Abstract：
:The present work was aimed to evaluate the contribution of interoception to the autonomic and behavioral responses to hypoxia. To address this issue, we studied whether the inactivation of the primary interoceptive posterior insular cortex (pIC) may disrupt the autonomic and behavioral effects of hypoxia in conscious rats. Rats were implanted with telemetric transmitters and microinjection cannulae placed bilaterally in the pIC. After one week, rats were injected with bupivacaine (26.5μM 1μL/side) and saline (1μL/side) into the pIC, and exposed to hypoxia (∼6% O2) for 150s, and autonomic and behavioral responses were recorded. Hypoxia produces hypertension, tachycardia followed by bradycardia, and hypothermia. When O2 dropped to ∼8%, rats showed escape behavior. Baseline cardiovascular variables and the pattern of hypoxia-induced autonomic and behavioral responses were not disrupted by pIC inactivation. However, pIC inactivation produced a modest but significant temperature decrease, higher bradycardic and hypertensive responses to hypoxia, and a minimal delay in escape onset. In addition, we measured the hypoxia-induced Fos activation in the nucleus tractus solitarius (NTS), the periaqueductal gray matter (PAG) and the pIC, which are key components of the interoceptive pathway. Hypoxia increased the number of Fos-positive neurons in the NTS and PAG, but not in the pIC. Present results suggest that pIC is not involved in the hypoxia-induced behavioral response, which seems to be processed in the NTS and PAG, but has a role in the efferent control of autonomic changes coping with hypoxia.
journal_name
Behav Brain Resjournal_title
Behavioural brain researchauthors
Casanova JP,Contreras M,Moya EA,Torrealba F,Iturriaga Rdoi
10.1016/j.bbr.2013.07.015subject
Has Abstractpub_date
2013-09-15 00:00:00pages
60-7eissn
0166-4328issn
1872-7549pii
S0166-4328(13)00414-2journal_volume
253pub_type
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