Activity of tryptophan hydroxylase and content of indolamines in discrete brain regions after a long-term hypoxic exposure in the rat

Poncet, Ludovic; Denoroy, Luc; Dalmaz, Y.; Péquignot, Jean-Marc

doi:10.1016/s0006-8993(97)00520-9

Cited by 32 publications

(21 citation statements)

References 41 publications

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“…On the other hand, prolonged exposures to CH affected TPH activity in the brain in a region-dependent manner. Thus CH (10% O 2 for 14 days) decreased TPH activity in the dorsal and median raphe, striatum, dorsomedian medulla oblongata, the locus coeruleus, and the anterior hypothalamic nucleus, whereas increased TPH activity in the ventrolateral medulla oblongata and the preoptic area (91). The effects of CH on TPH 1 and TPH 2 isoforms, however, remain to be studied.…”

Section: Effects Of Hypoxia On 5-ht Synthesismentioning

confidence: 94%

Hypoxia. 3. Hypoxia and neurotransmitter synthesis

Kumar

2011

American Journal of Physiology-Cell Physiology

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Central and peripheral neurons as well as neuroendocrine cells express a variety of neurotransmitters/modulators that play critical roles in regulation of physiological systems. The synthesis of several neurotransmitters/ modulators is regulated by O2-requiring rate-limiting enzymes. Consequently, hypoxia resulting from perturbations in O2 homeostasis can affect neuronal functions by altering neurotransmitter synthesis. Two broad categories of hypoxia are frequently encountered: continuous hypoxia (CH) and intermittent hypoxia (IH). CH is often seen during high altitude sojourns, whereas IH is experienced in sleep-disordered breathing with recurrent apneas (i.e., brief, repetitive cessations of breathing). This article presents what is currently known on the effects of both forms of hypoxia on neurotransmitter levels and neurotransmitter synthesizing enzymes in the central and peripheral nervous systems. biogenic amines; bioactive peptides; glutamate; ␥-amino butyric acid; gasotransmitters THE MAMMALIAN BRAIN represents 2% of the total body weight and consumes 20% of the total body oxygen for its normal function (108). This high level of oxygen consumption makes the brain an extremely sensitive tissue to changes in arterial blood oxygen levels. Many physiological systems are regulated by the nervous system, and neurotransmitters are critical for neuronal function. The rate-limiting enzymes associated with the synthesis of several neurotransmitters require molecular oxygen for their activity. Consequently, hypoxia (i.e., reduced oxygen availability) resulting from perturbations in O 2 homeostasis can profoundly impact neurotransmitter synthesis resulting in altered neuronal functions and consequently impact physiological systems.Hypoxia is experienced in a variety of physiological and pathological conditions. Two broad categories of hypoxia are most frequently encountered; continuous hypoxia (CH) and intermittent hypoxia (IH). For instance, CH is experienced by healthy humans during high altitude sojourns, whereas IH is encountered during sleep-disordered breathing with recurrent apneas; i.e., brief repetitive cessations of breathing wherein each episode lasts for tens of seconds. The purpose of this article is to provide a brief review of the effects of both forms of hypoxia on neurotransmitter levels, rate-limiting enzymes associated with neurotransmitter synthesis and the underlying mechanisms. Several of these molecules, which function as transmitters/modulators in the nervous system, are also expressed in nonneuronal tissues. However, because of space constraints, this review will focus on the effects of hypoxia on neurotransmitters in the central and peripheral nervous systems.Based on the chemical properties, neurotransmitters are divided into various groups as shown in Table 1. This review focuses on the impact of CH and IH on the synthesis of biogenic amines, acetylcholine, excitatory and inhibitory amino acids, bioactive peptides, and gasotransmitters (for examples see Table 1). BIOGENIC AMINESBiogenic ...

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Section: Effects Of Hypoxia On 5-ht Synthesismentioning

confidence: 94%

Hypoxia. 3. Hypoxia and neurotransmitter synthesis

Kumar

2011

American Journal of Physiology-Cell Physiology

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“…On the other hand, the ratio of the concentrations of 5-HIAA to 5-HT was not calculated, since this ratio may not be an accurate index of 5-HT turnover in long-term hypoxic rats [24].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, some of these CB-independent changes may also be secondary to morphological alterations induced by hypoxia. In this respect, the surface of the interface between the extraneuronal medium and the capillary system is enhanced following the angiogenesis and the higher capillary density [12], and should allow an increased clearance of 5-HIAA from blood and consequently a lowered tissue 5-HIAA content in hypoxic rats [24]. Moreover, the increased NPY-LI level in the striatum of hypoxic rats could also be linked to an increased capillary density, since NPY is present in striatal interneurons whose processes are often close to vascular cells [29].…”

