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Estelle B Gauda

Publications and source records attributed to Estelle B Gauda.

11 recordsLinked to original sources
PubMed2006

The effect of hyperoxia on reactive oxygen species (ROS) in rat petrosal ganglion neurons during development using organotypic slices.

Hyperoxia, during development in rats, results in hypoxic chemosensitivity ablation, carotid body hypoplasia, and reduced chemoafferents. We hypothesized that hyperoxia increases reactive oxygen species (ROS) in cell bodies of chemoafferents. Organotypic slices of petrosal-nodose ganglia from rats at day of life (DOL) 5-6 and 17-18 were exposed to 8%, 21%, or 95% O(2) for 4 h in the presence or absence of the ROS-sensitive fluorescent indicator, CM-H(2)DCFDA, and propidium iodide was used to determine the relationship between cell death and oxygen tension. In tissue slices from DOL 5-6 rats, fluorescence intensity was 182.5 +/- 2.9 for hypoxia, 217.5 +/- 3.3 for normoxia, and 336.6 +/- 3.8 for hyperoxia, (mean +/- SEM, p < 0.001, ANOVA). Normoxia increased ROS levels by 19.2% from hypoxia (p < 0.01) with a further increase of 54.8% from normoxia to hyperoxia (p < 0.001). In tissue slices from DOL 17-18 rats, ROS levels increased with increasing oxygen tension but were less than in younger animals (p < 0.01, ANOVA). The antioxidants, NAC and TEMPO-9-AC, attenuated ROS levels and cell death. Electron microscopy demonstrated that hyperoxia damages the ultrastructure within petrosal ganglion neurons. Hyperoxic-induced increased levels of ROS in petrosal ganglion neurons may contribute to loss of hypoxic chemosensitivity during early postnatal development.

Acetylcysteine↗
PubMed2006

Neonatal animal models of opiate withdrawal.

The symptoms of opiate withdrawal in infants are defined as neonatal abstinence syndrome (NAS). NAS is a significant cause of morbidity in term and preterm infants. Factors, such as polysubstance abuse, inadequate prenatal care, nutritional deprivation, and the biology of the developing central nervous system contribute to the challenge of evaluating and treating opiate-induced alterations in the newborn. Although research on the effects of opiates in neonatal animal models is limited, the data from adult animal models have greatly contributed to understanding and treating opiate tolerance, addiction, and withdrawal in adult humans. Yet the limited neonatal data that are available indicate that the mechanisms involved in these processes in the newborn differ from those in adult animals, and that neonatal models of opiate withdrawal are needed to understand and develop effective treatment regimens for NAS. In this review, the behavioral and neurochemical evidence from the literature is presented and suggests that mechanisms responsible for opiate tolerance, dependence, and withdrawal differ between adult and neonatal models. Also reviewed are studies that have used neonatal rodent models, the authors' preliminary data based on the use of neonatal rat and mouse models of opiate withdrawal, and other neonatal models that have been proposed for the study of neonatal opiate withdrawal.

Age Factors↗
PubMed2004

Maturation of peripheral arterial chemoreceptors in relation to neonatal apnoea.

Apnoea and periodic breathing are the hallmarks of breathing for the infant who is born prematurely. Sustained respiration is obtained through modulation of respiratory-related neurons with inputs from the periphery. The peripheral arterial chemoreceptors, uniquely and reflexly change ventilation in response to changes in oxygen tension. The chemoreflex in response to hypoxia is hyperventilation, bradycardia and vasoconstriction. The fast response time of the peripheral arterial chemoreceptors to changes in oxygen and carbon dioxide tension increases the risk of more periodicity in the breathing pattern. As a result of baseline hypoxaemia, peripheral arterial chemoreceptors contribute more to baseline breathing in premature than in term infants. While premature infants may have an augmented chemoreflex, infants who develop bronchopulmonary dysplasia have a blunted chemoreflex at term gestation. The development of chemosensitivity of the peripheral arterial chemoreceptors and environmental factors that might cause maldevelopment of chemosensitivity with continued maturation are reviewed in an attempt to help explain the physiology of apnoea of prematurity and the increased incidence of sudden infant death syndrome (SIDS) in infants born prematurely and those who are exposed to tobacco smoke.

Apnea↗
PubMed2004

Cannabinoid receptor expression in peripheral arterial chemoreceptors during postnatal development.

Prenatal exposure to tobacco smoke increases risk of sudden infant death syndrome (SIDS). Marijuana is frequently smoked in conjunction with tobacco, and perinatal exposure to marijuana is associated with increased incidence of SIDS. Abnormalities in peripheral arterial chemoreceptor responses during sleep may be operative in infants at risk for SIDS, and nicotine exposure adversely affects peripheral arterial chemoreceptor responses. To determine whether marijuana could potentially affect the activity of peripheral arterial chemoreceptors during early postnatal development, we used in situ hybridization histochemistry to characterize the pattern and level of mRNA expression for cannabinoid type 1 receptor (CB1R) in the carotid body, superior cervical ganglia (SCG), and nodose-petrosal-jugular ganglia (NG-PG-JG) complex in newborn rats. We used immunohistochemistry and light, confocal, and electron microscopy to characterize the pattern of CB1R and tyrosine hydroxylase protein expression. CB1R mRNA expression was intense in the NG-PG-JG complex, low to moderate in the SCG, and sparse in the carotid body. With maturation, CB1R gene expression significantly increased (P < 0.01) in the NG-PG-JG complex. CB1R immunoreactivity was localized to nuclei of ganglion cells in the SCG and NG-PG-JG complex, whereas tyrosine hydroxylase immunoreactivity was localized to the cytoplasm. Exposure to marijuana during early development could potentially modify cardiorespiratory responses via peripheral arterial chemoreceptors. The novel finding of nuclear localization of CB1Rs in peripheral ganglion cells suggests that these receptors may have an, as yet, undetermined role in nuclear signaling in sensory and autonomic neurons.

