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Stimulation of glossopharyngeal and laryngeal nerve afferents induces expulsion only when it is applied during retching in paralyzed decerebrate dogs
ELSEVIER
Neuroscience Letters 193 (1995) 117-120
Stimulation of glossopharyngeal and laryngeal nerve afferents induces expulsion only when it is applied during retching in paralyzed decerebrate dogs HiroyukiFukuda*,Tomoshige Koga Department of Physiology, KawasakiMedical School, 577 Matushima, Kurashiki, Okayama 701-01, Japan Received 10 April 1995; revised version received 25 May 1995; accepted 25 May 1995
Abstract
Stimulation of the oropharyngeal mucosa induces vomiting in humans, however, it has not been seen in animals. Thus, we attempted to induce fictive vomiting by stimulation of lingual and pharyngeal branch afferents of the glossopharyngeal nerve, and afferents of the superior and recurrent laryngeal nerves in paralyzed decerebrate dogs. The stimulation did not induce fictive vomiting when it was applied during eupnea, but induced fictive expulsion when it was applied during fictive retching. Threshold intensity for the induction decreased with the progress of retching.
Keywords: Vomiting, Glossopharyngeal nerve, Superior laryngeal nerve, Recurrent nerve, B6tzinger complex
To analyze the neuronal mechanisms for generation of retching, we systematically stimulated and partially cut the medulla oblongata of decerebrate paralyzed dogs and recorded its unitary neuronal activity [2,3] Based on our results, we postulated that the temporal patterns of muscle contractions in retching are generated by the central pattern generator (CPG) in the B6tzinger complex (Be)T). During retching, pulmonary ventilation almost stops, and, consequently, hypercapnia and hypoxia develop with the progress of retching [4]. When the changes in the blood gasses reach a threshold, retching stops; alternatively, an expulsion appears. Activation of the central and/or peripheral chemoreceptors changes firing patterns of BC)T neurons from the patterns of retching to the patterns of expulsion [5]. Thus, we postulated that stimulation of peripheral and central chemoreceptors activates the CPG for expulsion in the BC)T and induces expulsion. In humans, however, vomiting can be induced by stimulation of the oropharyngeal mucosa with a short latency which may not allow the development of blood gas changes. This fact seems to contradict our postulation and to indicate the existence of other neuronal mechanisms for in*Corresponding author, Tel.: +81 86 4621111; Fax: +81 86 4621199.
duction of expulsion. To the best of our knowledge, however, the fact that vomiting can be induced by stimulation of the oropharyngeal mucosa has not been seen in animals. Thus, we preliminarily attempted to induce vomiting by oropharyngo-esophageal mechanical stimulation in 2 non-paralyzed decerebrate dogs. The mechanical stimulation could not induce vomiting in ordinal conditions, but could when the stimulation was applied during stomach over distention which is known to induce retching [8]. This study was designed to confirm the preliminary result. This study was performed on 9 dogs, each weighing 7.5-11 kg. The dogs were anesthetized with ketamine hydrochloride (25 mg/kg, i.m.), paralyzed with gallamine triethiodide (2 mg/kg, i.v.), artificially ventilated, and precollicularly decerebrated. The body temperature was maintained at 37-39°C by 2 heating lamps and a heating plate. End-tidal CO2 was maintained within the range 2.0-3.0% to suppress spontaneous occurrence of expulsion at the end of retching [4]. Centrifugal activities were recorded as frequency histograms (100 ms bins) in the L1 abdominal muscle branch, the C5 phrenic root and the vagal pharyngo-esophageal branch in all 9 dogs, and in the trigeminal digastric muscle branch of 3 dogs. Fictive retching and expulsion were recognized from the activity
0304-39401951509.50 © 1995 Elsevier Science Ireland Ltd. All rights reserved SSDI 0 3 0 4 - 3 9 4 0 ( 9 5 ) 1 1 6 8 2 - J
118
H. Fukuda, T. Koga I Neuroscience Letters 193 (1995) 117-120
patterns of these nerves. Rhythmic bursts of highfrequency discharges, produced concomitantly by the phrenic and abdominal muscle nerves, were considered fictive retching. Fictive expulsion was considered an episode following retching in which the duration of the burst of the abdominal muscle nerve was prolonged both with respect to the corresponding expulsion burst of the phrenic nerve and to the bursts of the abdominal muscle nerve during the preceding retching phase [2,3,6,9-14,16] Fictive retching was produced by continuous stimulation (10 Hz, 0.5 ms duration, 20-25 V) of the central part of
the severed vagal trunks at the supra-diaphragmatic region. The central part of the severed pharyngeal (rostral and caudal) and lingual branches of the glossopharyngeal nerve, and the severed superior and recurrent laryngeal nerves were stimulated to induced fictive expulsion (2050 Hz, 2-10 V, 0.5 ms duration). During eupnea, stimulation of the glossopharyngeal branches and the laryngeal nerves produced activities like fictive swallowing or no-effect, or suppressed phrenic respiratory activities, but did not induce fictive retching and/or expulsion (Fig. 1B1-D1). Similarly, the stimula-
A Phrenic n.
