 4-week systemic exposure to HCY in adult
rats, and possible longer-term effects of HCY 4 weeks after exposure had ended. Contrary
to expectation, LTP was enhanced, not retarded after chronic HCY exposure relative
to controls. Basic synaptic transmission was not affected at this time point. However,
after the 4-week wash out period, a decrease in speed of basic synaptic transmission
emerged, and LTP was still partially enhanced, particularly for time points >30 min
post-tetanus. In summary, we provide first evidence for sustained HCY-induced changes
in hippocampal plasticity and a slow-onset disruption in synaptic transmission. These
changes may reflect the suggested (excito-)toxicity of HCY and its putative contribution
to neurodegenerative disease.