Document Detail

Role of GABAergic neurones in the nucleus tractus solitarii in modulation of cardiovascular activity.
MedLine Citation:
PMID:  20591977     Owner:  NLM     Status:  MEDLINE    
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.
Jasenka Zubcevic; Jeffrey T Potts
Related Documents :
20696147 - Central monoamine levels differ between rat strains used in studies of depressive behav...
19463097 - Analysis of mitochondrial dna somatic mutations in oxys and wistar strain rats.
8590047 - A comparative study of nadph-diaphorase in the sympathetic preganglionic neurons of the...
3241207 - Effects of felodipine on blood pressure and lymphocyte membrane characteristics in spon...
2626397 - The hepatic lipid peroxidation, copper and fibrosis in cholestatic rats.
12878447 - Liver oleic acid biogenesis is impaired during the prehypertensive period in the sponta...
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    
Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Baroreflex* / drug effects
Blood Pressure
Cardiovascular System / drug effects,  innervation*
Disease Models, Animal
GABA-A Receptor Antagonists / administration & dosage
Heart Rate
Hypertension / metabolism*,  physiopathology
Neural Inhibition
Neurons / drug effects,  metabolism*
Phrenic Nerve / physiopathology
Pyridazines / administration & dosage
Rats, Inbred SHR
Rats, Wistar
Respiratory Mechanics
Solitary Nucleus / drug effects,  metabolism*,  physiopathology
Time Factors
gamma-Aminobutyric Acid / metabolism*
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

Previous Document:  Periovulatory leukocyte infiltration in the rat ovary.
Next Document:  Sodium-bicarbonate cotransporter NBCn1 in the kidney medullary thick ascending limb cell line is upr...