imp/bin
]So° 6sec
Abdominal m.n.
~
]
5
o
o
Vagus n. 10Hz
Ssec
B2
B1
6sec
Vagus n. 10Hz, 25V
Superior laryngeal n. 20Hz, 10V
Superior-laryngealn. 50Hz, IOV
Cz
C1
6sec
E
I
II
Vagus n. 10Hz, 2 SV
Recurrent n. 50Hz, 10V
Recurrentn. 50Hz, 10V
Dz
D1
12sec
E
Lingual br. ZOHz, 10V
Vagus n. 10Hz
Lingualbr. 50Hz, 10V
Fig. I. Effects of continuous stimulation of the central part of the severed superior (B) and recurrent (C) laryngeal nerves, and the severed lingual branch of the giossopharyngeal nerve (D). From top to bottom, the traces represent frequency histograms (100 ms bins) of centrifugal discharges of the phrenic (phrenic n.) and abdominal muscle nerves (abdominal m. n.), and the pharyngo-esophageal branch of the vagus nerve and pulses of stimulation of the thracic vagal trunk (upward), and the laryngeal nerves and the lingual branch (downward). (A) Control. Only retching was induced by vagal stimulation: During eupnea (B1-D1), activities like swallowing were induced by stimulation of the superior laryngeal nerve (BI) and the lingual branch (Dl), but no obvious effect was produced by stimulation of the recurrent laryngeal nerve (C1). Stimulation of all 3 nerves induced an expulsion when it was applied during retching (B2-D2).
H. Fukuda, 7". Koga I Neuroscience Letters 193 (1995) 117-120
tion did not induce fictive retching and/or expulsion when it was superimposed on stimulation of the vagal trunk before fictive retching was induced by the vagal stimulation (not shown). In contrast, when stimulation of the glossopharyngeal branches and the laryngeal nerves was applied during fictive retching, it produced fictive expulsion (E), but not fictive swallowing (Fig. 1B2-D2). Activity of the pharyngo-esophageal branch almost disappeared during the fictive expulsion (Fig. 1B2-D2), and the digastric muscle branch of the trigeminal nerve produced a vigorous burst just after the expulsion (not shown, but confirmed in 3 dogs). The induction of fictive expulsion was confirmed in the lingual branch of 7 dogs, A1
A2
imp/bin
Abdominal r~ n.
~
lSoo
Pl~ryngo-esophageal br.
so
I
III
Vagus n. IOHz, 25V
B1
B2
1
s,
Ssec
lo
15
III
Vagus n. 10Hz, Z SV C2
CI
1
S
Lingual br. 50Hz, 4V
10
15
_.._UUUUUUUUtluuv v v MUUt . . . . ~ ]
III
Vagus n. 10Hz
D1
D2
t
21sec ~
Lingual br. 50Hz, ZV
s
_
lO
_
I I
Vagus n. 10Hz
]
II
I
Lingualbr. 50Hz, 4V
Fig. 2. Effects of stimulation of the central part of the severedlingual branch changed with the progressof retching. Furtherexplanations are in the text.
