PMID- 20102723
OWN - NLM
STAT- MEDLINE
DCOM- 20100318
LR  - 20151119
IS  - 1879-0631 (Electronic)
IS  - 0024-3205 (Linking)
VI  - 86
IP  - 9-10
DP  - 2010 Feb 27
TI  - Involvement of potassium channels in the antidepressant-like effect of 
      venlafaxine in mice.
PG  - 372-6
LID - 10.1016/j.lfs.2010.01.013 [doi]
AB  - 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.
CI  - Copyright 2010 Elsevier Inc. All rights reserved.
FAU - Bortolatto, Cristiani F
AU  - Bortolatto CF
AD  - 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.
FAU - Jesse, Cristiano R
AU  - Jesse CR
FAU - Wilhelm, Ethel A
AU  - Wilhelm EA
FAU - Nogueira, Cristina W
AU  - Nogueira CW
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100125
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Antidepressive Agents, Second-Generation)
RN  - 0 (Cyclohexanols)
RN  - 0 (Potassium Channel Blockers)
RN  - 0 (Potassium Channels)
RN  - 7D7RX5A8MO (Venlafaxine Hydrochloride)
SB  - IM
MH  - Animals
MH  - Antidepressive Agents, Second-Generation/*pharmacology
MH  - Cyclohexanols/*pharmacology/therapeutic use
MH  - Depression/drug therapy/physiopathology/psychology
MH  - Male
MH  - Mice
MH  - Motor Activity/drug effects/physiology
MH  - Potassium Channel Blockers/pharmacology/therapeutic use
MH  - Potassium Channels/metabolism/*physiology
MH  - Venlafaxine Hydrochloride
EDAT- 2010/01/28 06:00
MHDA- 2010/03/20 06:00
CRDT- 2010/01/28 06:00
PHST- 2009/09/23 00:00 [received]
PHST- 2010/01/13 00:00 [revised]
PHST- 2010/01/18 00:00 [accepted]
PHST- 2010/01/28 06:00 [entrez]
PHST- 2010/01/28 06:00 [pubmed]
PHST- 2010/03/20 06:00 [medline]
AID - S0024-3205(10)00031-7 [pii]
AID - 10.1016/j.lfs.2010.01.013 [doi]
PST - ppublish
SO  - Life Sci. 2010 Feb 27;86(9-10):372-6. doi: 10.1016/j.lfs.2010.01.013. Epub 2010 
      Jan 25.