title: Parabrachial nucleus influences the control of normal urinary bladder function and the response to bladder irritation in rats.
abstract: The contribution of the parabrachial nucleus to the mediation of bladder contraction was examined in the rat. Constant infusion (0.1 ml/min) of saline or 0.2% acetic acid evoked normal or abnormal bladder contractions, respectively. Single unit activity was recorded in the parabrachial nucleus with tungsten microelectrodes. Seven units with activity that was correlated with bladder contraction during saline infusion were located in the lateral subnuclei and three units were located in the medial subnuclei of the parabrachial nucleus. Twelve units with activity that was correlated with abnormal bladder contractions were found widely distributed in the parabrachial nucleus. An inverse correlation of activity to normal or abnormal bladder contractions was identified in 11 units in the parabrachial nucleus. Pressure injection of 5 mM CoCl(2) into the parabrachial nucleus was used to block synaptic transmission unilaterally. Normal bladder contractions evoked by saline infusion were disrupted by 5 of 10 injections, 4 of them in the medial subnuclei of the parabrachial nucleus and one in the lateral subnuclei. Abnormal bladder contractions were converted to a normal pattern in nine experiments where CoCl(2) injections lay in the lateral subnuclei of the parabrachial nucleus. In five experiments, CoCl(2) disrupted abnormal bladder contractions; four effective sites were located in the lateral subnucleus and one lay in the medial subnucleus of the parabrachial nucleus. These data demonstrated that single units responding to both normal and abnormal contractions were located throughout the parabrachial nuclei whereas the lateral subnuclei play a predominant role in mediation of abnormal bladder contractions and the medial subnuclei play a predominant role in the mediation of normal bladder contractions.
authors.affiliation: Department of Pharmacology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada. victor.liu@sandoz.com
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
authors.forename: G V
authors.initials: GV
authors.lastname: Allen
authors.forename: J W
authors.initials: JW
authors.lastname: Downie
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D016587:Antimutagenic Agents / Q000494:pharmacology; D001931:Brain Mapping; D003035:Cobalt / Q000494:pharmacology; D004576:Electromyography; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000502:physiology; D011149:Pons / Q000166:cytology / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D001743:Urinary Bladder / Q000502:physiology*; D001745:Urinary Bladder Diseases / Q000503:physiopathology*; D014554:Urination / Q000502:physiology*
chemical_list: D016587:Antimutagenic Agents; D003035:Cobalt; C018021:cobaltous chloride