119
in the rostral pharyngeal branch of 5 dogs, in the caudal pharyngeal branch of 3 dogs, in the superior laryngeal nerve of 7 dogs, and in the recurrent laryngeal nerve of 3 dogs. Threshold intensity for the induction of fictive expulsion was observed as shown in Fig. 2. In this dog, the stimulus of 50 Hz and 4 V induced an expulsion when it was applied just after the 15th retch, but the stimulation weakened to 2 V did not (Fig. 2B,C). The stimulus of 50 Hz and 4 V failed to induce expulsion when it was applied just after the 10th retch, but caused earlier termination of retching (Fig. 2D). This result indicates that the threshold intensity for the induction of expulsion decreases with the progress of retching. Similar decreases in the threshold intensity were observed in the superior laryngeal nerve of 5 dogs, in the lingual branch of 3 dogs, and in the recurrent laryngeal nerve and the rostral and caudal pharyngeal branches of 1 dog each. In these observations, 2 0 H z and 10 V stimulus of the rostral pharyngeal branch could induce an expulsion just after the first retch in 1 dog, but could not before the first retch. This study revealed the following similarities between both kinds of expulsions induced by oropharyngoesophageal afferents and by central and/or peripheral chemoreceptor afferents [4]: (1) quite similar firing patterns were exhibited during both kinds of expulsions by the phrenic nerve and the abdominal and digastric muscle nerves, and the vagal pharyngo-esophageal branch; (2) both kinds of expulsions were induced similarly only when the corresponding afferents were stimulated during retching; and (3) threshold intensity to induce both kinds of expulsions decreased similarly with the progress of retching. It is well established that neurosomas of motor fibers in the glossopharyngeal nerve and the pharyngeal branch of the vagus nerve are located in the retrofacial nucleus which is surrounded by the reticular part called the B 0 T [6,8,15]. Some neurons of the BOT responded not only to stimulation of sinus nerve afferents, but also to stimulation of superior laryngeal nerve afferents (Fukuda and Koga, unpublished results). Therefore, it can be assumed that the CPG for expulsion in the B 0 T induces expulsion when it is activated during retching by peripheral and/or central chemoreceptor afferents, as well as by oropharyngo-esophageal afferents. In humans, however, oropharyngeal stimulation can induce expulsion without preceding retching which is contrarily required to induce expulsion in decerebrate dogs. This difference, it is supposed, is due to the decerebration in this study, since the cerebrum can control occurrence of vomiting in some degrees in humans. This work was supported in part by Project Research Grants from Kawasaki Medical School. [1] Bianehi, A.L. and Grrlot. L., Converse motor output to inspiratory bulbospinal premotoneurones during vomiting, Neurosei.
120
H. Fukuda, T. Koga / Neuroscience Letters 193 (1995) 117-120
Lett., 104 (1989) 298-302. [2] Fukuda, H. and Koga, T., The BOtzinger complex as the pattern generator for retching and vomiting in the dog, Neurosci. Res., 12 (1991) 471-485. [3] Fukuda, H. and Koga, T., Non-respiratory neurons in the B0tzinger complex exhibiting appropriate firing patterns to generate the emetic act in dogs, Neurosci. Res., 14 (1992) 180-194. [4] Fukuda, H. and Koga, T., Hypercapnia and hypoxia which develop during retching participate in the transition from retching to expulsion in dogs, Neurosci. Res., 17 (1993) 205-215. [5] Fukuda, H. and Koga, T., Activation of peripheral and/or central chemoreceptors changes activities of B6tzinger complex neurons and induces expulsion in decerebrate dogs, Neurosci. Res., in press. [6] Gr61ot, L., Barillot, J.C. and Bianchi, A.L., Activity of respiratory-related oropharyngeal and laryngeal motoneurones during fictive vomiting in the decerebrate cat, Brain Res., 513 (1990) 101-105. [7] Gr61ot, L., Barillot, C.L. and Bianchi, A.L., Central distributions of the efferent and afferent components of the pharyngeal branches of the vagus and glossopharyngeal nerves: an HRP study in the cat, Exp. Brain Res., 78 (1989) 327-335. [8] Kitamura, S. and Ogata, K., An HRP study of location of the rabbit palatopharyngeal motoneurons and peripheral course of their axons, Anat. Rec., 228 (1990) 225-229. [9] Koga, T., Discharge patterns of bulbar respiratory neurons during
