Neuronal structures that mediate cardiovascular activation in response to alerting
and stressful stimuli have received a lot of attention in the previous research; yet
neuronal networks that mediate autonomic respiratory activation in response to such
stimuli have never been properly investigated. In the current study 3 groups of Wistar
rats (n = 8 each) received microinjections of GABAA agonist Muscimol or saline via bilateral guide cannulas targeting the dorsomedial
hypothalamus (DMH), the medial prefrontal cortex (mPFC) or the central amygdala (CAm)
and then were subjected to respiratory assessment using whole-body plethysmography
with presentation of 6 alerting acoustic stimuli (white noise, 0.5 msec, 40-90 dB) and restraint stress. Acoustic stimuli produced brief transient increases in respiratory
rate, proportional to the stimulus intensity, ranging from 12 ± 9 cpm increase over baseline in response to a 40 dB stimulus to 276 ± 67 cpm increase in response to a 90 dB stimulus. Inhibition of the DMH by Muscimol almost entirely abolished respiratory
responses to the alerting stimuli. Inhibition of the mPFC did not affect amplitudes
of the responses, but increased latency of responses to 70 and 80 dB stimuli (p = .014 & .024, respectively), while inhibition of the CAm did not affect latency of
responses, but reduced amplitude of responses to 70, 80 and 90 dB stimuli (p = .009, .021 & .043, respectively). Restraint stress significantly elevated respiratory
rate in all groups from 98 ± 12 to 155 ± 7 cpm (p < .001). Inhibition of the CAm reduced this stress-provoked increase in respiratory
rate during the first 5-minute interval of restraint from 57 ± 12 to 12 ± 15 cpm (p = .024), while inhibition of the mPFC reduced it during the last 5-minute interval of
restraint from 40 ± 10 to 11 ± 4 cpm (p = .02). In line with previous studies, we conclude that integrity of the DMH is essential
for autonomic responses to alerting stimuli, while the CAm contributes to the magnitude
of responses and the mPFC facilitates rapid responding.
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Publication history
Received:
May 15,
2013
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Copyright
© 2013 Published by Elsevier Inc.