Document Detail


Role of GABAergic neurones in the nucleus tractus solitarii in modulation of cardiovascular activity.
MedLine Citation:
PMID:  20591977     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
GABAergic neurones are interspersed throughout the nucleus tractus solitarii (NTS), and their tonic activity is crucial to the maintenance of cardiorespiratory homeostasis. However, the mechanisms that regulate the magnitude of GABAergic inhibition in the NTS remain unknown. We hypothesized that the level of GABAergic inhibition is proportionally regulated by the level of excitatory synaptic input to the NTS from baroreceptors. Using the in situ working heart-brainstem preparation in normotensive and spontaneously hypertensive rats, we blocked GABA(A) receptor-mediated neurotransmission in the NTS with gabazine (a specific GABA(A) receptor antagonist) at two levels of perfusion pressure (low PP, 60-70 mmHg; and high PP, 105-125 mmHg) while monitoring the immediate changes in cardiorespiratory variables. In normotensive rats, gabazine produced an immediate bradycardia consistent with disinhibition of NTS circuit neurones that regulate heart rate (HR) which was proportional to the level of arterial pressure (HR at low PP, 57 +/- 9 beats min(1); at high PP, 177 +/- 9 beats min(1); P < 0.001), suggesting that GABAergic circuitry in the NTS modulating heart rate was arterial pressure dependent. In contrast, there was no significant difference in the magnitude of gabazine-induced bradycardia in spontaneously hypertensive rats at low or high PP (HR at low PP, 45 +/- 10 beats min(1); at high PP, 58 +/- 7 beats min(1)). With regard to thoracic sympathetic nerve activity (tSNA), at high PP there was a significant reduction in tSNA during the inspiratory (I) phase of the respiratory cycle, but only in the normotensive rat (tSNA = 18.7 +/- 10%). At low PP, gabazine caused an elevation of the postinspiration phase of tSNA in both normotensive (tSNA = 23.7 +/- 2.9%) and hypertensive rats (tSNA = 44.2 +/- 14%). At low PP, gabazine produced no change in tSNA during the mid-expiration phase in either rat strain, but at high PP we observed a significant reduction in the mid-expiration phase tSNA, but only in the spontaneously hypertensive rat (tSNA = 25.2 +/- 8%). Gabazine at both low and high PP produced a reduction in the late expiration phase of tSNA in the hypertensive rat (low PP, tSNA = 29.4 +/- 4.4%; high PP, tSNA = 22.8 +/- 3%), whereas in the normotensive rat this was only significant at high PP (tSNA = 42.5 +/- 6.1%). Therefore, in the spontaneously hypertensive rat, contrary to the GABA(A) receptor-mediated control of HR, it appears that GABA(A) receptor-mediated control of tSNA in the NTS is arterial pressure dependent. This study provides new insight into the origin of GABAergic inhibition in NTS circuitry affecting heart rate and sympathetic activity.
Authors:
Jasenka Zubcevic; Jeffrey T Potts
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Publication Detail:
Type:  Journal Article     Date:  2010-06-30
Journal Detail:
Title:  Experimental physiology     Volume:  95     ISSN:  1469-445X     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-17     Completed Date:  2010-11-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  909-18     Citation Subset:  IM    
Affiliation:
Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. jasenka.zubcevic@uphs.upenn.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Baroreflex* / drug effects
Blood Pressure
Cardiovascular System / drug effects,  innervation*
Disease Models, Animal
GABA-A Receptor Antagonists / administration & dosage
Heart Rate
Hypertension / metabolism*,  physiopathology
Microinjections
Neural Inhibition
Neurons / drug effects,  metabolism*
Perfusion
Phrenic Nerve / physiopathology
Pyridazines / administration & dosage
Rats
Rats, Inbred SHR
Rats, Wistar
Respiratory Mechanics
Solitary Nucleus / drug effects,  metabolism*,  physiopathology
Time Factors
gamma-Aminobutyric Acid / metabolism*
Chemical
Reg. No./Substance:
0/GABA-A Receptor Antagonists; 0/Pyridazines; 104104-50-9/gabazine; 56-12-2/gamma-Aminobutyric Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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