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Dendritic release of VP mediates crosstalk between neuroendocrine and presympathetic PVN neurons: Role in osmotically‐driven homeostatic responses
Author(s) -
Son Sook Jin,
Filosa Jessica A.,
Zheng Hong,
Patel Kaushik P.,
Stern Javier E.
Publication year - 2012
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.26.1_supplement.1091.30
Subject(s) - chemistry , glutamate receptor , rostral ventrolateral medulla , medicine , endocrinology , nmda receptor , agonist , receptor , stimulation , homeostasis , neuron , neuroscience , biology , medulla oblongata , central nervous system , biochemistry
Dendritic release of vasopressin (VP) in the SON and PVN nuclei plays an important role in the autoregulation of VP neuronal activity. Here, we tested the hypothesis that dendritically‐released VP acts in a diffusible manner to influence the activity of neighboring presympathetic neurons. Patch‐clamp recordings in brain slices showed that focally applied VP depolarized and increased presympathetic PVN‐RVLM neurons (~450%, P< 0.01), an effect that persisted in the presence of GABA/glutamate receptor blockers. Activation of a single, identified eGFP‐VP neuron using photolysis of caged NMDA induced a Ca2+‐dependent, V1a‐mediated increased firing discharge in neighboring PVN‐RVLM neurons. Blockade of V1a receptors per se reduced PVN‐RVLM firing discharge (~75%, P< 0.02). Increasing (high K+, aminopeptidase blockade) and decreasing (κ opiod agonist) endogenous VP ambient levels, respectively, further increased/decreased PVN‐RVLM firing activity. Finally, a central osmotic stimulation (NaCl 0.3–2.1 omosl/l ICA) induced a prompt increase in RSNA, and effect that was blunted (~50%) when V1a receptors were locally blocked within the PVN (P<0.001). Collectively, our results demonstrate that dendritic release of VP mediates a functional crosstalk between neurosecretory and presympathetic PVN neurons, playing an important role in the generation of osmotically‐driven homeostatic responses. Supported by NIH HL‐090948 to JES and NIH HL‐62222 to KKP.