GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion
1 Department of Urology, Kanazawa University School of Medicine, and 2 Department of Pharmacology and Pharmaceutics, Graduate School of Natural Science and Technology, Kanazawa University, Ishikawa 920-8641, Japan To evaluate the influences of -aminobutyric acid (GABA) mechanisms on bladder hypera...
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creator | Kanie, Sayoko Yokoyama, Osamu Komatsu, Kazuto Kodama, Koichi Yotsuyanagi, Satoshi Niikura, Susumu Nagasaka, Yasuhiro Miyamoto, Ken-Ichi Namiki, Mikio |
description | 1 Department of Urology, Kanazawa University School of
Medicine, and 2 Department of Pharmacology and Pharmaceutics,
Graduate School of Natural Science and Technology, Kanazawa
University, Ishikawa 920-8641, Japan
To evaluate the
influences of -aminobutyric acid (GABA) mechanisms on bladder
hyperactivity after left middle cerebral artery occlusion, cystometric
recordings were obtained from unanesthetized female rats.
Intracerebroventricular administration of both muscimol (GABA A receptor agonist; 0.1-10 nmol) and baclofen
(GABA B receptor agonist; 0.1-3 nmol) produced
dose-dependent inhibitions of micturition with increases in bladder
capacity (BC). The effects of high doses (1-10 nmol) were similar
in sham-operated (SO) and cerebral-infarcted (CI) rats. However, lower
doses of muscimol (0.1 or 0.3 nmol) and baclofen (0.1 nmol) reduced BC
in CI rats. After bicuculline (GABA A receptor antagonist; 1 or 3 nmol) administration, BC in both SO and CI rats first decreased
and subsequently increased. An increase in urethral pressure was
observed after administration of bicuculline (3 nmol) but not with
either muscimol or baclofen. Infarct volumes in muscimol-,
bicuculline-, or baclofen-treated rats were not significantly different
from those of vehicle-treated rats. These results suggest that
GABAergic mechanisms inhibit the micturition reflex at the supraspinal
level but that this can change as a result of CI.
GABA or -aminobutyric acid; micturition reflex; cerebral
infarction |
doi_str_mv | 10.1152/ajpregu.2000.279.4.r1230 |
format | Article |
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Medicine, and 2 Department of Pharmacology and Pharmaceutics,
Graduate School of Natural Science and Technology, Kanazawa
University, Ishikawa 920-8641, Japan
To evaluate the
influences of -aminobutyric acid (GABA) mechanisms on bladder
hyperactivity after left middle cerebral artery occlusion, cystometric
recordings were obtained from unanesthetized female rats.
Intracerebroventricular administration of both muscimol (GABA A receptor agonist; 0.1-10 nmol) and baclofen
(GABA B receptor agonist; 0.1-3 nmol) produced
dose-dependent inhibitions of micturition with increases in bladder
capacity (BC). The effects of high doses (1-10 nmol) were similar
in sham-operated (SO) and cerebral-infarcted (CI) rats. However, lower
doses of muscimol (0.1 or 0.3 nmol) and baclofen (0.1 nmol) reduced BC
in CI rats. After bicuculline (GABA A receptor antagonist; 1 or 3 nmol) administration, BC in both SO and CI rats first decreased
and subsequently increased. An increase in urethral pressure was
observed after administration of bicuculline (3 nmol) but not with
either muscimol or baclofen. Infarct volumes in muscimol-,
bicuculline-, or baclofen-treated rats were not significantly different
from those of vehicle-treated rats. These results suggest that
GABAergic mechanisms inhibit the micturition reflex at the supraspinal
level but that this can change as a result of CI.
GABA or -aminobutyric acid; micturition reflex; cerebral
infarction</description><identifier>ISSN: 0363-6119</identifier><identifier>EISSN: 1522-1490</identifier><identifier>DOI: 10.1152/ajpregu.2000.279.4.r1230</identifier><identifier>PMID: 11003988</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Baclofen - administration & dosage ; Baclofen - pharmacology ; Bicuculline - administration & dosage ; Bicuculline - pharmacology ; Cerebral Infarction - physiopathology ; Cerebral Ventricles - drug effects ; Cerebral Ventricles - physiology ; Cerebral Ventricles - physiopathology ; Dose-Response Relationship, Drug ; Female ; GABA-A Receptor Agonists ; GABA-B Receptor Agonists ; Injections, Intraventricular ; Middle Cerebral Artery - physiology ; Muscimol - administration & dosage ; Muscimol - pharmacology ; Pressure ; Rats ; Rats, Sprague-Dawley ; Seizures - physiopathology ; Urinary Bladder - drug effects ; Urinary Bladder - physiology ; Urinary Bladder - physiopathology ; Urination - drug effects ; Urination - physiology</subject><ispartof>American journal of physiology. Regulatory, integrative and comparative physiology, 2000-10, Vol.279 (4), p.1230-R1238</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-bdc97e709ff5665793f00b7a56bee2c9bd73f05535d35d03d17199ef9e46e86b3</citedby><cites>FETCH-LOGICAL-c467t-bdc97e709ff5665793f00b7a56bee2c9bd73f05535d35d03d17199ef9e46e86b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,3026,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11003988$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kanie, Sayoko</creatorcontrib><creatorcontrib>Yokoyama, Osamu</creatorcontrib><creatorcontrib>Komatsu, Kazuto</creatorcontrib><creatorcontrib>Kodama, Koichi</creatorcontrib><creatorcontrib>Yotsuyanagi, Satoshi</creatorcontrib><creatorcontrib>Niikura, Susumu</creatorcontrib><creatorcontrib>Nagasaka, Yasuhiro</creatorcontrib><creatorcontrib>Miyamoto, Ken-Ichi</creatorcontrib><creatorcontrib>Namiki, Mikio</creatorcontrib><title>GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><description>1 Department of Urology, Kanazawa University School of
Medicine, and 2 Department of Pharmacology and Pharmaceutics,
Graduate School of Natural Science and Technology, Kanazawa
University, Ishikawa 920-8641, Japan
To evaluate the
influences of -aminobutyric acid (GABA) mechanisms on bladder
hyperactivity after left middle cerebral artery occlusion, cystometric
recordings were obtained from unanesthetized female rats.
