No abstract

Vocalizations of South African clawed frogs are produced by contractions of laryngeal muscles innervated by motor neurons of the caudal medulla (within cranial nerve nucleus IX-X). We have traced afferents to laryngeal motor neurons in male and female frogs using retrograde axonal transport of horseradish peroxidase conjugated to wheat germ agglutinin (HRP-WGA). After iontophoretic injection of HRP-WGA into n. IX-X, retrogradely labelled neurons were seen in the contralateral n. IX-X, in rhombencephalic reticular nuclei, and in the pre-trigeminal nucleus of the dorsal tegmental area (DTAM) of both males and females.

Neonatal rats produce ultrasonic vocalizations in response to cold stress. The rate and intensity of these vocalizations decrease dramatically as the pup reaches maturity. The laryngeal nerves controlling the production of ultrasounds and their nuclei of origin were investigated in 10-day-old rat pups. Unilateral and bilateral transections of the inferior laryngeal nerve reduced ultrasounds to undetectable levels. Transecting the superior laryngeal nerve either unilaterally or bilaterally reduced the sound pressure level, reduced the rate, and increased the fundamental frequency of the ultrasounds. Retrograde transport of horseradish peroxidase revealed that the efferent axonb in the inferior laryngeal nerve arise from the cells of the dorsal formation of the nucleus ambiguus and that efferents in the superior laryngeal nerve originate from the ventral formation of the nucleus ambiguus. Therefore, different aspects of the production of pup ultrasounds appear to be controlled by distinct neuronal subpopulations of the nucleus ambiguus.

In six conscious dogs we compared the action of the M1-receptor antagonist telenzepine (20.25-81.0 nmol.kg-1.h-1), the cholecystokinin (CCK) antagonist L-364,718 (0.025-0.1 mg.kg-1.h-1), and combinations of both on the pancreatic secretory response to intraduodenal tryptophan, given against a secretin background before and after truncal vagotomy. Before vagotomy, the higher doses of telenzepine and of L-364,718 significantly (P < 0.05) decreased the protein response to tryptophan by up to 97%. After vagotomy, all doses of L-364,718 abolished the protein response, whereas telenzepine had no further effect. Before and after vagotomy, all combinations abolished the protein response. The plasma CCK-like immunoreactivity basally, during secretin, and in response to tryptophan was not altered by vagotomy, telenzepine, and/or L-364,718. These findings indicate that in dogs 1) potentiation exists between M1 receptors and CCK for stimulation of the pancreatic enzyme response to intraduodenal tryptophan, 2) the cholinergic fibers of the enteropancreatic reflex activated by tryptophan run within the vagus nerves and end at least in part on M1 receptors, 3) CCK acts in part independently of the vagal nerves, and 4) the CCK release by intestinal tryptophan is not influenced by vagotomy, telenzepine, and/or L-364,718.