Hippocampal synaptic plasticity was studied in transgenic mice over-expressing human α-synuclein containing the A30P Parkinson's disease mutation. Medial perforant path-dentate granule cell synapses showed enhanced paired-pulse depression (PPD) for short interpulse intervals (< 200 ms), without differences in basal transmission. Extracellular calcium reduction failed to rescue the enhanced PPD. Paired-pulse facilitation in the CAI region was normal in slices from transgenic mice, but enhanced synaptic depression was revealed upon repetitive stimulation of the Schaffer collaterals. Long-term potentiation in the CAI field was not impaired in slices from transgenic mice. These results suggest that mutant α-synuclein accumulation impairs short-term changes in synaptic strength when neurotransmitter availability is limited due to enhanced release probability or repetitive synaptic activity.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Feb 10 2003|
- Brain slices
- Field potential
- Parkinson's disease
- Synaptic plasticity