Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/9544
Title: Phenotypic identification of rat rostroventrolateral medullary presympathetic vasomotor neurons inhibited by exogenous cholecystokinin.
Authors: Sartor, Daniela M;Verberne, Anthony J M
Affiliation: Clinical Pharmacology and Therapeutics Unit, Austin and Repatriation Medical Centre, Department of Medicine, University of Melbourne, Heidelberg 3084, Victoria, Australia.
Issue Date: 27-Oct-2003
Citation: The Journal of Comparative Neurology; 465(4): 467-79
Abstract: Systemic administration of the gastrointestinal hormone cholecystokinin (CCK) selectively inhibits splanchnic sympathetic vasomotor discharge and differentially affects presympathetic vasomotor neurons of the rostroventrolateral medulla (RVLM). Stimulation of the sympathoexcitatory region of the periaqueductal grey (PAG) produces profound mesenteric vasoconstriction. In this study, our aim was to identify phenotypically different populations of RVLM presympathetic vasomotor neurons using juxtacellular neuronal labelling and immunohistochemical detection of the adrenergic neuronal marker phenylethanolamine-N-methyl transferase (PNMT) and to determine whether the PAG provides functional excitatory input to these neurons. Fifty-eight percent (36/62) of RVLM presympathetic neurons were inhibited by systemic administration of CCK. These cells had conduction velocities (3.6 +/- 0.2 m/sec) in the non-C-fiber range consistent with neurons possessing lightly myelinated spinal axons. Of these, 79% (22/28) were excited by PAG stimulation, and 59% (10/17) were not immunoreactive for PNMT. Conversely, 42% (26/62) of RVLM presympathetic neurons were either unaffected or activated by CCK administration and had slower conduction velocities (1.4 +/- 0.3 m/sec) than cells inhibited by CCK. Fifty percent (11/22) of these cells were driven by PAG stimulation, and most (11/14 or 79%) were PNMT-positive. These results suggest that cardiovascular responses elicited by PAG stimulation occur via activation of non-C1 and C1 RVLM presympathetic neurons. RVLM neurons inhibited by CCK were more likely to be driven by PAG stimulation and may be a subset of neurons responsible for driving gastrointestinal sympathetic vasomotor tone. CCK-induced inhibition of a subpopulation of RVLM presympathetic neurons may be implicated in postprandial hyperemia and postprandial hypotension.
Internal ID Number: 12975810
URI: http://ahro.austin.org.au/austinjspui/handle/1/9544
DOI: 10.1002/cne.10840
URL: http://www.ncbi.nlm.nih.gov/pubmed/12975810
Type: Journal Article
Subjects: Animals
Axons.drug effects.physiology
Biotin.analogs & derivatives.diagnostic use
Blood Pressure.drug effects.physiology
Cell Size.physiology
Cholecystokinin.metabolism.pharmacology
Efferent Pathways.cytology.drug effects.metabolism
Epinephrine.metabolism
Male
Medulla Oblongata.cytology.drug effects.metabolism
Mesenteric Arteries.innervation.physiology
Neural Conduction.drug effects.physiology
Neural Inhibition.drug effects.physiology
Neurons.cytology.drug effects.metabolism
Periaqueductal Gray.cytology.drug effects.physiology
Phenotype
Phenylethanolamine N-Methyltransferase.metabolism
Rats
Rats, Sprague-Dawley
Regional Blood Flow.drug effects.physiology
Spinal Cord.drug effects.physiology
Sympathetic Nervous System.cytology.drug effects.metabolism
Vasomotor System.drug effects.physiology
Appears in Collections:Journal articles

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