Section: Hypoxia-induced Change Reduced By Csntmentioning

confidence: 99%

“…Moreover, the serotonin (5-hydroxytryptamine, 5-HT) content is increased in the DMM and in the frontal cortex of long-term hypoxic rats. The content of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) is decreased in the raphe nuclei, the DMM, the VLM, the hypothalamic periventricular nucleus and the frontal cortex [24].…”

Section: Introductionmentioning

confidence: 99%

“…For that purpose, rats deprived of the carotid sinus nerve (CSNT rats) as well as intact rats were exposed for 14 days to moderate normobaric hypoxia or to normoxia. Thereafter, NPY-LI and indolamines were determined in some peripheral structures (CB, superior cervical ganglia) and in discrete brain regions in which these neurotransmitters are known to be altered by longterm hypoxia in intact animals [23,24].…”

Section: Introductionmentioning

confidence: 99%

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Effects of carotid sinus nerve transection on changes in neuropeptide Y and indolamines induced by long-term hypoxia in rats

Poncet

Denoroy²,

Dalmaz

et al. 1998

Pfl�gers Archiv European Journal of Physiology

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Long-term hypoxia induces changes in neuropeptide-Y-like immunoreactivity (NPY-LI) and/or in the content of serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) at the central level. To determine whether these alterations depend on the integrity of carotid body (CB) chemoreceptors, intact rats or those whose carotid sinus nerve was transected (CSNT) were exposed to hypoxia (10% O2) or to normoxia for 14 days. Thereafter, NPY-LI, 5-HT and 5-HIAA levels in discrete brain regions were determined. The increase in NPY-LI in the ventrolateral medulla oblongata (VLM) of intact hypoxic rats was mostly abolished after CSNT and therefore is mainly mediated by CB chemoreceptors. In contrast, other hypoxia-induced changes were similar or even enhanced in CSNT as compared to intact rats and therefore do not depend on the integrity of CB chemoreceptors. This was the case for the increase of NPY-LI in the striatum and the caudal dorsomedian medulla oblongata (DMM), as well as for all the changes in 5-HT and 5-HIAA in the DMM, the VLM, the raphe nuclei, the striatum and the frontal cortex. We propose that long-term hypoxia alters brain NPY-LI and indolamine content through the stimulation of CB chemoreceptors or ancillary chemoreceptors, as well as through local biochemical or morphological mechanisms.

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Long‐term prenatal hypoxia alters maturation of brain catecholaminergic systems and motor behavior in rats

Perrin

Mamet

Scarna

et al. 2004

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In order to determine the influence of long-term prenatal hypoxia on the maturation of the brain catecholaminergic structures involved in motor and cognitive functions, pregnant rats were subjected to hypoxia (10% O2) from the 5th to 20th day of gestation. The in vivo activity of tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, was assessed, by accumulation of L-DOPA after i.p. administration of NSD-1015, in the motor cortex areas, the hippocampus, and the striatum at birth and at the 3rd, 7th, 14th, 21st, and 68th postnatal days. The motor reactivity to novelty and the circadian motor activity were measured at the 21st and 68th postnatal days. Exposure to prenatal hypoxia strongly altered the developmental pattern of in vivo TH activity in restricted noradrenergic terminals of the brain. In the 21-day-old prenatal hypoxic rats, the TH activity was reduced by 80% in the motor cortex areas and by 43% in the hippocampus, compared to control rats, while no differences could be detected in the striatum. Compared to control rats, the prenatal hypoxic pups exhibited a higher motor reactivity to novelty and a nocturnal motor hypoactivity at the 21st postnatal day. The neurochemical and behavioral alterations were no longer observed at the 68th postnatal day. The altered in vivo TH activity in the young rats might be part of the neural mechanisms contributing to the motor behavioral impairments induced by prenatal hypoxia. Long-term prenatal hypoxia could be linked to the development of psychopathologies that can be detected in infancy.

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Activity of tryptophan hydroxylase and content of indolamines in discrete brain regions after a long-term hypoxic exposure in the rat

Cited by 32 publications

References 41 publications

Hypoxia. 3. Hypoxia and neurotransmitter synthesis

Hypoxia. 3. Hypoxia and neurotransmitter synthesis

Effects of carotid sinus nerve transection on changes in neuropeptide Y and indolamines induced by long-term hypoxia in rats

Long‐term prenatal hypoxia alters maturation of brain catecholaminergic systems and motor behavior in rats

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