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1 Department of Biology, Ithaca College, Ithaca, NY, USA
2 Department of Physiology and Functional Genomics, University of Florida, Gainesville, FL, USA
* To whom correspondence should be addressed. E-mail: jhardwick{at}ithaca.edu.
Histamine, released from mast cells, can modulate the activity of intrinsic neurons in the guinea pig cardiac plexus. The current study examined the ionic mechanisms underlying the histamine-induced responses in these cells. Histamine evokes a small membrane depolarization and an increase in neuronal excitability. Using intracellular voltage recording from individual intracardiac neurons, we were able to demonstrate that removal of extracellular sodium reduced the membrane depolarization, whereas inhibition of K+ channels by 1 mM Ba2+, 2 mM Cs+, or 5 mM TEA had no effect. The depolarization was also not inhibited by either 10 µM Gd3+, or a reduced Cl- solution. The histamine-induced increase in excitability was unaffected by K+ channel inhibitors, however it was reduced by either blockage of voltage-gated Ca2+ channels with 200 µM Cd2+ or replacement of extracellular Ca2+ with Mg2+. Conversely, alterations in intracellular calcium with thapsigargin or caffeine did not inhibit the histamine-induced effects. However, in cells treated with both thapsigargin and caffeine to deplete internal calcium stores, the histamine-induced increase in excitability was decreased. Treatment with the phospholipase C inhibitor U73122 also prevented both the depolarization and the increase in excitability. From these data, we conclude that histamine, via activation of H1 receptors, activates PLC, which results in (1) the opening of a non-specific cation channel such as a TRPC4 or TRPC5 channel, and (2) in combination with either the influx of Ca2+ through voltage-gated channels or the release of internal calcium stores, leads to an increase in excitability.
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