Regional specificity of the long-term regulation of tyrosine hydroxylase in some catecholaminergic rat brainstem areas. I. Influence of long-term hypoxia

Schmitt, Pascal; Garcia, Christine; Pujol, J.F.; Péquignot, Jean-Marc

doi:10.1016/0006-8993(93)91776-o

Cited by 24 publications

(14 citation statements)

References 47 publications

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“…CSH increased the activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, in the NTS including A2 cell group (Pepin et al, 1996; Soulier et al, 1995), the ventrolateral medulla (Schmitt et al, 1993) and the locus coeruleus (Schmitt et al, 1993). Furthermore, CSH increased NE turnover in A2 cell group, but decreased that in A5 cell group and locus coeruleus with no significant effect in A1 cell group (Soulier et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Chronic Sustained Hypoxia Enhances Both Evoked EPSCs and Norepinephrine Inhibition of Glutamatergic Afferent Inputs in the Nucleus of the Solitary Tract

Zhang

Carreño²,

Cunningham³

et al. 2009

J. Neurosci.

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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% FIO 2 ). Whole-cell recordings of NTS second-order neurons identified by DiA (1,1Ј-dilinoleyl-3,3,3Ј,3Ј-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. NE dose dependently decreased the amplitude of eEPSCs. NE increased the paired-pulse ratio of eEPSCs and reduced the frequency of miniature EPSCs, suggesting a presynaptic mechanism. EC 50 of NE inhibition of eEPSCs was lower in CSH cells (3.0 Ϯ 0.9 M; n ϭ 5) than in normoxic (NORM) cells (7.6 Ϯ 1.0 M; n ϭ 7; p Ͻ 0.01). NE (10 M) elicited greater inhibition of eEPSCs in CSH cells (63 Ϯ 2%; n ϭ 16) than NORM cells (45 Ϯ 3%; n ϭ 21; p Ͻ 0.01). The ␣-adrenoreceptor antagonist phentolamine abolished NE inhibition of eEPSCs. CSH enhanced the ␣2-adrenoreceptor agonist clonidine-mediated inhibition (3 M; NORM, 23 Ϯ 2%, n ϭ 5 vs CSH, 44 Ϯ 5%, n ϭ 4; p Ͻ 0.05) but attenuated ␣1-adrenoreceptor agonist phenylephrine-mediated inhibition (40 M; NORM, 36 Ϯ 2%, n ϭ 11 vs CSH, 26 Ϯ 4%, n ϭ 6; p Ͻ 0.05). The ␣2-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 ␣2-adrenoreceptors. These changes represent central neural adaptations to CSH.

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Section: Discussionmentioning

confidence: 99%

Chronic Sustained Hypoxia Enhances Both Evoked EPSCs and Norepinephrine Inhibition of Glutamatergic Afferent Inputs in the Nucleus of the Solitary Tract

Zhang

Carreño²,

Cunningham³

et al. 2009

J. Neurosci.

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“…1987; Finley & Katz, 1992). Long‐term hypoxia stimulates selectively the noradrenaline turnover and increases the TH amount in the caudal A2/C2 subset, whereas hypotension activates the catecholaminergic neurons in the rostral A2/C2 subset (Schmitt et al . 1993a; 1993b).…”

Section: Discussionmentioning

confidence: 99%

“…1993). By contrast, the amount of TH protein was increased after 14 days of sustained hypoxia and was unaffected by acute hypoxia (Schmitt et al . 1993a).…”

Section: Discussionmentioning

confidence: 99%

O₂‐sensing after carotid chemodenervation: hypoxic ventilatory responsiveness and upregulation of tyrosine hydroxylase mRNA in brainstem catecholaminergic cells

Roux

Péquignot

Dumas

et al. 2000

Eur J of Neuroscience

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Ventilatory responses to acute and long-term hypoxia are classically triggered by carotid chemoreceptors. The chemosensory inputs are carried within the carotid sinus nerve to the nucleus tractus solitarius and the brainstem respiratory centres. To investigate whether hypoxia acts directly on brainstem neurons or secondarily via carotid body inputs, we tested the ventilatory responses to acute and long-term hypoxia in rats with bilaterally transected carotid sinus nerves and in sham-operated rats. Because brainstem catecholaminergic neurons are part of the chemoreflex pathway, the ventilatory response to hypoxia was studied in association with the expression of tyrosine hydroxylase (TH). TH mRNA levels were assessed in the brainstem by in situ hybridization and hypoxic ventilatory responses were measured in vivo by plethysmography. After long-term hypoxia, TH mRNA levels in the nucleus tractus solitarius and ventrolateral medulla increased similarly in chemodenervated and sham-operated rats. Ventilatory acclimatization to hypoxia developed in chemodenervated rats, but to a lesser extent than in sham-operated rats. Ventilatory response to acute hypoxia, which was initially low in chemodenervated rats, was fully restored within 21 days in long-term hypoxic rats, as well as in normoxic animals which do not overexpress TH. Therefore, activation of brainstem catecholaminergic neurons and ventilatory adjustments to hypoxia occurred independently of carotid chemosensory inputs. O2-sensing mechanisms unmasked by carotid chemodenervation triggered two ventilatory adjustments: (i) a partial acclimatization to long-term hypoxia associated with TH upregulation; (ii) a complete restoration of acute hypoxic responsivity independent of TH upregulation.

