Preferential neuron loss in the rat piriform cortex following pilocarpine-induced status epilepticus

Epilepsy Res. 2007 Apr;74(1):1-18. doi: 10.1016/j.eplepsyres.2006.11.008. Epub 2006 Dec 27.

Abstract

Structures within the piriform cortex (PC) including the endopiriform nucleus (DEN) and pre-endopiriform nucleus (pEn) have been implicated to be involved in seizure genesis in models of temporal lobe epilepsy. We used stereological methods to examine the specificity and extent of neuron loss in the PC of pilocarpine-treated rats. Both 7 days and 2 months post-status epilepticus rats showed significant neuron loss in the pEn and DEN, layer III of the intermediate PC, and layers II and III of the caudal PC. Total losses in the PC were 40 and 46% in 7 days and 2 months post-status epilepticus rats, respectively (p<0.01). The numbers of parvalbumin (PV)- and cholecystokinin (CCK)-immunopositive neuron profiles significantly decreased, and somatostatin (SS)-immunopositive neuron profiles tended to decrease. A large decrease in the number of PV-immunopositive neuron profiles occurred in the pEn, adjoining parts of the DEN and deep layer III of the PC, portions of the DEN bordering the claustrum and agranular insular cortex, and layer III of the caudal PC. The regions with decreased numbers of PV-, CCK-, and SS-immunopositive neuron profiles overlapped with those where many Nissl-stained neurons were lost and many degenerating cell bodies were detected. These results suggest that the decreases in the numbers of PV/SS/CCK-immunopositive neurons are related to neuron loss rather than to a low rate of synthesis of their peptides or proteins.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death
  • Cerebral Cortex / pathology*
  • Cholecystokinin / metabolism
  • Disease Models, Animal
  • Immunohistochemistry
  • Male
  • Neurons / pathology*
  • Nissl Bodies
  • Parvalbumins / metabolism
  • Pilocarpine
  • Rats
  • Rats, Sprague-Dawley
  • Seizures / pathology*
  • Somatostatin / metabolism
  • Status Epilepticus / chemically induced
  • Status Epilepticus / metabolism
  • Status Epilepticus / pathology*

Substances

  • Parvalbumins
  • Pilocarpine
  • Somatostatin
  • Cholecystokinin