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抄録 Alzheimer型老年痴呆において,無名質より大脳皮質へ投射するコリンニューロンの脱落が,その病因との関係において注目されている。しかしこれまで,このニューロンの生理学的な同定はなされていない。我々はネコを用いて,このニューロンを逆行性反応によって電気生理学的に同定することに成功した。この系のニューロンは一般に極めて遅い伝導速度を示すが,その中にも平均2.3m/secと比較的速い伝導速度を示す有髄線維と思われる線維群と,伝導速度が平均1.0m/secと極めて遅い無髄線維と思われる線維群とが混在しているようである。また無名質より大脳皮質に至るニューロンの神経終末は,電気生理学的に側頭葉と頭頂葉に最も多く分布していることが明らかとなり,これは解剖学的な結果と一致した。アトロピンの投与も試みたが,この系の逆行性反応は潜時,振幅とも明らかな変化を認めず,少なくとも自己あるいは近傍の細胞体に対する軸索側枝の存在する可能性は少ないものと考えられた。
Recently in senile dementia of Alzheimer type, neuronal loss of cholinergic neurons in the subs-tantia innominata is described. However thesefindings are based on morphological studies and, so far, these neurons have mot been identified physiologically. In this study we tried to record these neurons electrophysiologically by antidromic activation.
Cats were anesthetized with sodium pentobar-bital and paralyzed with gallamine triethiodide. Three arreys of 3 or 4 silver-ball stimulating electrodes were fixed to the surface of the cere-bral cortex. Each electrode was stimulated by rectangular pulses of 1 msec duration. Recording electrodes were glass micropipettes filled with 2 M NaC1 saturated with fast green FCF and in-serted into the ipsilateral substantia innominata stereotaxically.
Twenty-eight neurons were constituted of mainly negative component; suggesting that they were recorded from cell bodies, not from axons. Also they responded in an all-or-none manner and show-ed constant latencies when stimulus intensities were at threshold level. When paired stimuli were applied, the latency of the action potential to the second stimulus was equal to that of the first one. These neurons were, therefore, considered to be activated antidromically.
These neurons had axons of very slow conduc-tion velocities. They are divided into two groups according to conduction velocities. The first group had mean conduction velocity of 2.3 m/sec and they responded to rather high frequency stimuli. The second group had mean conduction velocity of 1.0 m/sec and neurons belonging to this group showed quite long refractory periods. Based on conduction velocity analysis, the former is thought to include neurons with myelinated axons and the latter those with unmyelinated ones. Anatomical findings indicate that the ratio between myelina-ted and unmyelinated fibers is 1 to 2. In our study, ratio of myelinated fibers is rather high compared to the anatomical findings; being ex-plained by the difference of the techniques.
In our electrophysiological study stimulating sites with the lowest threshold were situated in the temporal and parietal cortices and, therefore, axon terminals of these neurons were thought to end mainly in the temporal and parietal cortices. This conclusion is in good agreement with the anatomical findings.
In some cases 120 pg/kg of atropine was admi-nistered intravenously. Neither latency nor ampli-tude of the action potentials was affected.
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