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“…Previous studies from our laboratory support a functional subdivision of noradrenergic neurons within the NTS. The caudal A 2 subset is indeed selectively affected by carotid chemosensory inputs, whereas the rostral part of A 2 is affected by pharmacological handling of arterial blood pressure [27][28][29]31]. In this context, the ovariectomy-induced alterations of noradrenergic activity in the caudal A 2 portion might be consecutive to stimulation of primary chemosensory afferents rather than to a direct effect of female steroids on NTS neurons.…”

Section: Neurochemical Studiesmentioning

confidence: 95%

“…In addition, noradrenergic neurons located in the ventrolateral medulla, an area that is reciprocally connected with the NTS, constitute the A 1 cell group and are intricate with neurons of the ventral respiratory group. The neural activity of both cell groups can be altered by exposure to hypoxia [27,29,31]. Other medullary noradrenergic cell groups, the locus coeruleus (A 6 ) and A 5 in the pons medulla are reciprocally connected with the NTS and are also affected by carotid chemoreceptor stimulation [9,31].…”

Section: Introductionmentioning

confidence: 99%

Influence of gender and endogenous sex steroids on catecholaminergic structures involved in physiological adaptation to hypoxia

Pequignot

Spielvogel

Caceres

et al. 1997

Pfl�gers Archiv European Journal of Physiology

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Mechanisms underlying sex-related differences in adaptation to high altitude were investigated by assessing the turnover of dopamine and noradrenaline in structures of the chemoafferent pathway, i.e. carotid body and brainstem noradrenergic cell groups (A1, A5, A6, A2 to which chemosensory fibres project). The influence of gender was assessed in male and female rats reared at an altitude of 3600 m, whereas the influence of endogenous sex hormones was evaluated by castration. Haematocrit, red blood cell count and plasma erythropoietin levels were lower in females than in males (-5%, -15%, -53%, respectively). Dopamine and noradrenaline turnover were higher in female structures (carotid body: +51%; A2: +140%; A1: +54%; A5: +27%). Dopamine and noradrenaline turnover in carotid body and brainstem cell groups were differently affected by castration, i. e. enhanced by orchidectomy (carotid body: +134%; A2: +120%; A1: +69%; A5: +67%) but inhibited by ovariectomy (carotid body: -33%; A2: -92%). Orchidectomy elicited a reduction in haematocrit (-10%), haemoglobin concentration (-8%) and red blood cell count (-24%), whereas haematological status remained unaltered after ovariectomy. Therefore, both gender and endogenous sex steroids may control catecholamine activity differently in structures involved in the chemoafferent pathway, thus providing a neurochemical basis for sex-related differences in adaptation to hypoxia.

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Regional specificity of the long-term regulation of tyrosine hydroxylase in some catecholaminergic rat brainstem areas. I. Influence of long-term hypoxia

Cited by 24 publications

References 47 publications

Chronic Sustained Hypoxia Enhances Both Evoked EPSCs and Norepinephrine Inhibition of Glutamatergic Afferent Inputs in the Nucleus of the Solitary Tract

Chronic Sustained Hypoxia Enhances Both Evoked EPSCs and Norepinephrine Inhibition of Glutamatergic Afferent Inputs in the Nucleus of the Solitary Tract

O₂‐sensing after carotid chemodenervation: hypoxic ventilatory responsiveness and upregulation of tyrosine hydroxylase mRNA in brainstem catecholaminergic cells

Influence of gender and endogenous sex steroids on catecholaminergic structures involved in physiological adaptation to hypoxia

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Regional specificity of the long-term regulation of tyrosine hydroxylase in some catecholaminergic rat brainstem areas. I. Influence of long-term hypoxia

Cited by 24 publications

References 47 publications

Chronic Sustained Hypoxia Enhances Both Evoked EPSCs and Norepinephrine Inhibition of Glutamatergic Afferent Inputs in the Nucleus of the Solitary Tract

Chronic Sustained Hypoxia Enhances Both Evoked EPSCs and Norepinephrine Inhibition of Glutamatergic Afferent Inputs in the Nucleus of the Solitary Tract

O2‐sensing after carotid chemodenervation: hypoxic ventilatory responsiveness and upregulation of tyrosine hydroxylase mRNA in brainstem catecholaminergic cells

Influence of gender and endogenous sex steroids on catecholaminergic structures involved in physiological adaptation to hypoxia

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O₂‐sensing after carotid chemodenervation: hypoxic ventilatory responsiveness and upregulation of tyrosine hydroxylase mRNA in brainstem catecholaminergic cells