A 12-year-old, castrated male Yorkshire terrier dog presented with frequent regurgitations that had begun 45 days earlier and become more progressive. Radiographs revealed an air-trap region behind the cranial esophageal sphincter muscle in the esophagus and esophagographies with barium contrast showed mild esophageal dilation with decreased motility. Esophageal motility increased within 5 min of neostigmine methylsulfate administration and acetylcholine receptor antibodies titer increased to beyond the normal range. Based on these findings, acquired myasthenia gravis with focal form was diagnosed, making this the first such case diagnosed by an acetylcholine receptor antibody test in Korea.

Substance P (SP) is colocalized with ACh in splanchnic nerves that innervate into adrenal medulla and the peptide has been shown to inhibit nicotinic agonists-induced catecholamine secretion. To elucidate the effects of SP on cytosolic Ca(2+) dynamics, the present study was conducted using fura-2-loaded isolated bovine adrenal chromaffin cells. Stimulation of the cells with nicotine (10-100mu-M) produced a rapid rise of cytosolic Ca(2+) concentration ([Ca(2+)]i), the peak level of which increased in a dose-dependent manner, followed by a gradual decay. In the presence of 10mu-M SP, the dose-response relationship of the peak levels shifted downward. Quantitative analyses implied that SP inhibits the nicotine-induced Ca(2+) influx in a noncompetitive manner. Nicotinic acetylcholine receptor is composed of two major functional domains: an agonist-binding site and an ionophore or channel domain. Agonist binding activates ionophore / channel domain and causes mainly Na(+) influx. This Na(+) influx depolarizes the cell and activates voltage-dependent Ca(2+) channels. Based on this fact, the present results indicate that SP dose not block nicotine binding sites but interferes with other sites of nicotinic receptor / channel molecule, most probably a channel domain. It was suggested that SP colocalized with ACh in splanchnic nerves functions as a physiological modulator of catecholamine secretion by non-competitively suppressing ACh-induced cytosolic Ca(2+) dynamics in bovine a