両側無名質破壊による辺縁系発作の抑制効果

LIMBIC SEIZURE AND IBOTENIC ACID-INDUCED LESIONS OF SUBSTANTIA INNOMINATA IN CATS

　抄録　無名質は，コリン作動性神経細胞が多数存在し，大脳皮質に神経線維を投射している。我々は，無名質のアセチルコリン系が辺縁系発作に及ぼす影響を検討するため，次の実験をおこなった。猫の両側無名質をイボテン酸で破壊した後で，無麻酔，無拘束の状態でカイニン酸を左扁桃核に注入し辺縁系発作を誘発した。コントロール群は，両側無名質にリン酸緩衝液を注入した後，カイニン酸を左扁桃核に注入した。コントロール群では，初期の辺縁系発作が終息しtransfer stageを経た後に二次性全般化発作を起こすようになった。両側無名質破壊群では，初期の辺縁系発作はコントロール群と同様におこったが，二次性全般化発作には発展しなかった。アセチルコリン系である無名質の破壊は，カイニン酸誘発による辺縁系発作の二次性全般化に抑制的に働くと考えられた。

The substantia innominata (SI) contains a lot of cholinergic neurons and mainly project their fibers to the cerebral cortex and to the amygdala. De-generative lesions were made in the bilateral SI and influences of these lesions upon kainic acid-induced limbic seizure were studied. Eleven adult cats were stereotaxically implanted and 2. 5 ,ug ofibotenic acid (IBO) was injected into the bilateral SI in 6 cats (IBO group) and 1,u1 of phosphate buffer (PB) in 5 cats (PB group). All animals were given freedom at least 8 days to recover from the operation. Kainic acid microinjection was made into the left amygdala and electroclinical observation was done. In PB group, the limbic status was elicited and these seizures persisted for about 3 days after the KA injection. Seizures were subsided but interictal discharges were ob-served at the injected site of the amygdala. Then, limbic seizures reappeared within 10 days and a slowly progressive development of limbic seizure was observed. These seizures developed further. Occasionally, these limbic seizures successively developed and secondarily generalized seizures oc-curred once or twice a week. Otherwise, theirclinical behaviors were normal during the inter-ictal periods. In IBO group, the limbic status were elicited and lasted for about 3 days after the KA injection. Although interictal discharges reap-peared at the injected site of the amygdala, suc-cessive development of the limbic seizure was not observed. The secondarily generalized seizure never occurred in the IBO group. Histopathologi-cal studies revealed circumscribed degenerative changes in the bilateral SI. The KA microinjec-tion into the amygdala resulted stereotyped amy-gdaloid degenerative lesions in both groups. Au-thors insisted that cholinergic connections between SI and amygdala or cerebral cortex have a facilita-tory action upon the secondarily generalization of limbic seizures.