[I0]
[11]
[12]
[13]
[14]
[15]
[16]
retching and vomiting in decerebrate dogs, Jpn. J. Physiol., 41 (1991) 233-249. Koga, T. and Fukuda, H., Characteristic behavior of the respiratory muscles, esophagus, and external anal and urethral sphincters during straining, retching, and vomiting in the decerebrate dog, Jpn. J. Physiol., 40 (1990) 789-807. Koga, T. and Fukuda, H., Augmenting inspiratory neurons in the ventral respiratory area may participate in contractions of the diaphragm during vomiting in decerebrate dogs, Neurosci. Lett, 180 (1994) 257-260. Miller, A.D., Lakos, S.F. and Tan, L.K., Central motor program for relaxation of periesophageal diaphragm during the expulsive phase of vomiting, Brain Res., 456 (1988) 367-370. Miller, A.D. and Nonaka, S., B6tzinger expiratory neurons may inhibit phrenic motomeurons and medullary inspiratory neurons during vomiting, Brain Res., 521 (1990) 352-354. Miller, A.D. and Ezure, K., Behavior of inhibitory and excitatory propriobulbar respiratory neurons during fictive vomiting, Brain Res., 578 (1992) 168-176. Strutz, J., Hammerich, T. and Amedee, R., The motor innervation of the soft palate: an anatomical study in guinea pigs and monkeys, Arch. Otho-Rhino-Laryngol., 245 (1988) 180-184. Tan, L.K. and Miller, A.D., Innervation of periesophageal region of cat's diaphragm: implication for studies of control of vomiting, Neurosci. Lett., 68 (1986) 339-344.
Neuroscience Letters 193 (1995) 117-120
Stimulation of glossopharyngeal and laryngeal nerve afferents induces expulsion only when it is applied during retching in paralyzed decerebrate dogs HiroyukiFukuda*,Tomoshige Koga Department of Physiology, KawasakiMedical School, 577 Matushima, Kurashiki, Okayama 701-01, Japan Received 10 April 1995; revised version received 25 May 1995; accepted 25 May 1995
Abstract
Stimulation of the oropharyngeal mucosa induces vomiting in humans, however, it has not been seen in animals. Thus, we attempted to induce fictive vomiting by stimulation of lingual and pharyngeal branch afferents of the glossopharyngeal nerve, and afferents of the superior and recurrent laryngeal nerves in paralyzed decerebrate dogs. The stimulation did not induce fictive vomiting when it was applied during eupnea, but induced fictive expulsion when it was applied during fictive retching. Threshold intensity for the induction decreased with the progress of retching.
Keywords: Vomiting, Glossopharyngeal nerve, Superior laryngeal nerve, Recurrent nerve, B6tzinger complex
To analyze the neuronal mechanisms for generation of retching, we systematically stimulated and partially cut the medulla oblongata of decerebrate paralyzed dogs and recorded its unitary neuronal activity [2,3] Based on our results, we postulated that the temporal patterns of muscle contractions in retching are generated by the central pattern generator (CPG) in the B6tzinger complex (Be)T). During retching, pulmonary ventilation almost stops, and, consequently, hypercapnia and hypoxia develop with the progress of retching [4]. When the changes in the blood gasses reach a threshold, retching stops; alternatively, an expulsion appears. Activation of the central and/or peripheral chemoreceptors changes firing patterns of BC)T neurons from the patterns of retching to the patterns of expulsion [5]. Thus, we postulated that stimulation of peripheral and central chemoreceptors activates the CPG for expulsion in the BC)T and induces expulsion. In humans, however, vomiting can be induced by stimulation of the oropharyngeal mucosa with a short latency which may not allow the development of blood gas changes. This fact seems to contradict our postulation and to indicate the existence of other neuronal mechanisms for in*Corresponding author, Tel.: +81 86 4621111; Fax: +81 86 4621199.
