The Supraoptic Nucleus of the Hypothalamus Modulates Autonomic, Neuroendocrine, and Behavioral Responses to Acute Restraint Stress in Rats

2019 ◽  
Vol 110 (1-2) ◽  
pp. 10-22 ◽  
Author(s):  
Silvana Lopes-Azevedo ◽  
Eduardo Albino Trindade Fortaleza ◽  
Cristiane Busnardo ◽  
América Augusto Scopinho ◽  
Melina Matthiesen ◽  
...  

Aims: Acute restraint stress (RS) has been reported to cause neuronal activation in the supraoptic nucleus of the hypothalamus (SON). The aim of the study was to evaluate the role of SON on autonomic (mean arterial pressure [MAP], heart rate [HR], and tail temperature), neuroendocrine (corticosterone, oxytocin, and vasopressin plasma levels), and behavioral responses to RS. Methods: Guide cannulas were implanted bilaterally in the SON of male Wistar rats for microinjection of the unspecific synaptic blocker cobalt chloride (CoCl2, 1 mM) or vehicle (artificial cerebrospinal fluid, 100 nL). A catheter was introduced into the femoral artery for MAP and HR recording. Rats were subjected to RS, and it was studied the effect of microinjection of CoCl2 or vehicle into the SON on pressor and tachycardic responses, drop in tail temperature, plasma oxytocin, vasopressin, and corticosterone levels, and anxiogenic-like effect induced by RS. Results: SON pretreatment with CoCl2 reduced the RS-induced MAP and HR increase, without affecting the RS-evoked tail temperature decrease. Microinjection of CoCl2 into areas surrounding the SON did not affect RS-induced increase in MAP and HR, reinforcing the idea that SON influences RS-evoked cardiovascular responses. Also, SON pretreatment with CoCl2 reduced RS-induced increase in corticosterone and oxytocin, without affecting vasopressin plasma levels, suggesting its involvement in RS-induced neuroendocrine responses. Finally, the CoCl2 microinjection into SON inhibited the RS-caused delayed anxiogenic-like effect. Conclusion: The results indicate that SON is an important component of the neural pathway that controls autonomic, neuroendocrine, and behavioral responses induced by RS.

2009 ◽  
Vol 156 (1) ◽  
pp. 181-188 ◽  
Author(s):  
Leonardo B.M. Resstel ◽  
Rodrigo F. Tavares ◽  
Sabrina F.S. Lisboa ◽  
Sâmia R.L. Joca ◽  
Fernando M.A. Corrêa ◽  
...  

2017 ◽  
Vol 175 ◽  
pp. 16-21 ◽  
Author(s):  
Josiane O. Duarte ◽  
Karina S. Gomes ◽  
Ricardo L. Nunes-de-Souza ◽  
Carlos C. Crestani

2012 ◽  
Vol 26 (10) ◽  
pp. 1366-1374 ◽  
Author(s):  
Fábio C Cruz ◽  
Sheila A Engi ◽  
Rodrigo M Leão ◽  
Cleopatra S Planeta ◽  
Carlos C Crestani

2016 ◽  
Vol 173 (19) ◽  
pp. 2833-2844 ◽  
Author(s):  
Lucas Gomes-de-Souza ◽  
Leandro A Oliveira ◽  
Ricardo Benini ◽  
Patrícia Rodella ◽  
Willian Costa-Ferreira ◽  
...  

Stress ◽  
2009 ◽  
Vol 12 (3) ◽  
pp. 268-278 ◽  
Author(s):  
C. C. Crestani ◽  
F. H. F. Alves ◽  
R. F. Tavares ◽  
F. M. A. Corrêa

2010 ◽  
Vol 1333 ◽  
pp. 57-63 ◽  
Author(s):  
Fernando H.F. Alves ◽  
Carlos C. Crestani ◽  
Fernando M.A. Corrêa

1996 ◽  
Vol 270 (5) ◽  
pp. E787-E792 ◽  
Author(s):  
M. Ludwig ◽  
M. F. Callahan ◽  
R. Landgraf ◽  
A. K. Johnson ◽  
M. Morris

The effects of lesioning of the anteroventral third ventricle (AV3V) region on vasopressin (VP) release into the supraoptic nucleus (SON) and blood in response to central and systemic osmotic stimulation were determined. Microdialysis probes were implanted bilaterally within the SON of male urethan-anesthetized rats with sham or AV3V lesions. Osmotic stimuli were administered intraperitoneally (3.5 M NaCl, 600 microliters/100 g body wt) and then via the microdialysis probes (1 M NaCl-artificial cerebrospinal fluid). AV3V lesions attenuated the response to systemic osmotic stimulation. The lesioned rats showed no increase in intranuclear VP release and reduced plasma VP (increase of 42.6 +/- 8.4 vs. 78.0 +/- 16.4 pg/ml) and blood pressure responses (7.1 +/- 2.3 vs. 19.6 +/- 3.2 mmHg) to intraperitoneal NaCl. In contrast, the endocrine and cardiovascular responses to direct osmotic stimulation of the nucleus were as seen in previous studies and seemed to be unaffected by the lesion. These results show that lesion of the AV3V region interrupts neuronal inputs which trigger VP secretion from the posterior pituitary as well as release into the extracellular compartment of the SON.


2010 ◽  
Vol 158 (1-2) ◽  
pp. 51-57 ◽  
Author(s):  
Cristiane Busnardo ◽  
Rodrigo F. Tavares ◽  
Leonardo B.M. Resstel ◽  
Lucila L.K. Elias ◽  
Fernando M.A. Correa

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