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Neuropeptide Y (NPY) expression is increased in explanted guinea pig parasympathetic cardiac ganglia neurons
S W Lynch1, K M Braas, S A Harakall
1Department of Anatomy and Neurobiology, College of Medicine, University of Vermont, Burlington, VT 05405, USA.
Abstract:
While expression of neuropeptides by sympathetic neurons is altered by decentralization and axotomy, it is not known whether similar experimental paradigms also modulate the chemical phenotype of parasympathetic cardiac ganglia neurons. The present study tested whether guinea pig parasympathetic neuron neuropeptide Y (NPY) expression was altered when cardiac ganglia preparations were maintained as organ explants in the presence or absence of colchicine. Two experimental approaches were used to examine NPY expression. First, immunocytochemical techniques were used to quantitate numbers of neurons within the cardiac ganglia exhibiting NPY-immunoreactivity; second, reverse transcription PCR was used to examine proNPY mRNA expression. In control cardiac ganglia preparations, approximately 4% of ganglia neurons exhibited NPY-immunoreactivity. The percentage of NPY-immunopositive neurons in 30- and 72-h explanted cardiac ganglia preparations, maintained in the absence of colchicine, increased to 11 and 16%, respectively. Colchicine treatment of explanted preparations further increased the percentage of NPY-positive ganglia cells 24% (30 h) and 32% (72 h). All NPY-immunoreactive neurons from control ganglia and explanted ganglia were choline acetyltransferase(ChAT)-immunoreactive, indicating retention of the cholinergic phenotype. ProNPY mRNA also was increased following ganglia explantation, consistent with the increase in the numbers of NPY-immunoreactive neurons. NPY transcripts were further increased after 30 h, but not after 72 h in colchicine-treated, explanted cardiac ganglia preparations. These results demonstrate that NPY expression is altered in explanted cardiac ganglia preparations, providing evidence that the chemical phenotype of parasympathetic cardiac neurons can be modulated.