Intracerebroventricular administration of both muscimol (GABA A receptor agonist; 0.1-10 nmol) and baclofen
(GABA B receptor agonist; 0.1-3 nmol) produced
dose-dependent inhibitions of micturition with increases in bladder
capacity (BC). The effects of high doses (1-10 nmol) were similar
in sham-operated (SO) and cerebral-infarcted (CI) rats. However, lower
doses of muscimol (0.1 or 0.3 nmol) and baclofen (0.1 nmol) reduced BC
in CI rats. After bicuculline (GABA A receptor antagonist; 1 or 3 nmol) administration, BC in both SO and CI rats first decreased
and subsequently increased. An increase in urethral pressure was
observed after administration of bicuculline (3 nmol) but not with
either muscimol or baclofen. Infarct volumes in muscimol-,
bicuculline-, or baclofen-treated rats were not significantly different
from those of vehicle-treated rats. These results suggest that
GABAergic mechanisms inhibit the micturition reflex at the supraspinal
level but that this can change as a result of CI.
GABA or -aminobutyric acid; micturition reflex; cerebral
infarction</description><subject>Animals</subject><subject>Baclofen - administration & dosage</subject><subject>Baclofen - pharmacology</subject><subject>Bicuculline - administration & dosage</subject><subject>Bicuculline - pharmacology</subject><subject>Cerebral Infarction - physiopathology</subject><subject>Cerebral Ventricles - drug effects</subject><subject>Cerebral Ventricles - physiology</subject><subject>Cerebral Ventricles - physiopathology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>GABA-A Receptor Agonists</subject><subject>GABA-B Receptor Agonists</subject><subject>Injections, Intraventricular</subject><subject>Middle Cerebral Artery - physiology</subject><subject>Muscimol - administration & dosage</subject><subject>Muscimol - pharmacology</subject><subject>Pressure</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Seizures - physiopathology</subject><subject>Urinary Bladder - drug effects</subject><subject>Urinary Bladder - physiology</subject><subject>Urinary Bladder - physiopathology</subject><subject>Urination - drug effects</subject><subject>Urination - physiology</subject><issn>0363-6119</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kF1rFDEYhYModlv9C5Ir72aaj5nJxLu1tFUoCNLe9Cbk453dlOzOmGS08-_NsivVCyEQODnPCTwIYUpqSlt2qZ-mCJu5ZoSQmglZN3WkjJNXaFWeWUUbSV6jFeEdrzpK5Rk6T-mplBve8LfojFJCuOz7FXq8XX9eQ9x4i-24z9GbOftxj_OIo87YBO0cRLxdJojaZv_T5wXrIZds550LgC1EMFEHrGNJFzxaG-ZUNt6hN4MOCd6f7gv0cHN9f_Wluvt2-_VqfVfZphO5Ms5KAYLIYWi7rhWSD4QYodvOADArjRMlaVveunIId1RQKWGQ0HTQd4ZfoI_H3SmOP2ZIWe18shCC3sM4JyUYk5z2rBT7Y9HGMaUIg5qi3-m4KErUwas6eVUHr6p4VY36fvBa0A-nP2azA_cCnkSWQn0sbP1m-8tHUNN2KRbCuFleZv9Z_PR_4GYO4R6e8x_yL1BNbuC_AY6bnZ8</recordid><startdate>20001001</startdate><enddate>20001001</enddate><creator>Kanie, Sayoko</creator><creator>Yokoyama, Osamu</creator><creator>Komatsu, Kazuto</creator><creator>Kodama, Koichi</creator><creator>Yotsuyanagi, Satoshi</creator><creator>Niikura, Susumu</creator><creator>Nagasaka, Yasuhiro</creator><creator>Miyamoto, Ken-Ichi</creator><creator>Namiki, Mikio</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20001001</creationdate><title>GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion</title><author>Kanie, Sayoko ; Yokoyama, Osamu ; Komatsu, Kazuto ; Kodama, Koichi ; Yotsuyanagi, Satoshi ; Niikura, Susumu ; Nagasaka, Yasuhiro ; Miyamoto, Ken-Ichi ; Namiki, Mikio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c467t-bdc97e709ff5665793f00b7a56bee2c9bd73f05535d35d03d17199ef9e46e86b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Baclofen - administration & dosage</topic><topic>Baclofen - pharmacology</topic><topic>Bicuculline - administration & dosage</topic><topic>Bicuculline - pharmacology</topic><topic>Cerebral Infarction - physiopathology</topic><topic>Cerebral Ventricles - drug effects</topic><topic>Cerebral Ventricles - physiology</topic><topic>Cerebral Ventricles - physiopathology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>GABA-A Receptor Agonists</topic><topic>GABA-B Receptor