本研究的目的是想在天竺鼠疑核與後疑核尋找並鑑定與呼吸有關的
神經元，並進一步探討其對二氧化碳濃度提高的反應。動物以urethane
(2g/kg，i.p.) 麻醉，麻痺肌肉，切斷兩側迷走神經後，以人工呼吸機
維持生命，分離並記錄膈神經活動，以金屬電極或玻璃電極記錄單一神
經元。
在所記錄的 285個神經元中，可分為吸氣神經元 (I)、呼氣神經元
(E)、 及跨期神經元 (P-S)等三種類型。其分布主要集中在閂前方 0-
2.0 mm，中線外側 1.2-2.0 mm， 表面下深約 2.0-4.5 mm 的區域內。
增加呼氣末二氧化碳濃度，會使呼吸週期縮短，膈神經活動增強，
呼吸神經元的放電率有些增加，有些則反而降低。當呼氣末二氧化碳濃
度從 0.04 升高到 0.06 與 0.09 時，在 I神經元中，有17個神經元的
平均放電率分別從每秒 31.2+3.8 spikes增到 45.9+6.5 spikes，再增
加到 47.5+6.8 spikes (p<0.05) ；另有13個神經元的平均放電率則從
每秒 67.2+10.6 spikes 降到 49.5+6.5 spikes，再降到 45.0+8.3
spikes (p<0.05) 。至於 E神經元，有11個神經元的平均放電率從每秒
10.0+2.7 spikes 增加到 15.5+3.7 spikes，再增加到 16.4+3.5
spikes；另有 9個神經元的平均放電率則從每秒 20.7+5.6 spikes降到
15.1+4.9 spikes，再降到 11.3+4.9 spikes。P-S神經元的平均放電率
對呼氣末二氧化碳濃度升高的反應也可分為增加(n=28)與降低(n=20)兩
組。增加放電率的 P-S神經元，其平均放電率在吸氣時間內從正常二氧
化碳濃度的每秒 21.1+2.8 spikes增加到 35.0+5.1 spikes及34.5+5.6
，在呼氣時間內則從每秒 24.3+4.7 spikes升高到 36.5+5.6 spikes與
38.2+6.8 spikes， 都有明顯的差異(p<0.05)。降低者也是如此，在吸
氣時間內的平均放電率從每秒 26.4+3.8 spikes降到 16.3+2.9 spikes
和11.6+2.1 spikes ，呼氣時間內的平均放電率則從每秒 25.7+2.5
spikes降到 0.06 時的 18.6+2.6 spikes，再降為 0.09 時的10.5+1.6
spikes (p<0.01)。 此外，切斷兩側迷走神經，除降低呼吸頻率外，還
會減弱天竺鼠膈神經對高濃度二氧化碳的反應。
這些結果顯示：天竺鼠疑核和後疑核內的確含有許多呼吸神經元，
且其放電率會受到二氧化碳濃度的影響，而迷走神經的完整與否，則會
影響天竺鼠對高濃度二氧化碳的反應。因此，這些呼吸神經元對呼吸神
經管制可能扮演著重要角色，同時迷走神經的傳入訊息對天竺鼠的正常
呼吸調節應該相當重要。

The aim of the present study was to localize and charact-
erize the respiratory-related neurons in the nucleus ambiguus
(NA) and nucleus retroambigualis (NRA) of the guinea pig. The
animals was anethetized with urethane(2g/kg,i.p.),bilaterally
vagotomized,paralyzed and artificially ventilated.The phrenic
nerve activity was isolated and its activity was monitored .
Single unit activity was recorded with metal or glass micro-
electrods.
Activities of 285 neurons from 48 animals were observed
and showed a respiratory-related rhythm. They were classified
into inspiratory (I), expiratory (E), and phase-spanning (P-S)
patterns according to their timing in relation to respiratory
cycle by phrenic nerve discharge . The distribution of these
neurons was concentrated in the area extending from 0-2.0 mm
rostral to the obex, 1.2-2.0 mm lateral to the midline, and
2.0-4.5 mm below the surface.
In response to hypercapnia, the duration of the respiratory
cycle shortened, but phrenic nerve activity enhanced. In res-
ponse to different levels of hypercapnia, mean discharge rateS
of some neurons diminished, whereas some augmented. When FETCO2
was raised from 0.04 (control) to 0.06, and further to 0.09,
mean discharge rate of 17 I neurons increased from 31.2+3.8
spikes/sec (control) to 45.9+6.5 spikes/sec (p<0.05) and 47.5+
6.8 spikes/sec (p<0.05), respectively. However, mean discharge
rate of the other 13 I neurons reduced from 67.2+10.6 spikes/sec
to 49.5+6.5 spikes/sec and 45.0+8.3 spikes/sec (p<0.05). For
the E neurons, mean discharge rate of 11 neurons increased
from 10.0+2.7 spikes/sec to 15.5+3.7 spikes/sec and 16.4+3.5
spikes/sec, but the other 9 neurons decreased from 20.7+5.6
spikes/sec to 15.1+4.9 spikes/sec and 11.3+4.9 spikes/sec.
Similar patterns of responses to hypercapnia were also observed
in P-S neurons with some were excited (n=28), and some were
inhibited (n=20). For those P-S neurons excited by hypercapnia,
mean discharged rate increased from 21.1+2.8 spikes/sec to
35.0+5.1 spikes/sec (p<0.05) and 34.5+5.6 spikes/sec (p<0.05)
during Ti, and from 24.3+4.7 spikes/sec to 36.5+5.6 spikes/sec
and 38.2+6.8 spikes/sec (p<0.05) during Te. In contrast, neurons
inhibited by CO2 reduced their meaan discharge rate from
26.4+3.8 spikes/sec to 16.3+2.9 spikes/sec (p<0.05) and 11.6+2.1
spikes/sec (p<0.01) during Ti, and from 25.7+2.5 spikes/sec
to 18.6+2.6 spikes/sec (p<0.05) and 10.5+1.6 spikes/sec (p<0.01)
during Te. In addtion, bilateral vagotomy produced a decrease
in the respiratory frequency and a diminish of phrenic nerve
response to hypercapnia.
It was concluded that there were respiratory-related
neurons, which may play an important role in the neural control
mechanism of respiration, were concentrated in the area of the
NA and NRA in guinea pigs. The discharge rate of these neurons
can be modulated by CO2 concentration. In addtion, vagal inputs
may also play a role in the response of the phrenic nerve to
severe hypercapnia in the guinea pig. It was suggested that
the respiratory-related neurons and the vagal inputs are
essential for the normal respiration in this anmal.
The aim of the present study was to localize and charact-