Temporal Patterns of Vasopressin Release Following Electrical Stimulation of the Amygdala and the Neuroendocrine Pathway in the Monkey

1977 ◽  
Vol 23 (2) ◽  
pp. 61-75 ◽  
Author(s):  
J.N. Hayward ◽  
K. Murgas ◽  
K. Pavasuthipaisit ◽  
F.R. Perez-Lopez ◽  
M.V. Sofroniew
Keyword(s):  
Electrical Stimulation ◽  
Temporal Patterns ◽  
Vasopressin Release ◽  
Stimulation Of

scholarly journals Detection of activity-dependent vasopressin release from neuronal dendrites and axon terminals using sniffer cells

2018 ◽  
Vol 120 (3) ◽  
pp. 1386-1396 ◽  
Author(s):  
Cristian Zaelzer ◽  
Claire Gizowski ◽  
Christopher K. Salmon ◽  
Keith K. Murai ◽  
Charles W. Bourque
Keyword(s):  
Electrical Stimulation ◽  
Response Analysis ◽  
Living Tissue ◽  
Vasopressin Release ◽  
Human Embryonic Kidney Cells ◽  
Functional Roles ◽  
Axon Terminals ◽  
Neuronal Dendrites ◽  
Calcium Indicator ◽  
Stimulation Of

Our understanding of neuropeptide function within neural networks would be improved by methods allowing dynamic detection of peptide release in living tissue. We examined the usefulness of sniffer cells as biosensors to detect endogenous vasopressin (VP) release in rat hypothalamic slices and from isolated neurohypophyses. Human embryonic kidney cells were transfected to express the human V1a VP receptor (V1aR) and the genetically encoded calcium indicator GCaMP6m. The V1aR couples to Gq11, thus VP binding to this receptor causes an increase in intracellular [Ca2+] that can be detected by a rise in GCaMP6 fluorescence. Dose-response analysis showed that VP sniffer cells report ambient VP levels >10 pM (EC50 = 2.6 nM), and this effect could be inhibited by the V1aR antagonist SR 49059. When placed over a coverslip coated with sniffer cells, electrical stimulation of the neurohypophysis provoked a reversible, reproducible, and dose-dependent increase in VP release using as few as 60 pulses delivered at 3 Hz. Suspended sniffer cells gently plated over a slice adhered to the preparation and allowed visualization of VP release in discrete regions. Electrical stimulation of VP neurons in the suprachiasmatic nucleus caused significant local release as well as VP secretion in distant target sites. Finally, action potentials evoked in a single magnocellular neurosecretory cell in the supraoptic nucleus provoked significant VP release from the somatodendritic compartment of the neuron. These results indicate that sniffer cells can be used for the study of VP secretion from various compartments of neurons in living tissue. NEW & NOTEWORTHY The specific functional roles of neuropeptides in neuronal networks are poorly understood due to the absence of methods allowing their real-time detection in living tissue. Here, we show that cultured “sniffer cells” can be engineered to detect endogenous release of vasopressin as an increase in fluorescence.

Alpha 2-adrenergic regulation of galanin and norepinephrine release from canine pancreas

1992 ◽  
Vol 262 (5) ◽  
pp. R819-R825 ◽  
Author(s):  
A. J. Scheurink ◽  
T. O. Mundinger ◽  
B. E. Dunning ◽  
R. C. Veith ◽  
G. J. Taborsky
Keyword(s):  
Electrical Stimulation ◽  
Direct Evidence ◽  
Endocrine Pancreas ◽  
Temporal Patterns ◽  
Norepinephrine Release ◽  
Adrenergic Regulation ◽  
Adrenergic Mechanisms ◽  
Noradrenergic Nerves ◽  
Highly Correlated ◽  
Stimulation Of

We found previously that electrical stimulation of the mixed autonomic pancreatic nerves (MPNS) is anesthesized dogs elicits marked and rapid increases of pancreatic output of both norepinephrine (NE) and galanin, and on that basis hypothesized a role for galanin as a sympathetic cotransmitter in the endocrine pancreas. In the present study, direct evidence was sought for the co-release of galanin and NE from canine pancreas by determining whether pancreatic galanin output is subject to modulation by presynaptic alpha 2-adrenergic mechanisms as has been established for NE. During MPNS (8 Hz, 1 ms, 10 mA, 10 min) in anesthesized dogs, both pancreatic NE and galanin outflow were increased with similar temporal patterns during consecutive stimulations. Blockade of presynaptic alpha 2-adrenoceptors with yohimbine increased and stimulation of presynaptic alpha 2-adrenoceptors with clonidine reduced NE and galanin outflow. Over all experiments, pancreatic spillover of galanin was highly correlated with that of NE. It is concluded that presynaptic alpha 2-adrenergic mechanisms modulate not only NE but also pancreatic galanin release, suggesting that galanin is co-released with NE from noradrenergic nerves in the endocrine pancreas.

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