Selective protection of neuropeptide containing dentate hilar interneurons by non-NMDA receptor blockade in an animal model of status epilepticus.

We used a 24 h perforant path stimulation model of status epilepticus to study the role of non-NMDA receptors in the loss of hilar interneurons and paired pulse inhibition associated with the model. In one experiment, NBQX administered i.v. at 1.0 mg/kg/h significantly reduced the loss of hematoxylin and eosin-stained hilar neurons from 360.2 to 125.3 but failed to protect against the loss of paired pulse inhibition. In a second experiment, i.v. NBQX at 1.5 mg/kg/h significantly protected against loss of SS- and NPY-positive hilar interneurons but also failed to protect against loss of paired pulse inhibition. These results demonstrate that the neuronal loss associated with sustained stimulation of this excitatory pathway is mediated in part through non-NMDA receptors. The lack of protection against loss of paired pulse inhibition suggests that SS- and NPY-immunoreactive interneurons may not be responsible for frequency-dependent paired-pulse inhibition of dentate granule cells.