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Involvement of potassium channels in the antidepressant-like effect of venlafaxine in mice.
Life Sci. 2010 Feb 27; 86(9-10):372-6.LS

Abstract

AIMS

Studies have shown that the acute administration of venlafaxine elicits an antidepressant-like effect in the mouse forced swim test (FST) by a mechanism dependent on the l-arginine-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway. Because it has been reported that NO activates different types of potassium (K(+)) channels in the brain, this study investigated the involvement of K(+) channels in the antidepressant-like effect of venlafaxine in the mouse FST.

MAIN METHODS

Male adult Swiss mice were pretreated with different K(+) channel inhibitors or openers 15 min before venlafaxine administration. After 30 min, the open-field test (OFT) and FST were carried out.

KEY FINDINGS

Intracerebroventricular (i.c.v.) pretreatment of mice with subeffective doses of tetraethylammonium (TEA, a non-specific inhibitor of K(+) channels, 25 pg/site), glibenclamide (an ATP-sensitive K(+) channel inhibitor, 0.5 pg/site), charybdotoxin (a large- and intermediate-conductance calcium-activated K(+) channel inhibitor, 25 pg/site) or apamin (a small-conductance calcium-activated K(+) channel inhibitor, 10 pg/site) was able to potentiate the action of a subeffective dose of venlafaxine (2mg/kg, i.p.). Moreover, the reduction in the immobility time elicited by an effective dose of venlafaxine (8 mg/kg, i.p.) in the FST was prevented by the pretreatment of mice with the K(+) channel openers cromakalim (10 microg/site, i.c.v.) and minoxidil (10 microg/site, i.c.v.). The drugs used in this study did not produce any change in locomotor activity.

SIGNIFICANCE

The results demonstrate that the neuromodulatory effects of venlafaxine, via the inhibition of K(+) channels, are possibly involved in its anti-immobility activity in the mouse FST.

Authors+Show Affiliations

Laboratory of Synthesis, Reactivity, Pharmacological and Toxicological Evaluation of Organochalcogens, Natural Science Institute, Federal University of Santa Maria, Santa Maria, CEP 97105-900, RS, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20102723

Citation

Bortolatto, Cristiani F., et al. "Involvement of Potassium Channels in the Antidepressant-like Effect of Venlafaxine in Mice." Life Sciences, vol. 86, no. 9-10, 2010, pp. 372-6.
Bortolatto CF, Jesse CR, Wilhelm EA, et al. Involvement of potassium channels in the antidepressant-like effect of venlafaxine in mice. Life Sci. 2010;86(9-10):372-6.
Bortolatto, C. F., Jesse, C. R., Wilhelm, E. A., & Nogueira, C. W. (2010). Involvement of potassium channels in the antidepressant-like effect of venlafaxine in mice. Life Sciences, 86(9-10), 372-6. https://doi.org/10.1016/j.lfs.2010.01.013
Bortolatto CF, et al. Involvement of Potassium Channels in the Antidepressant-like Effect of Venlafaxine in Mice. Life Sci. 2010 Feb 27;86(9-10):372-6. PubMed PMID: 20102723.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of potassium channels in the antidepressant-like effect of venlafaxine in mice. AU - Bortolatto,Cristiani F, AU - Jesse,Cristiano R, AU - Wilhelm,Ethel A, AU - Nogueira,Cristina W, Y1 - 2010/01/25/ PY - 2009/09/23/received PY - 2010/01/13/revised PY - 2010/01/18/accepted PY - 2010/1/28/entrez PY - 2010/1/28/pubmed PY - 2010/3/20/medline SP - 372 EP - 6 JF - Life sciences JO - Life Sci. VL - 86 IS - 9-10 N2 - AIMS: Studies have shown that the acute administration of venlafaxine elicits an antidepressant-like effect in the mouse forced swim test (FST) by a mechanism dependent on the l-arginine-nitric oxide (NO)-cyclic guanosine monophosphate (cGMP) pathway. Because it has been reported that NO activates different types of potassium (K(+)) channels in the brain, this study investigated the involvement of K(+) channels in the antidepressant-like effect of venlafaxine in the mouse FST. MAIN METHODS: Male adult Swiss mice were pretreated with different K(+) channel inhibitors or openers 15 min before venlafaxine administration. After 30 min, the open-field test (OFT) and FST were carried out. KEY FINDINGS: Intracerebroventricular (i.c.v.) pretreatment of mice with subeffective doses of tetraethylammonium (TEA, a non-specific inhibitor of K(+) channels, 25 pg/site), glibenclamide (an ATP-sensitive K(+) channel inhibitor, 0.5 pg/site), charybdotoxin (a large- and intermediate-conductance calcium-activated K(+) channel inhibitor, 25 pg/site) or apamin (a small-conductance calcium-activated K(+) channel inhibitor, 10 pg/site) was able to potentiate the action of a subeffective dose of venlafaxine (2mg/kg, i.p.). Moreover, the reduction in the immobility time elicited by an effective dose of venlafaxine (8 mg/kg, i.p.) in the FST was prevented by the pretreatment of mice with the K(+) channel openers cromakalim (10 microg/site, i.c.v.) and minoxidil (10 microg/site, i.c.v.). The drugs used in this study did not produce any change in locomotor activity. SIGNIFICANCE: The results demonstrate that the neuromodulatory effects of venlafaxine, via the inhibition of K(+) channels, are possibly involved in its anti-immobility activity in the mouse FST. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/20102723/Involvement_of_potassium_channels_in_the_antidepressant_like_effect_of_venlafaxine_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(10)00031-7 DB - PRIME DP - Unbound Medicine ER -