Korean J Urol.  2002 Dec;43(12):1078-1085.

The Actions of Adenosine on Voltage-dependent K+ Currents in Neurons of Male Rat Major Pelvic Ganglia

Affiliations
  • 1Department of Physiology and Institute of Basic Medical Science, Korea.
  • 2Department of Urology, Yonsei University Wonju College of Medicine, Korea.
  • 3Department of Urology, University of Ulsan College of Medicine, Kangnung Asan Hospital, Gangneung, Korea. jypark@knh.co.kr

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.

Keyword

Autonomic ganglia; Adenosine; Potassium channels

MeSH Terms

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
Adenosine
Calcium
Neurotransmitter Agents
Potassium
Potassium Channels
Receptors, Purinergic P1
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