duction of expulsion. To the best of our knowledge, however, the fact that vomiting can be induced by stimulation of the oropharyngeal mucosa has not been seen in animals. Thus, we preliminarily attempted to induce vomiting by oropharyngo-esophageal mechanical stimulation in 2 non-paralyzed decerebrate dogs. The mechanical stimulation could not induce vomiting in ordinal conditions, but could when the stimulation was applied during stomach over distention which is known to induce retching [8]. This study was designed to confirm the preliminary result. This study was performed on 9 dogs, each weighing 7.5-11 kg. The dogs were anesthetized with ketamine hydrochloride (25 mg/kg, i.m.), paralyzed with gallamine triethiodide (2 mg/kg, i.v.), artificially ventilated, and precollicularly decerebrated. The body temperature was maintained at 37-39°C by 2 heating lamps and a heating plate. End-tidal CO2 was maintained within the range 2.0-3.0% to suppress spontaneous occurrence of expulsion at the end of retching [4]. Centrifugal activities were recorded as frequency histograms (100 ms bins) in the L1 abdominal muscle branch, the C5 phrenic root and the vagal pharyngo-esophageal branch in all 9 dogs, and in the trigeminal digastric muscle branch of 3 dogs. Fictive retching and expulsion were recognized from the activity
0304-39401951509.50 © 1995 Elsevier Science Ireland Ltd. All rights reserved SSDI 0 3 0 4 - 3 9 4 0 ( 9 5 ) 1 1 6 8 2 - J
118
H. Fukuda, T. Koga I Neuroscience Letters 193 (1995) 117-120
patterns of these nerves. Rhythmic bursts of highfrequency discharges, produced concomitantly by the phrenic and abdominal muscle nerves, were considered fictive retching. Fictive expulsion was considered an episode following retching in which the duration of the burst of the abdominal muscle nerve was prolonged both with respect to the corresponding expulsion burst of the phrenic nerve and to the bursts of the abdominal muscle nerve during the preceding retching phase [2,3,6,9-14,16] Fictive retching was produced by continuous stimulation (10 Hz, 0.5 ms duration, 20-25 V) of the central part of
the severed vagal trunks at the supra-diaphragmatic region. The central part of the severed pharyngeal (rostral and caudal) and lingual branches of the glossopharyngeal nerve, and the severed superior and recurrent laryngeal nerves were stimulated to induced fictive expulsion (2050 Hz, 2-10 V, 0.5 ms duration). During eupnea, stimulation of the glossopharyngeal branches and the laryngeal nerves produced activities like fictive swallowing or no-effect, or suppressed phrenic respiratory activities, but did not induce fictive retching and/or expulsion (Fig. 1B1-D1). Similarly, the stimula-
A Phrenic n.
imp/bin
]So° 6sec
Abdominal m.n.
~
]
5
o
o
Vagus n. 10Hz
Ssec
B2
B1
6sec
Vagus n. 10Hz, 25V
Superior laryngeal n. 20Hz, 10V
Superior-laryngealn. 50Hz, IOV
Cz
C1
6sec
E
I
II
Vagus n. 10Hz, 2 SV
Recurrent n. 50Hz, 10V
Recurrentn. 50Hz, 10V
Dz
D1
12sec
E
Lingual br. ZOHz, 10V
Vagus n. 10Hz
Lingualbr. 50Hz, 10V
Fig. I. Effects of continuous stimulation of the central part of the severed superior (B) and recurrent (C) laryngeal nerves, and the severed lingual branch of the giossopharyngeal nerve (D). From top to bottom, the traces represent frequency histograms (100 ms bins) of centrifugal discharges of the phrenic (phrenic n.) and abdominal muscle nerves (abdominal m. n.), and the pharyngo-esophageal branch of the vagus nerve and pulses of stimulation of the thracic vagal trunk (upward), and the laryngeal nerves and the lingual branch (downward). (A) Control. Only retching was induced by vagal stimulation: During eupnea (B1-D1), activities like swallowing were induced by stimulation of the superior laryngeal nerve (BI) and the lingual branch (Dl), but no obvious effect was produced by stimulation of the recurrent laryngeal nerve (C1). Stimulation of all 3 nerves induced an expulsion when it was applied during retching (B2-D2).
