Decreases in excitatory synaptic transmission and increases in recurrent inhibition in the rat dentate gyrus after transient cerebral ischemia.
Excitatory transmission along the perforant path from the entorhinal cortex to the granule cells of the dentate gyrus was evaluated two days after 10 min of transient cerebral ischemia in the rat. The amplitude of the population spike, and the amplitude and the initial slope of the population excitatory postsynaptic potential (EPSP) evoked by the perforant path stimulation were measured across a range of stimulus intensities, and were compared with control values. Inhibitory interactions were evaluated using the paradigm of paired pulse stimulation, comparing the amplitude of the population spike evoked by the second pulse of a pair to the initial spike. The maximal values of the initial slope of the population EPSP and the population spike were reduced in the ischemic group. Also, the extent of paired pulse inhibition was greater in the ischemic group. These results suggest that: (1) excitatory synaptic transmission along the perforant path is impaired in the postischemic period, (2) inhibition of the dentate granule cells is enhanced in this period. These results are not consistent with the hypothesis that there is a hyperactivation of the tri-synaptic circuit in the chronic postischemic period that accounts for the excitotoxic death of CA1 neurons.
Chang
H S
HS
Department of Neurosurgery, University of Virginia School of Medicine, Charlottesville 22908.
Steward
O
O
Kassell
N F
NF
D000200:Action Potentials; D000818:Animals; D004558:Electric Stimulation; D006624:Hippocampus / Q000503:physiopathology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D009433:Neural Inhibition; D051381:Rats; D011919:Rats, Inbred Strains