Autonomic Responses Associated with Severe Gagging Elicited by Stimulation of the Superior Laryngeal Nerve in Rats

Tactile stimulation of the pharyngo-laryngeal region elicits severe gagging, which is characterized by simultaneous contraction of the costal diaphragm and abdominal muscles. While severe gagging is associated with problems in oral feeding in children, routine dental treatment and gastrointestinal endoscopy, little is known about the neural mechanism of this reflex. In the present study using decerebrate rats, we observed dynamic changes in the activities of the costal and crural diaphragm, abdominal muscles, and infrahyoid muscles, and in pharyngeal and esophageal pressure during severe gagging, and determined the most suitable stimulation of the superior laryngeal nerve (SLN) for induction. High-frequency stimulation of the SLN at 50 Hz (30 μA, 50 pulses) elicited severe gagging in all of the rats. Severe gagging had the following characteristics: 1) simultaneous activation of the costal diaphragm and abdominal muscles, but relaxation of the crural diaphragm; 2) infrahyoid muscle contraction and temporary decrease in pharyngeal pressure; 3) retrograde contraction of esophageal striated muscles; and 4) decrease of blood pressure, which was mediated by a vagal muscarinic pathway. The identification of characteristic changes in respiratory muscles and autonomic responses should assist future studies on the mechanism of severe gagging

Somatosensory Evoked Potentials in Cerebral Infarction Model Rats Induced by Microsphere Injection to Cerebral Artery

Microspheres, monodisperse polystyrene beads, are used for the study of cerebral infarction by injection into the cerebral artery. Cerebral infarction model rats were made by injecting 2,600 microspheres into the right internal carotid artery in this study. Motor ability was assessed by the rotarod test in which cling duration on the accelerating rotating rod was measured. Significant decrease in the motor ability was recognized on 3 and 15 days after the embolization compared with before surgery (p<0.05). However, sham-operated rats did not show significant change of motor ability. Each rat was reanaesthetized 15 days after surgery, and somatosensory evoked potentials (SEPs) induced by stimulation of the sciatic nerve of the contralateral hind limb were averaged. Latencies of N_1 and N_2 waves in SEPs were compared between sham-operated rats and embolized rats 15 days after surgery. No significant differences in N_1 and N_2 latencies were recognized between the two groups. These results suggest that motor ability was impaired at chronic periods of the embolization, while SEPs recovered, although latencies of N_1 and N_2 in SEPs were reported to increase at acute periods in embolized rats

Changes in the lactate threshold during treadmill exercise after microsphere-induced infarction in rats.

The aim of this study was to clarify changes in the lactate threshold (LT) in the acute period after cerebral infarction. Cerebral infarction was induced by the injection of microspheres (MS) into the right internal carotid artery. To estimate the degree of neurologic deficit caused by surgery, the behaviors of all rats were evaluated in terms of typical symptoms of stroke in rats. The rotarod test was used to evaluate equilibrium function. Rats were forced to perform stepwise treadmill exercises, and serial changes in blood lactate concentration were measured for determination of the LT. The average treadmill speed at the LT and the rotarod test performance in MS rats was significantly lower than those in sham-operated rats on postsurgery day 2. However, although neurologic deficits disappeared on postsurgery day 7 in MS rats, LT level and rotarod test performance were significantly lower than in sham-operated rats. These results suggest that the decrease in LT in the acute period after cerebral infarction might be induced by impaired equilibrium function. Other possibilities are discussed as well