TRIETHYLTIN INTOXICATION ALTERS ACETYLCHOLINE-RELEASE FROM RAT PHRENIC NERVE-HEMIDIAPHRAGM

  • 1 January 1982
    • journal article
    • research article
    • Vol. 4  (2) , 251-254
Abstract
Triethyltin (TET) exposure produces, among other symptoms, muscular weakness. The etiology of this phenomenon is obscure, but the symptoms suggest impaired cholinergic transmission at the neuromuscular junctrion. Acetylcholine (ACh) release was assessed in the vascularly perfused phrenic nerve-hemidiaphragm isolated from rats subjected to acute or chronic in vivo exposure to TET. Adult male hooded Long-Evans rats (250-350 g) were exposed acutely to 1 injection of TET (10 mg/kg i.p.) or chronically to TET (30 mg/l) in their drinking water. Hemidiaphragms were obtained from treated and age-matched control rats 24 h after acute exposure or 1, 2 or 3 wk after initiation of the chronic exposure regimen. ACh release was assessed during unstimulated (spontaneous), stimulated (7 Hz) and suprastimulated (20 Hz) conditions. ACh release was not altered in the hemidiaphragms of acutely exposed rats. Rats chronically exposed to TET showed normal spontaneous release, a trend towards decreased stimulated (7 Hz) release and an almost complete failure to release ACh in response to 20 Hz stimulation. Data were discussed with respect to known TET effects on cellular bioenergetics and the consequences for neurotransmitter synthesis and release mechanisms.