Lasting increase in excitatory amino acid receptor-mediated polyphosphoinositide hydrolysis in the amygdala/pyriform cortex of amygdala-kindled rats

Kazufumi Akiyama, Norihito Yamada, Saburo Otsuki

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

We previously demonstrated that ibotenate-stimulated polyphosphoinositide hydrolysis, determined as the accumulation of [3H]inositol 1-phosphate, significantly increase in the amygdala/pyriform cortex (AM/PC) 24 h and 7 days after the last seizure in AM-kindled rats. The present study examined whether the increase in ibotenate-stimulated polyphosphoinositide hydrolysis in the AM/PC is longer lasting. AM-kindled rats with a tripolar electrode implanted into the left AM and sham-operated controls were decapitated either 1, 2 or 4 weeks after the last seizure. Ibotenate (10-3 M)-stimulated accumulation of [3H]inositol 1-phosphate significantly increased by 90% (P <0.01), 110% (P <0.051) and 73% (P <0.05) in the AM/PC 1, 2 and 4 weeks, respectively, after the last seizure. Four weeks after the last seizure, there were significant increases of a similar magnitude in the contralateral (right) AM/PC (by 83%, P <0.001) and the ipsilateral (left) AM/PC (by 63%, P <0.01). There was no change in the hippocampus or limbic forebrain at any of these times. Also 4 weeks after the last seizure, accumulation of [3H]inositol 1-phosphate significantly (P <0.05) increased at ibotenate concentrations of 2 × 10-4 M, 5 × 10-4 M and 10-3 M in the kindled AM/PC. In light of the view that the AM/PC are the crucial brain structures for sustaining seizure susceptibility, the marked and lasting increase in the ibotenate-stimulated polyphosphoinositide hydrolysis coupled to excitatory amino acid receptors in the kindled AM/PC may be associated with the development of kindling and long-term maintenance of kindled events.

Original languageEnglish
Pages (from-to)95-101
Number of pages7
JournalBrain Research
Volume485
Issue number1
DOIs
Publication statusPublished - Apr 17 1989

Fingerprint

Phosphatidylinositol Phosphates
Glutamate Receptors
Amygdala
Hydrolysis
Seizures
Implanted Electrodes
Piriform Cortex
Prosencephalon
Hippocampus
Brain

Keywords

  • Amygdala
  • Excitatory amino acid
  • Ibotenate
  • Kindling
  • Polyphosphoinositide hydrolysis
  • Seizure susceptibility

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Lasting increase in excitatory amino acid receptor-mediated polyphosphoinositide hydrolysis in the amygdala/pyriform cortex of amygdala-kindled rats. / Akiyama, Kazufumi; Yamada, Norihito; Otsuki, Saburo.

In: Brain Research, Vol. 485, No. 1, 17.04.1989, p. 95-101.

Research output: Contribution to journalArticle

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abstract = "We previously demonstrated that ibotenate-stimulated polyphosphoinositide hydrolysis, determined as the accumulation of [3H]inositol 1-phosphate, significantly increase in the amygdala/pyriform cortex (AM/PC) 24 h and 7 days after the last seizure in AM-kindled rats. The present study examined whether the increase in ibotenate-stimulated polyphosphoinositide hydrolysis in the AM/PC is longer lasting. AM-kindled rats with a tripolar electrode implanted into the left AM and sham-operated controls were decapitated either 1, 2 or 4 weeks after the last seizure. Ibotenate (10-3 M)-stimulated accumulation of [3H]inositol 1-phosphate significantly increased by 90{\%} (P <0.01), 110{\%} (P <0.051) and 73{\%} (P <0.05) in the AM/PC 1, 2 and 4 weeks, respectively, after the last seizure. Four weeks after the last seizure, there were significant increases of a similar magnitude in the contralateral (right) AM/PC (by 83{\%}, P <0.001) and the ipsilateral (left) AM/PC (by 63{\%}, P <0.01). There was no change in the hippocampus or limbic forebrain at any of these times. Also 4 weeks after the last seizure, accumulation of [3H]inositol 1-phosphate significantly (P <0.05) increased at ibotenate concentrations of 2 × 10-4 M, 5 × 10-4 M and 10-3 M in the kindled AM/PC. In light of the view that the AM/PC are the crucial brain structures for sustaining seizure susceptibility, the marked and lasting increase in the ibotenate-stimulated polyphosphoinositide hydrolysis coupled to excitatory amino acid receptors in the kindled AM/PC may be associated with the development of kindling and long-term maintenance of kindled events.",
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AB - We previously demonstrated that ibotenate-stimulated polyphosphoinositide hydrolysis, determined as the accumulation of [3H]inositol 1-phosphate, significantly increase in the amygdala/pyriform cortex (AM/PC) 24 h and 7 days after the last seizure in AM-kindled rats. The present study examined whether the increase in ibotenate-stimulated polyphosphoinositide hydrolysis in the AM/PC is longer lasting. AM-kindled rats with a tripolar electrode implanted into the left AM and sham-operated controls were decapitated either 1, 2 or 4 weeks after the last seizure. Ibotenate (10-3 M)-stimulated accumulation of [3H]inositol 1-phosphate significantly increased by 90% (P <0.01), 110% (P <0.051) and 73% (P <0.05) in the AM/PC 1, 2 and 4 weeks, respectively, after the last seizure. Four weeks after the last seizure, there were significant increases of a similar magnitude in the contralateral (right) AM/PC (by 83%, P <0.001) and the ipsilateral (left) AM/PC (by 63%, P <0.01). There was no change in the hippocampus or limbic forebrain at any of these times. Also 4 weeks after the last seizure, accumulation of [3H]inositol 1-phosphate significantly (P <0.05) increased at ibotenate concentrations of 2 × 10-4 M, 5 × 10-4 M and 10-3 M in the kindled AM/PC. In light of the view that the AM/PC are the crucial brain structures for sustaining seizure susceptibility, the marked and lasting increase in the ibotenate-stimulated polyphosphoinositide hydrolysis coupled to excitatory amino acid receptors in the kindled AM/PC may be associated with the development of kindling and long-term maintenance of kindled events.

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