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Discharge evoked by N2 inhalation is increased in catecholaminergic and non‐catecholaminergic neurons in caudal NTS following chronic exposures to hypoxia
Author(s) -
HerreraRosales Myrna,
Mifflin Steve
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a562-d
Subject(s) - catecholaminergic , inhalation , catecholaminergic cell groups , chemoreceptor , hypoxia (environmental) , chemistry , reflex , medicine , anesthesia , endocrinology , neuroscience , biology , dopamine , oxygen , receptor , organic chemistry
To determine if the responses of neurons within caudal portions of the nucleus of the solitary tract (cNTS) to chemoreceptor activation are altered following chronic hypoxia, action potential (AP) discharge evoked by N 2 inhalation (2–15 sec) was recorded in cNTS neurons in Inactin anesthetized rats exposed to room air (NORM) or 10% FIO 2 (CH) for 7 days. Juxtacellular labeling with Neurobiotin followed by immunohistochemistry for tyrosine hydroxylase immunoreactivity (TH‐IR) was used to identify catecholaminergic neurons. In NORM rats, the number of APs evoked by 10sec N 2 inhalation was not different comparing 8 TH‐IR cNTS neurons (6±2 APs) and 14 cNTS neurons that were not TH‐IR (7±2 APs). Above threshold, the slope of the curve relating discharge to the duration of N 2 inhalation was 1.7±.2 APs/sec of N 2 inhalation. In CH rats, the number of APs evoked by 10sec N 2 inhalation was not different comparing 5 TH‐IR cNTS neurons (12±4 APs) and 12 cNTS neurons that were not TH‐IR (10±3 APs). Above threshold, the slope of the curve relating discharge to the duration of N 2 inhalation was 3.1±.4 APs/sec of N 2 inhalation, significantly greater than that in NORM rats (p<.05). The results indicate that discharge evoked by chemoreceptor activation is increased in cNTS neurons in rats exposed to hypoxia for 7 days. Enhanced discharge of cNTS neurons following chronic exposures to hypoxia could form a basis for enhanced chemoreflex function in chronic hypoxic states (e.g., travel to altitude, heart failure).