The Actions of Adenosine on Voltage-dependent K+ Currents in Neurons of Male Rat Major Pelvic Ganglia.
- Author:
Kyu Sang PARK
1
;
Seung Kyu CHA
;
Keon Il LEE
;
Seong Woo JEONG
;
Sung Jin KIM
;
Jong Yeon PARK
;
In Deok KONG
;
Joong Woo LEE
Author Information
1. Department of Physiology and Institute of Basic Medical Science, Korea.
- Publication Type:Original Article
- Keywords:
Autonomic ganglia;
Adenosine;
Potassium channels
- MeSH:
Adenosine*;
Animals;
Autonomic Pathways;
Calcium;
Fires;
Ganglia*;
Ganglia, Autonomic;
Humans;
Male*;
Neurons*;
Neurotransmitter Agents;
Patch-Clamp Techniques;
Penis;
Potassium;
Potassium Channels;
Prostate;
Rats*;
Receptors, Purinergic P1;
Urinary Bladder
- From:Korean Journal of Urology
2002;43(12):1078-1085
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The major pelvic ganglia (MPG) function as a relay center for autonomic pathways to the urogenital organs, such as the urinary bladder, vas deference, and penis. It is well known that adenosine acts as an important neuromodulator in various neuronal tissues. Several studies have suggested that some of these actions are coupled with potassium conductances. However, the exact mechanisms are unclear. Therefore, the roles of adenosine on the various potassium channels, in MPG neurons, were investigated. MATERIALS AND METHODS: Single neurons of the MPGs, located on the lateral surfaces of the prostate gland, from male rats were enzymatically dissociated. Ionic currents were recorded using the whole-cell variant patch-clamp technique. RESULTS: Two types of voltage-dependent outward potassium channels were isolated in the MPG neurons using whole-cell voltage protocols. One was the transient outward potassium current (type A-current, IA), the other was the delayed rectifier potassium current (IKDR). The IA and IKDR were recorded in both adrenergic and nonadrenergic neurons, which were distinguished by the existence of T-type calcium currents. Both the adrenergic and nonadrenergic neurons had the same kind of outward potassium currents. Application of adenosine (10(-4)M) increased the IA reversibly. N-cyclopentyladenosine (CPA, 10(-5)M), an A1 selective agonist, produced the same effect. However, the delayed rectifier components were not affected by the adenosine or CPA. The effects of adenosine and CPA on the IA were mostly prevented by pretreatment with DPCPX, an A1 selective antagonist. CONCLUSIONS: Adenosine increased the IA only, via the selective activation of A1 adenosine receptors. The augmentation of A-currents by adenosine may reduce neuronal firings, and then contribute to regulation of neuronal excitability in male rat MPG neurons.
