The excitatory NT(s) in the cat cb's response to hypoxia, hypercapnia, and acidosis is (are) yet to be identified. Four sets of experiments were designed to: (A) Measure the release of ACh from the cb with HPLC techniques; (B) Locate cholinergic receptors in the cat cb with immunocytochemical techniques; (C) Block "pre" and "post" putative cholinergic synaptic components of the chemotransductive unit pharmacologically; (D) Fluorometrically determine the effect of cholinergic agents on intracellular calcium (Ca++i) in cat cb Type I cells. RESULTS: (A) ACh release during hypoxia/hypercapnia was 0.226pmoles/min vs. 0.079 during hyperoxia/normocapnia. (B) Positive signals for the α4 subunit of the neuronal nicotinic receptor has been foundin the cb, and for the α7 subunit in the cb, carotid sinus nerve, and petrosal ganglion. (C) Use of presynaptic inhibitors of ACh synthesis (hemicholinium) or release (cetiedil, vesamicol), or postsynaptic inhibitors (atropine, mecamylamine) depressed the cb response to hypoxic perfusates in a dose-related manner; M1 and M2 receptor activity was also detected in the cb with pirenzepine and gallamine. (D) nicotinic, but not muscarinic, agonists produced a dose-dependent rise in Type I cell Ca++i; ACh also increased petrosal ganglion cell Ca++i. These data suggest that ACh may play an important pre- and post-synaptic excitatory role in the cat cb during hypoxia.
|Original language||English (US)|
|State||Published - 1997|
ASJC Scopus subject areas
- Molecular Biology