Change in cerebral glucose metabolism during limbic seizures elicited from lateral septal nucleus

Epilepsy Res. 1998 May;30(3):167-76. doi: 10.1016/s0920-1211(98)00006-0.

Abstract

The roles of the amygdala and hippocampus have been extensively studied in limbic seizures. Although the septal nuclei have a close connection to the hippocampus and affect emotional behavior, the effect on limbic seizures is still unclear. We have reported that characteristic sham-rage seizures were observed in cats, by administering a local injection of kainic acid (KA) into the lateral septal nucleus (LSN). This study investigated the electrophysiological features of KA-induced septal seizures in rats and analyzed the process in relation to the cerebral glucose metabolism using [14C]deoxyglucose autoradiography. On EEG, epileptic discharge eliciting from the LSN rapidly propagated to the hippocampus and the amygdala. Behavioral change was similar to that in limbic seizures induced by intraamygdaloid KA. Sham-rage seizure was not observed in rats. However, the local cerebral glucose metabolism during the seizures increased not only in the limbic structures including the LSN but also in the hypothalamus and periaqueductal grey matter of the midbrain. The findings were distinctive of septal seizures as compared with amygdaloid seizures. The results suggested that sham-rage seizures in cats might be caused by a secondary epileptogenic excitation in the hypothalamus or periaqueductal grey matter of the midbrain. The septal nuclei may play an important role in emotional behavior associated with limbic seizures even if there is a species difference in its function.

MeSH terms

  • Animals
  • Behavior, Animal / physiology
  • Brain / metabolism*
  • Brain / pathology
  • Electroencephalography
  • Excitatory Amino Acid Agonists
  • Glucose / metabolism*
  • Kainic Acid
  • Limbic System / physiopathology*
  • Rats
  • Rats, Wistar
  • Seizures / chemically induced
  • Seizures / physiopathology*
  • Seizures / psychology
  • Septal Nuclei / physiopathology*

Substances

  • Excitatory Amino Acid Agonists
  • Glucose
  • Kainic Acid