This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bosch, M. A. Articles by Rønnekleiv, O. K. Search for Related Content PubMed PubMed Citation Articles by Bosch, M. A. Articles by Rønnekleiv, O. K.

Distribution, Neuronal Colocalization, and 17ß-E2 Modulation of Small Conductance Calcium-Activated K⁺ Channel (SK3) mRNA in the Guinea Pig Brain

Department of Physiology/Pharmacology, Oregon Health Sciences University, Portland, Oregon 97201; Division of Neuroscience, Oregon Regional Primate Research Center, Beaverton, Oregon 97206

Address all correspondence and requests for reprints to: Dr. Oline K. Rønnekleiv, Department of Physiology/Pharmacology, Oregon Health Sciences University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97201. E-mail: . ronnekle{at}ohsu.edu

Molecular cloning has revealed the existence of three distinct small conductance (SK1–3) Ca²⁺-activated K⁺ channels. Because SK channels underlie the afterhyperpolarization (AHP) that is critical for sculpturing phasic firing in hypothalamic neurons, we investigated the distribution of these channels in the female guinea pig. Both SK1 and SK3 cDNA fragments were cloned using PCR, and ribonuclease protection assay as well as in situ hybridization analysis illustrated that the SK3 channel was the predominant subtype expressed in the guinea pig hypothalamus. Combined in situ hybridization and fluorescence immunocytochemistry revealed that SK3 mRNA was expressed in GnRH, dopamine, and vasopressin neurons, and all of these neurons exhibited an AHP current. Moreover, SK3 mRNA was found in other brain areas, including the septum, bed nucleus, amygdala, thalamus, midbrain, and hippocampus. Using quantitative ribonuclease protection assay, the rank order of SK3 mRNA expression was septum midbrain > rostral thalamus rostral basal hypothalamus caudal thalamus preoptic area >> caudal basal hypothalamus hippocampus. Moreover, 17ß-E2 treatment, which reduces plasma LH during the negative feedback phase, significantly increased SK3 mRNA levels in the rostral basal hypothalamus (P < 0.05; n = 6). Therefore, these findings suggest that estrogen increases the mRNA expression of SK3 channels, which may represent a mechanism by which estrogen regulates hypothalamic neuronal excitability during negative feedback.

This article has been cited by other articles:

				X. Liu and A. E. Herbison Small-Conductance Calcium-Activated Potassium Channels Control Excitability and Firing Dynamics in Gonadotropin-Releasing Hormone (GnRH) Neurons Endocrinology, July 1, 2008; 149(7): 3598 - 3604. [Abstract] [Full Text] [PDF]

				S. L. Pierce, J. D.K. Kresowik, K. G. Lamping, and S. K. England Overexpression of SK3 Channels Dampens Uterine Contractility to Prevent Preterm Labor in Mice Biol Reprod, June 1, 2008; 78(6): 1058 - 1063. [Abstract] [Full Text] [PDF]

				M. L. Palmer, K. R. Schiller, and S. M. O'Grady Apical SK potassium channels and Ca2+-dependent anion secretion in endometrial epithelial cells J. Physiol., February 1, 2008; 586(3): 717 - 726. [Abstract] [Full Text] [PDF]

				D. J. Spergel Calcium and Small-Conductance Calcium-Activated Potassium Channels in Gonadotropin-Releasing Hormone Neurons before, during, and after Puberty Endocrinology, May 1, 2007; 148(5): 2383 - 2390. [Abstract] [Full Text] [PDF]

				D. W. Waring and J. L. Turgeon Estradiol Inhibition of Voltage-Activated and Gonadotropin-Releasing Hormone-Induced Currents in Mouse Gonadotrophs Endocrinology, December 1, 2006; 147(12): 5798 - 5805. [Abstract] [Full Text] [PDF]

				Z. Chu and S. M. Moenter Physiologic Regulation of a Tetrodotoxin-Sensitive Sodium Influx That Mediates a Slow Afterdepolarization Potential in Gonadotropin-Releasing Hormone Neurons: Possible Implications for the Central Regulation of Fertility. J. Neurosci., November 15, 2006; 26(46): 11961 - 11973. [Abstract] [Full Text] [PDF]

				M. Kato, N. Tanaka, S. Usui, and Y. Sakuma The SK channel blocker apamin inhibits slow afterhyperpolarization currents in rat gonadotropin-releasing hormone neurones J. Physiol., July 15, 2006; 574(2): 431 - 442. [Abstract] [Full Text] [PDF]

				A. J. McNeish, S. L. Sandow, C. B. Neylon, M. X. Chen, K. A. Dora, and C. J. Garland Evidence for Involvement of Both IKCa and SKCa Channels in Hyperpolarizing Responses of the Rat Middle Cerebral Artery Stroke, May 1, 2006; 37(5): 1277 - 1282. [Abstract] [Full Text] [PDF]

				J. Ledoux, M. E. Werner, J. E. Brayden, and M. T. Nelson Calcium-Activated Potassium Channels and the Regulation of Vascular Tone Physiology, February 1, 2006; 21(1): 69 - 78. [Abstract] [Full Text] [PDF]

				M. S. Taylor, A. D. Bonev, T. P. Gross, D. M. Eckman, J. E. Brayden, C. T. Bond, J. P. Adelman, and M. T. Nelson Altered Expression of Small-Conductance Ca2+-Activated K+ (SK3) Channels Modulates Arterial Tone and Blood Pressure Circ. Res., July 25, 2003; 93(2): 124 - 131. [Abstract] [Full Text] [PDF]