Differential effects of long-term hypoxia on norepinephrine turnover in brain stem cell groups

Abstract

The influence of long-term hypoxia on noradrenergic cell groups in the brain stem was assessed by estimating the changes in norepinephrine (NE) turnover in A1, A2 (subdivided into anterior and posterior parts), A5, and A6 groups in rats exposed to hypoxia (10% O2-90% N2) for 14 days. The NE turnover was decreased in A5 and A6 groups but failed to change significantly in A1. The NE turnover was increased in the posterior part of A2 and remained unaltered in the anterior part. In normoxic rats, the hypotensive drug dihydralazine induced a reverse effect, namely increased NE turnover in anterior A2 and no change in posterior A2. The neurochemical responses to hypoxia were abolished by transection of carotid sinus nerves. The results show that long-term hypoxia exerts differential effects on the noradrenergic cell groups located in the brain stem. Peripheral chemosensory inputs control the hypoxia-induced noradrenergic alterations. The A2 cell group displays a functional subdivision: the posterior part is influenced by peripheral chemosensory inputs, whereas the anterior part may be concerned with barosensitivity.

Modulation of Synaptic Transmission to Second-Order Peripheral Chemoreceptor Neurons in Caudal Nucleus Tractus Solitarius by α1-Adrenoreceptors

“…Chronic intermittent cold exposure significantly increased ␣ 1 -adrenoreceptor-mediated responses in the paraventricular nucleus of the hypothalamus without significant changes in extracellular NE levels, suggesting enhanced ␣ 1 -adrenoreceptor sensitivity (Ma and Morilak, 2005). Chronic sustained hypoxia increases the activity and expression of tyrosine hydroxylase in the NTS (Soulier et al, 1992;Schmitt et al, 1994). If this results in increased NE release within the NTS, ␣ 1 -adrenoreceptormediated inhibition could provide neuroprotection to secondorder neurons receiving increased excitatory afferent inputs from peripheral chemoreceptors.…”

Role of nitric oxide in hypoxia-induced hyperventilation and hypothermia: participation of the locus coeruleus

“…In a wide variety of animal species, hypoxia elicits a number of compensatory responses, including increased ventilation and cardiac output (5). Decreases in PaO 2 are monitored by peripheral arterial chemoreceptors that evoke excitation of chemosensory fibers projecting in the brainstem within the nucleus tractus solitarius (NTS) (12). In the brainstem, these afferent inputs are processed and integrated together with other inputs to yield a final command to the respiratory motoneurons resulting in an increase in respiratory drive (22).…”

“…Activity in LC neurons is highest during wakefulness, particularly under conditions requiring increased alertness (28). The major component of adaptive responses to hypoxia is the stimulation of the sympathoadrenal system (9,11), and sympathetic neurons are under the control of noradrenergic cell groups located in the brainstem (12), where the LC is the major noradrenergic nucleus. Recently, it has been reported that noradrenergic LC neurons send axons to spinal motoneurons, where they may participate in the control of respiratory movements (29).…”

“…Sympathetic neurons receive both excitatory and inhibitory influences from noradrenergic cell groups located in the brainstem (12). The locus coeruleus (LC), a pair of nuclei located in the pons, is an assembly of densely packed noradrenergic neurons; its extensive projections provide noradrenergic innervation to many brain areas and to the spinal cord (13).…”

Long‐term influence of neonatal hypoxia on catecholamine activity in carotid bodies and brainstem cell groups of the rat.

“…This region contains a well-defined group of noradrenergic neurones called the A2 cell group (Dahlstr6m & Fuxe, 1964). Previous studies from our laboratory have indicated that in adult rats, A2 neural activity is altered by hypoxia (Soulier, Cottet-Emard, Pequignot, Hanchin, Peyrin & Pequignot, 1992) and may be involved in the control of ventilatory acclimatization to highi altitude (Schmitt, Soulier, Pequignot, Pujol & Denavit-Saubie, 1994). In addition to A2, other noradrenergic cell groups of the brainstem (Al, A5 and A6 or locus coeruleus) display changes in their neural activity during hypoxia (Soulier et al 1992).…”