H. Fukuda, 7". Koga I Neuroscience Letters 193 (1995) 117-120
tion did not induce fictive retching and/or expulsion when it was superimposed on stimulation of the vagal trunk before fictive retching was induced by the vagal stimulation (not shown). In contrast, when stimulation of the glossopharyngeal branches and the laryngeal nerves was applied during fictive retching, it produced fictive expulsion (E), but not fictive swallowing (Fig. 1B2-D2). Activity of the pharyngo-esophageal branch almost disappeared during the fictive expulsion (Fig. 1B2-D2), and the digastric muscle branch of the trigeminal nerve produced a vigorous burst just after the expulsion (not shown, but confirmed in 3 dogs). The induction of fictive expulsion was confirmed in the lingual branch of 7 dogs, A1
A2
imp/bin
Abdominal r~ n.
~
lSoo
Pl~ryngo-esophageal br.
so
I
III
Vagus n. IOHz, 25V
B1
B2
1
s,
Ssec
lo
15
III
Vagus n. 10Hz, Z SV C2
CI
1
S
Lingual br. 50Hz, 4V
10
15
_.._UUUUUUUUtluuv v v MUUt . . . . ~ ]
III
Vagus n. 10Hz
D1
D2
t
21sec ~
Lingual br. 50Hz, ZV
s
_
lO
_
I I
Vagus n. 10Hz
]
II
I
Lingualbr. 50Hz, 4V
Fig. 2. Effects of stimulation of the central part of the severedlingual branch changed with the progressof retching. Furtherexplanations are in the text.
119
in the rostral pharyngeal branch of 5 dogs, in the caudal pharyngeal branch of 3 dogs, in the superior laryngeal nerve of 7 dogs, and in the recurrent laryngeal nerve of 3 dogs. Threshold intensity for the induction of fictive expulsion was observed as shown in Fig. 2. In this dog, the stimulus of 50 Hz and 4 V induced an expulsion when it was applied just after the 15th retch, but the stimulation weakened to 2 V did not (Fig. 2B,C). The stimulus of 50 Hz and 4 V failed to induce expulsion when it was applied just after the 10th retch, but caused earlier termination of retching (Fig. 2D). This result indicates that the threshold intensity for the induction of expulsion decreases with the progress of retching. Similar decreases in the threshold intensity were observed in the superior laryngeal nerve of 5 dogs, in the lingual branch of 3 dogs, and in the recurrent laryngeal nerve and the rostral and caudal pharyngeal branches of 1 dog each. In these observations, 2 0 H z and 10 V stimulus of the rostral pharyngeal branch could induce an expulsion just after the first retch in 1 dog, but could not before the first retch. This study revealed the following similarities between both kinds of expulsions induced by oropharyngoesophageal afferents and by central and/or peripheral chemoreceptor afferents [4]: (1) quite similar firing patterns were exhibited during both kinds of expulsions by the phrenic nerve and the abdominal and digastric muscle nerves, and the vagal pharyngo-esophageal branch; (2) both kinds of expulsions were induced similarly only when the corresponding afferents were stimulated during retching; and (3) threshold intensity to induce both kinds of expulsions decreased similarly with the progress of retching. It is well established that neurosomas of motor fibers in the glossopharyngeal nerve and the pharyngeal branch of the vagus nerve are located in the retrofacial nucleus which is surrounded by the reticular part called the B 0 T [6,8,15]. Some neurons of the BOT responded not only to stimulation of sinus nerve afferents, but also to stimulation of superior laryngeal nerve afferents (Fukuda and Koga, unpublished results). Therefore, it can be assumed that the CPG for expulsion in the B 0 T induces expulsion when it is activated during retching by peripheral and/or central chemoreceptor afferents, as well as by oropharyngo-esophageal afferents. In humans, however, oropharyngeal stimulation can induce expulsion without preceding retching which is contrarily required to induce expulsion in decerebrate dogs. This difference, it is supposed, is due to the decerebration in this study, since the cerebrum can control occurrence of vomiting in some degrees in humans. This work was supported in part by Project Research Grants from Kawasaki Medical School. [1] Bianehi, A.L. and Grrlot. L., Converse motor output to inspiratory bulbospinal premotoneurones during vomiting, Neurosei.
