https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23827 Wed 09 Feb 2022 15:57:43 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16906 A agonist muscimol or saline into the amygdala bilaterally and were subjected to a respiratory recording using whole body plethysmography. Presentation of acoustic stimuli (500-ms white noise, 40–90 dB) caused transient responses in respiratory rate that were proportional to the stimulus intensity, ranging from +13 ± 9 cpm to +276 ± 67 cpm for 40- and 90-dB stimuli, respectively. Inhibition of the amygdala significantly suppressed respiratory rate responses to the high-intensity stimuli (70–90dB). Submitting rats to the restraint stress significantly elevated the mean respiratory rate (+72 ± 8 cpm) and the dominant respiratory rate (+1 ± 12 cpm), as well as the fraction of high-frequency respiratory rate (+10 ± 3%). Inhibition of the amygdala by muscimol significantly suppressed these responses. We conclude that the amygdala is one of the key structures that are essential for expression of respiratory responses to stressful or alerting stimuli in rats.]]> Tue 31 Jul 2018 15:18:15 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16912 A receptor antagonist) into sites within a circumscribed region in the deep layers of the superior colliculus and in the central and external nuclei of the inferior colliculus evoked a response characterized by intense and highly synchronized bursts of renal sympathetic nerve activity (RSNA) and phrenic nerve activity (PNA). Each burst of RSNA had a duration of ~300–400 ms and occurred slightly later (peak to peak latency of 41 ± 8 ms) than the corresponding burst of PNA. The bursts of RSNA and PNA were also accompanied by transient increases in arterial pressure and, in most cases, heart rate. Synchronized bursts of RSNA and PNA were also evoked after neuromuscular blockade, artificial ventilation, and vagotomy and so were not dependent on afferent feedback from the lungs. We propose that the synchronized sympathetic-respiratory responses are driven by a common population of neurons, which may normally be activated by an acute threatening stimulus.]]> Sat 24 Mar 2018 07:59:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27703 Sat 24 Mar 2018 07:40:10 AEDT ]]>