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Altered balance of excitatory/inhibitory synaptic inputs in supraoptic (SON) and paraventricular (PVN) neurosecretory neurons in heart failure rats.
Author(s) -
Potapenko Evgeniy,
Biancardi Vinicia Campana,
Stern Javier E
Publication year - 2010
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.24.1_supplement.1019.6
Subject(s) - excitatory postsynaptic potential , inhibitory postsynaptic potential , supraoptic nucleus , medicine , chemistry , glutamate receptor , endocrinology , neuroscience , vasopressin , biology , receptor
Neurohumoral hyperactivation, including enhanced vasopressin (VP) release, is a hallmark of heart failure (HF). VP release from neurosecretory neurons in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei is tightly controlled by their electrical activity, which in turn depends on a balanced glutamate (GLU) excitatory and GABA inhibitory synaptic inputs. Here, we investigated if changes in the GABA/GLU balance in SON neurons may constitute an underlying mechanism in VP overactivation in HF. GABA and GLU IPSCs/EPSCs were simultaneously recorded in SON neurons from sham and coronary ligated HF rats (n= 17 and 27, respectively). Our data indicate an enhanced excitatory synaptic strength (~60% longer lasting and ~52% larger potency EPSCs), concomitant with a blunted inhibitory synaptic strength (~ 35% faster and ~38% reduced potency IPSCs) in neurons from HF rats. The GABA/GLU strength ratio within each cell was decreased in HF rats (~50%, P<0.01). Blockade of GABA inputs with 15 μM gabazine prolonged EPSCs duration by ~20%, in sham but not in HF rats. These results support that a shift in the GABA/GLU balance towards an excitatory predominance may contribute to enhanced VP release in HF. Supported by NIH HL68725.