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Altered balance of GABAergic and glutamatergic afferent inputs in PVN‐RVLM neurons of renovascular hypertensive rats
Author(s) -
Biancardi Vinicia Campana,
Campos Ruy Ribeiro,
Stern Javier Eduardo
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.958.13
Subject(s) - glutamatergic , excitatory postsynaptic potential , gabaergic , medicine , endocrinology , inhibitory postsynaptic potential , glutamate receptor , neuroscience , chemistry , biology , receptor
Altered hypothalamic synaptic function contributes to exacerbated neurohumoral drive in hypertension. Using immunohistochemistry and tract‐tracing techniques, we determined if remodeling of afferent GABAergic and glutamatergic inputs in PVN‐RVLM neurons contributes to the imbalanced excitatory/inhibitory function observed in renovascular hypertensive rats (RVH). The density of GAD67ir and VGLUT2ir boutons increased in PVN‐RVLM neurons from RVH rats (P< 0.001). Despite this concomitant increase, time‐dependent and compartment‐specific differences in their reorganization resulted in an altered balance of excitatory/inhibitory inputs. In SHAM and early stage RVH rats (3 weeks), cell body VGLUT2ir predominated over GAD67ir (P< 0.001); no differences were observed in proximal dendrites. Conversely, in late‐stage RVH rats (6 weeks), the somatic VGLUT2/GAD67 predominance diminished (P>0.5), while this relationship in proximal dendrites increased (P< 0.05). Our results support that anatomical remodeling of GABA and glutamate afferent inputs in the PVN, resulting in a net predominance of excitatory over inhibitory inputs, may contribute as an underlying mechanism to enhanced neurohumoral drive in renovascular hypertension. This work was supported by NIH HL090948‐01 to Stern JE and CAPES BEX0325/03‐1 (Brazil).