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- Title
Chronic Sustained Hypoxia Enhances Both Evoked EPSCs and Norepinephrine Inhibition of Glutamatergic Afferent Inputs in the Nucleus of the Solitary Tract.
- Authors
Weirong Zhang; Carreño, Flávia R.; Cunningham, J. Thomas; Mifflin, Steve W.
- Abstract
The nucleus of the solitary tract (NTS) receives inputs from both arterial chemoreceptors and central noradrenergic neural structures activated during hypoxia. We investigated norepinephrine (NE) modulation of chemoreceptor afferent integration after a chronic exposure to sustained hypoxia (CSH) (7- 8 d at 10% FIO2 ). Whole-cell recordings of NTS second-order neurons identified by DiA (1,1′- dilinoleyl-3,3,3′,3′-tetra-methylindocarbocyanine, 4-chlorobenzenesulphonate) labeling of carotid bodies were obtained in a brain slice. Electrical stimulation of the solitary tract was used to evoke EPSCs. CSH exposure increased evoked EPSC (eEPSC) amplitude via both presynaptic and postsynaptic mechanisms.NEdose dependently decreased the amplitude of eEPSCs.NEincreased the paired-pulse ratio of eEPSCs and reduced the frequency of miniature EPSCs, suggesting a presynaptic mechanism.EC50 of NEinhibition of eEPSCs was lower in CSH cells (3.0±0.9μM; n=5) than in normoxic (NORM) cells (7.6±1.0μM; n=7; p<0.01). NE (10μM) elicited greater inhibition of eEPSCs in CSH cells (63±2%; n=16) than NORM cells (45±3%; n=21; p<0.01). The α-adrenoreceptor antagonist phentolamine abolished NE inhibition of eEPSCs. CSH enhanced the α2-adrenoreceptor agonist clonidine-mediated inhibition (3 μM; NORM, 23±2%, n=5 vs CSH, 44±5%, n=4; p<0.05) but attenuated α1-adrenoreceptor agonist phenylephrine-mediated inhibition (40 μM; NORM, 36±2%, n=11 vs CSH, 26±4%, n=6; p<0.05). The α2-adrenoreceptor antagonist yohimbine abolished CSH-induced enhancement of NE inhibition of eEPSCs. These results demonstrate that CSH increases evoked excitatory inputs to NTS neurons receiving arterial chemoreceptor inputs. CSH also enhances NE inhibition of glutamate release from inputs to these neurons via presynaptic α2- adrenoreceptors. These changes represent central neural adaptations to CSH.
- Subjects
SOLITARY nucleus; CEREBRAL anoxia; AUDITORY evoked response; CHEMORECEPTORS; SENSORY receptors; NORADRENERGIC neurons; NORADRENERGIC mechanisms
- Publication
Journal of Neuroscience, 2009, Vol 29, Issue 10, p3093
- ISSN
0270-6474
- Publication type
Article
- DOI
10.1523/JNEUROSCI.2648-08.2009