title: Baro-activated neurons with pulse-modulated activity in the rat caudal ventrolateral medulla express GAD67 mRNA.
abstract: GABAergic neurons in the caudal ventrolateral medulla (CVLM) are believed to mediate the sympathetic baroreceptor reflex by inhibiting presympathetic neurons in the rostral ventrolateral medulla (RVLM). Accordingly, some CVLM neurons are activated by increased arterial pressure (AP; baro-activated), have activity strongly modulated by the AP pulse (pulse-modulated), and can be antidromically activated from the RVLM. This study examined whether baro-activated, pulse-modulated CVLM neurons are indeed GABAergic and examined their structures. We recorded extracellularly from 19 baro-activated, pulse-modulated CVLM neurons in chloralose-anesthetized rats. Most of these cells (13/19) were silenced by decreasing AP with nitroprusside, but some (6/19) remained active at low AP levels. They were also excited by phenyl biguanide (17/17) but inhibited by noxious tail pinch (8/11). Twelve baro-activated cells were filled with biotinamide and examined for expression of GAD67 mRNA. Because adjacent vagal motor neurons are also activated by increased AP, we examined choline acetyltransferase (ChAT) immunoreactivity. Most baro-activated cells (9/12) expressed high levels of GAD67 mRNA, the rest (3/12) displayed lower levels of GAD67 mRNA, but none showed ChAT immunoreactivity. In contrast, adjacent baro-inhibited CVLM cells had no GAD67 mRNA (n = 5) but were instead tyrosine hydroxylase immunoreactive (n = 7). Reconstruction of baro-activated CVLM neurons revealed axons that projected dorsomedially and rostrally with several axon collaterals. These data demonstrate the existence of GABAergic CVLM neurons with the physiological characteristics expected of interneurons that mediate the sympathetic baroreceptor reflex. In addition, baro-activated GABAergic CVLM neurons appear to integrate several types of inputs and provide inhibition to multiple targets.
authors.affiliation: Department of Pharmacology, University of Virginia Health System, Charlotttesville, Virginia 22908-0735, USA. ASchreihofer@mail.mcg.edu
authors.forename: Ann M
authors.initials: AM
authors.lastname: Schreihofer
authors.forename: Patrice G
authors.initials: PG
authors.lastname: Guyenet
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D017704:Baroreflex / Q000502:physiology*; D001710:Biotin / Q000031:analogs & derivatives*; D002452:Cell Count; D004594:Electrophysiology; D015971:Gene Expression Regulation, Enzymologic; D005968:Glutamate Decarboxylase / Q000235:genetics*; D007527:Isoenzymes / Q000235:genetics*; D008297:Male; D008526:Medulla Oblongata / Q000166:cytology / Q000502:physiology*; D009433:Neural Inhibition / Q000502:physiology; D009475:Neurons, Afferent / Q000201:enzymology*; D010641:Phenotype; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D007527:Isoenzymes; D012333:RNA, Messenger; C093086:biotinamide; D001710:Biotin; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1