Role of ventrolateral periaqueductal gray neurons in the behavioral and cardiovascular responses to contextual conditioned fear and poststress recovery

Neuroscience ◽  
2003 ◽  
Vol 116 (3) ◽  
pp. 897-912 ◽  
Author(s):  
P Walker ◽  
P Carrive
2014 ◽  
Author(s):  
Molly Ann Metz ◽  
Heidi Kane ◽  
Thery Prok ◽  
Christena Cleveland ◽  
Nancy Collins

2021 ◽  
Vol 11 (4) ◽  
pp. 423
Author(s):  
Markus Fendt ◽  
Claudia Paulina Gonzalez-Guerrero ◽  
Evelyn Kahl

Rats can acquire fear by observing conspecifics that express fear in the presence of conditioned fear stimuli. This process is called observational fear learning and is based on the social transmission of the demonstrator rat’s emotion and the induction of an empathy-like or anxiety state in the observer. The aim of the present study was to investigate the role of trait anxiety and ultrasonic vocalization in observational fear learning. Two experiments with male Wistar rats were performed. In the first experiment, trait anxiety was assessed in a light–dark box test before the rats were submitted to the observational fear learning procedure. In the second experiment, ultrasonic vocalization was recorded throughout the whole observational fear learning procedure, and 22 kHz and 50 kHz calls were analyzed. The results of our study show that trait anxiety differently affects direct fear learning and observational fear learning. Direct fear learning was more pronounced with higher trait anxiety, while observational fear learning was the best with a medium-level of trait anxiety. There were no indications in the present study that ultrasonic vocalization, especially emission of 22 kHz calls, but also 50 kHz calls, are critical for observational fear learning.


2006 ◽  
Vol 172 (2) ◽  
pp. 294-298 ◽  
Author(s):  
Leonardo B.M. Resstel ◽  
Sâmia R.L. Joca ◽  
Fabrício A. Moreira ◽  
Fernando M.A. Corrêa ◽  
Francisco S. Guimarães

2010 ◽  
Vol 1328 ◽  
pp. 49-56 ◽  
Author(s):  
Ahmad Mohammadi-Farani ◽  
Mousa Sahebgharani ◽  
Zargham Sepehrizadeh ◽  
Elham Jaberi ◽  
Mahmoud Ghazi-Khansari

1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.


1999 ◽  
Vol 276 (1) ◽  
pp. H63-H70 ◽  
Author(s):  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen

To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Sham-operated or lesioned Wistar rats were administered ouabain (50 μg/day) or placebo for 3 wk from subcutaneously implanted controlled release pellets or artificial cerebrospinal fluid (CSF) or CSF containing 0.8 mol/l NaCl (5 μl/h) infused intracerebroventricularly for 2 wk. At the end of the experiment, mean arterial pressure (MAP) and heart rate at rest and in response to ganglionic blockade by intravenous hexamethonium (30 mg/kg) were assessed. In rats infused with hypertonic saline, responses to air jet stress were also assessed. Baseline MAP in sham-operated rats receiving intracerebroventricular hypertonic saline or subcutaneous ouabain was significantly higher than in control rats (115 ± 1 vs. 97 ± 3 and 121 ± 3 vs. 103 ± 3 mmHg, respectively). vAV3V lesions abolished the increase in MAP elicited by chronic infusion of hypertonic saline or administration of ouabain. Sham-operated rats treated with hypertonic saline or ouabain exhibited significantly enhanced decreases in MAP to hexamethonium, but lesioned rats did not. Rats infused with hypertonic saline demonstrated enhanced responses to air jet stress that were similar in sham-operated and lesioned rats. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. Cardiovascular responses to air jet stress appear not to be mediated by the vAV3V.


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