Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 597, Issue 1, Pages 283-301Publisher
WILEY
DOI: 10.1113/JP276467
Keywords
baroreflex; glycine; GABA; rostral ventrolateral medulla; patch-clamp
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Funding
- National Institute of Health [R01 HL122829, R01 HL098602]
- Australian Research Council Future Fellowship [FT170100363]
- National Health and Medical Research Council of Australia [GNT1079680]
- High Blood Pressure Research Council of Australia
- Rebecca L Cooper Medical Foundation
- VictorianGovernment through the Operational Infrastructure Scheme
- Centre for Neuroanatomy with Neurotropic Viruses [P40 OD10996]
- Australian Research Council [FT170100363] Funding Source: Australian Research Council
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The arterial baroreflex is a rapid negative-feedback system that compensates changes in blood pressure by adjusting the output of presympathetic neurons in the rostral ventrolateral medulla (RVLM). GABAergic projections from the caudal VLM (CVLM) provide a primary inhibitory input to presympathetic RVLM neurons. Although glycine-dependent regulation of RVLM neurons has been proposed, its role in determining RVLM excitability is ill-defined. The present study aimed to determine the physiological role of glycinergic neurotransmission in baroreflex function, identify the mechanisms for glycine release, and evaluate co-inhibition of RVLM neurons by GABA and glycine. Microinjection of the glycine receptor antagonist strychnine (4 mm, 100 nL) into the RVLM decreased the duration of baroreflex-mediated inhibition of renal sympathetic nerve activity (control = 12 +/- 1 min; RVLM-strychnine = 5.1 +/- 1 min), suggesting that RVLM glycine plays a critical role in regulating the time course of sympathoinhibition. Blockade of output from the nucleus tractus solitarius and/or disinhibition of the CVLM unmasked tonic glycinergic inhibition of the RVLM. To evaluate cellular mechanisms, RVLM neurons were retrogradely labelled (prior injection of pseudorabies virus PRV-152) and whole-cell, patch clamp recordings were obtained in brainstem slices. Under steady-state conditions GABAergic inhibition of RVLM neurons predominated and glycine contributed less than 25% of the overall inhibition. By contrast, stimulation of synaptic inputs in the RVLM decreased GABAergic inhibition to 53%; and increased glycinergic inhibition to 47%. Thus, under conditions of increased synaptic activity in the RVLM, glycinergic inhibition is recruited to strengthen sympathoinhibition.
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