Agonists</topic><topic>Injections, Intraventricular</topic><topic>Middle Cerebral Artery - physiology</topic><topic>Muscimol - administration & dosage</topic><topic>Muscimol - pharmacology</topic><topic>Pressure</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Seizures - physiopathology</topic><topic>Urinary Bladder - drug effects</topic><topic>Urinary Bladder - physiology</topic><topic>Urinary Bladder - physiopathology</topic><topic>Urination - drug effects</topic><topic>Urination - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kanie, Sayoko</creatorcontrib><creatorcontrib>Yokoyama, Osamu</creatorcontrib><creatorcontrib>Komatsu, Kazuto</creatorcontrib><creatorcontrib>Kodama, Koichi</creatorcontrib><creatorcontrib>Yotsuyanagi, Satoshi</creatorcontrib><creatorcontrib>Niikura, Susumu</creatorcontrib><creatorcontrib>Nagasaka, Yasuhiro</creatorcontrib><creatorcontrib>Miyamoto, Ken-Ichi</creatorcontrib><creatorcontrib>Namiki, Mikio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kanie, Sayoko</au><au>Yokoyama, Osamu</au><au>Komatsu, Kazuto</au><au>Kodama, Koichi</au><au>Yotsuyanagi, Satoshi</au><au>Niikura, Susumu</au><au>Nagasaka, Yasuhiro</au><au>Miyamoto, Ken-Ichi</au><au>Namiki, Mikio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><date>2000-10-01</date><risdate>2000</risdate><volume>279</volume><issue>4</issue><spage>1230</spage><epage>R1238</epage><pages>1230-R1238</pages><issn>0363-6119</issn><eissn>1522-1490</eissn><abstract>1 Department of Urology, Kanazawa University School of
Medicine, and 2 Department of Pharmacology and Pharmaceutics,
Graduate School of Natural Science and Technology, Kanazawa
University, Ishikawa 920-8641, Japan
To evaluate the
influences of -aminobutyric acid (GABA) mechanisms on bladder
hyperactivity after left middle cerebral artery occlusion, cystometric
recordings were obtained from unanesthetized female rats.
Intracerebroventricular administration of both muscimol (GABA A receptor agonist; 0.1-10 nmol) and baclofen
(GABA B receptor agonist; 0.1-3 nmol) produced
dose-dependent inhibitions of micturition with increases in bladder
capacity (BC). The effects of high doses (1-10 nmol) were similar
in sham-operated (SO) and cerebral-infarcted (CI) rats. However, lower
doses of muscimol (0.1 or 0.3 nmol) and baclofen (0.1 nmol) reduced BC
in CI rats. After bicuculline (GABA A receptor antagonist; 1 or 3 nmol) administration, BC in both SO and CI rats first decreased
and subsequently increased. An increase in urethral pressure was
observed after administration of bicuculline (3 nmol) but not with
either muscimol or baclofen. Infarct volumes in muscimol-,
bicuculline-, or baclofen-treated rats were not significantly different
from those of vehicle-treated rats. These results suggest that
GABAergic mechanisms inhibit the micturition reflex at the supraspinal
level but that this can change as a result of CI.
GABA or -aminobutyric acid; micturition reflex; cerebral
infarction</abstract><cop>United States</cop><pmid>11003988</pmid><doi>10.1152/ajpregu.2000.279.4.r1230</doi></addata></record> |
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language | eng |
recordid | cdi_pubmed_primary_11003988 |
source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
subjects | Animals Baclofen - administration & dosage Baclofen - pharmacology Bicuculline - administration & dosage Bicuculline - pharmacology Cerebral Infarction - physiopathology Cerebral Ventricles - drug effects Cerebral Ventricles - physiology Cerebral Ventricles - physiopathology Dose-Response Relationship, Drug Female GABA-A Receptor Agonists GABA-B Receptor Agonists Injections, Intraventricular Middle Cerebral Artery - physiology Muscimol - administration & dosage Muscimol - pharmacology Pressure Rats Rats, Sprague-Dawley Seizures - physiopathology Urinary Bladder - drug effects Urinary Bladder - physiology Urinary Bladder - physiopathology Urination - drug effects Urination - physiology |
title | GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion |
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