120
H. Fukuda, T. Koga / Neuroscience Letters 193 (1995) 117-120
Lett., 104 (1989) 298-302. [2] Fukuda, H. and Koga, T., The BOtzinger complex as the pattern generator for retching and vomiting in the dog, Neurosci. Res., 12 (1991) 471-485. [3] Fukuda, H. and Koga, T., Non-respiratory neurons in the B0tzinger complex exhibiting appropriate firing patterns to generate the emetic act in dogs, Neurosci. Res., 14 (1992) 180-194. [4] Fukuda, H. and Koga, T., Hypercapnia and hypoxia which develop during retching participate in the transition from retching to expulsion in dogs, Neurosci. Res., 17 (1993) 205-215. [5] Fukuda, H. and Koga, T., Activation of peripheral and/or central chemoreceptors changes activities of B6tzinger complex neurons and induces expulsion in decerebrate dogs, Neurosci. Res., in press. [6] Gr61ot, L., Barillot, J.C. and Bianchi, A.L., Activity of respiratory-related oropharyngeal and laryngeal motoneurones during fictive vomiting in the decerebrate cat, Brain Res., 513 (1990) 101-105. [7] Gr61ot, L., Barillot, C.L. and Bianchi, A.L., Central distributions of the efferent and afferent components of the pharyngeal branches of the vagus and glossopharyngeal nerves: an HRP study in the cat, Exp. Brain Res., 78 (1989) 327-335. [8] Kitamura, S. and Ogata, K., An HRP study of location of the rabbit palatopharyngeal motoneurons and peripheral course of their axons, Anat. Rec., 228 (1990) 225-229. [9] Koga, T., Discharge patterns of bulbar respiratory neurons during
[I0]
[11]
[12]
[13]
[14]
[15]
[16]
retching and vomiting in decerebrate dogs, Jpn. J. Physiol., 41 (1991) 233-249. Koga, T. and Fukuda, H., Characteristic behavior of the respiratory muscles, esophagus, and external anal and urethral sphincters during straining, retching, and vomiting in the decerebrate dog, Jpn. J. Physiol., 40 (1990) 789-807. Koga, T. and Fukuda, H., Augmenting inspiratory neurons in the ventral respiratory area may participate in contractions of the diaphragm during vomiting in decerebrate dogs, Neurosci. Lett, 180 (1994) 257-260. Miller, A.D., Lakos, S.F. and Tan, L.K., Central motor program for relaxation of periesophageal diaphragm during the expulsive phase of vomiting, Brain Res., 456 (1988) 367-370. Miller, A.D. and Nonaka, S., B6tzinger expiratory neurons may inhibit phrenic motomeurons and medullary inspiratory neurons during vomiting, Brain Res., 521 (1990) 352-354. Miller, A.D. and Ezure, K., Behavior of inhibitory and excitatory propriobulbar respiratory neurons during fictive vomiting, Brain Res., 578 (1992) 168-176. Strutz, J., Hammerich, T. and Amedee, R., The motor innervation of the soft palate: an anatomical study in guinea pigs and monkeys, Arch. Otho-Rhino-Laryngol., 245 (1988) 180-184. Tan, L.K. and Miller, A.D., Innervation of periesophageal region of cat's diaphragm: implication for studies of control of vomiting, Neurosci. Lett., 68 (1986) 339-344.