Alpha1-Adrenoceptor Antagonists Improve Memory by Activating N-methyl-D-Aspartate-Induced Ion Currents in the Rat Hippocampus.
10.5213/inj.2015.19.4.228
- Author:
Chang Hee KIM
1
;
Il Gyu KO
;
Sung Eun KIM
;
Mal Soon SHIN
;
Yeon Ho KANG
;
Jung Wan CHO
;
Key Moon SHIN
;
Chang Ju KIM
;
Baek Vin LIM
;
Khae Hawn KIM
Author Information
1. Department of Urology, Gachon University Gil Medical Center, Gachon University School of Medicine, Incheon, Korea. kimcho99@gilhospital.com
- Publication Type:Original Article
- Keywords:
Tamsulosin;
Memory;
Apoptosis;
Patch-Clamp Techniques;
Receptors, N-methyl-D-aspartate
- MeSH:
Animals;
Apoptosis;
Blood-Brain Barrier;
Brain;
Central Nervous System;
Dentate Gyrus;
Hippocampus*;
In Situ Nick-End Labeling;
Learning;
Lower Urinary Tract Symptoms;
Memory*;
Memory, Short-Term;
N-Methylaspartate;
Neurons;
Patch-Clamp Techniques;
Rats*;
Receptors, Ionotropic Glutamate;
Receptors, Kainic Acid;
Receptors, N-Methyl-D-Aspartate;
Urinary Bladder, Overactive
- From:International Neurourology Journal
2015;19(4):228-236
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Alpha1 (alpha1)-adrenoceptor antagonists are widely used to treat lower urinary tract symptoms. These drugs not only act on peripheral tissues, but also cross the blood-brain barrier and affect the central nervous system. Therefore, alpha1-adrenoceptor antagonists may enhance brain functions. In the present study, we investigated the effects of tamsulosin, an alpha1-adrenoceptor antagonist, on short-term memory, as well as spatial learning and memory, in rats. METHODS: The step-down avoidance test was used to evaluate short-term memory, and an eight-arm radial maze test was used to evaluate spatial learning and memory. TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling) staining was performed in order to evaluate the effect of tamsulosin on apoptosis in the hippocampal dentate gyrus. Patch clamp recordings were used to evaluate the effect of tamsulosin on ionotropic glutamate receptors, such as N-methyl-D-aspartate (NMDA), amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), and kainate receptors, in hippocampal CA1 neurons. RESULTS: Tamsulosin treatment improved short-term memory, as well as spatial learning and memory, without altering apoptosis. The amplitudes of NMDA-induced ion currents were dose-dependently increased by tamsulosin. However, the amplitudes of AMPA- and kainate-induced ion currents were not affected by tamsulosin. CONCLUSIONS: Tamsulosin enhanced memory function by activating NMDA receptor-mediated ion currents in the hippocampus without initiating apoptosis. The present study suggests the possibility of using tamsulosin to enhance memory under normal conditions, in addition to its use in treating overactive bladder.