Animals↗
PubMed2004

Autonomic microganglion cells: a source of acetylcholine in the rat carotid body.

Hypoxic chemosensitivity of peripheral arterial chemoreceptors and the ventilatory response to O2 deprivation increases with postnatal development. Multiple putative neurotransmitters, which are synthesized in the carotid body (CB), are thought to mediate signals generated by hypoxia. Acetylcholine (ACh) is believed to be a major excitatory neurotransmitter participating in hypoxic chemosensitivity. However, it is not known whether ACh originates from type I cells in the CB. In these studies, we tested the hypothesis that choline acetyltransferase (ChAT) and vesicular ACh transporter (VAChT) mRNAs are expressed in the CB and that mRNA levels would increase with postnatal maturation or exposure to hypoxia. Semiquantitative in situ hybridization histochemistry and immunohistochemistry were used to localize cholinergic markers within neurons and cells of the rat CB, the nodose-petrosal-jugular ganglion complex, and the superior cervical ganglion up to postnatal day 28. We show that the pattern of distribution, in tissue sections, is similar for both ACh markers; however, the level of VAChT mRNA is uniformly greater than that of ChAT. VAChT mRNA and immunoreactivity are detected abundantly in the nodose-petrosal-jugular ganglion complex in a number of microganglion cells embedded in nerve fibers innervating the CB for all postnatal groups, whereas ChAT mRNA is detected in only a few of these cells. Contrary to our hypothesis, postnatal maturation caused a reduction in ACh trait expression, whereas hypoxic exposure did not induce the upregulation of VAChT and ChAT mRNA levels in the CB, microganglion, or within the ganglion complex. The present findings indicate that the source of ACh in the CB is likely within autonomic microganglion cells and cholinergic nerve terminals.

Acetylcholine↗
PubMed2002

Gene expression in peripheral arterial chemoreceptors.

The peripheral arterial chemoreceptors of the carotid body participate in the ventilatory responses to hypoxia and hypercapnia, the arousal responses to asphyxial apnea, and the acclimatization to high altitude. In response to an excitatory stimuli, glomus cells in the carotid body depolarize, their intracellular calcium levels rise, and neurotransmitters are released from them. Neurotransmitters then bind to autoreceptors on glomus cells and postsynaptic receptors on chemoafferents of the carotid sinus nerve. Binding to inhibitory or excitatory receptors on chemoafferents control the electrical activity of the carotid sinus nerve, which provides the input to respiratory-related brainstem nuclei. We and others have used gene expression in the carotid body as a tool to determine what neurotransmitters mediate the response of peripheral arterial chemoreceptors to excitatory stimuli, specifically hypoxia. Data from physiological studies support the involvement of numerous putative neurotransmitters in hypoxic chemosensitivity. This article reviews how in situ hybridization histochemistry and other cellular localization techniques confirm, refute, or expand what is known about the role of dopamine, norepinephrine, substance P, acetylcholine, adenosine, and ATP in chemotransmission. In spite of some species differences, review of the available data support that 1). dopamine and norepinephrine are synthesized and released from glomus cells in all species and play an inhibitory role in hypoxic chemosensitivity; 2). substance P and acetylcholine are not synthesized in glomus cells of most species but may be made and released from nerve fibers innervating the carotid body in essentially all species; 3). adenosine and ATP are ubiquitous molecules that most likely play an excitatory role in hypoxic chemosensitivity.

Animals↗
PubMed2002

CO(2)-induced c-Fos expression in brainstem preprotachykinin mRNA containing neurons.

Tachykinin peptides are found in brainstem regions involved in central chemoreception and they may play a modulatory role in ventilatory response to hypercapnia. We determined whether tachykinin peptide containing neurons are activated by CO(2) by combining in situ hybridization and immunohistochemistry (IHH). Experiments were performed in 21-day-old rats exposed to 12% CO(2) for 1 h. c-Fos expression was identified by IHH on free floating sections (40 microm) that were mounted and then hybridized with anti-sense 35S labeled ribonucleotide probe of the rat preprotachykinin A (PPT-A) gene. Sections were analyzed for expression of the PPT-A gene, c-Fos protein and colocalization of PPT-A gene with c-Fos protein. Within the chemosensory region of the nucleus tractus solitarius (nTS), 19% of c-Fos positive cells expressed PPT-A mRNA after hypercapnic loading. In medullary raphe nuclei, 64% of c-Fos positive cells expressed the PPT-A gene after exposure to CO(2), while 21% of c-Fos labeled neurons in parapyramidal nuclei also expressed PPT-A mRNA. These results indicate that a subpopulation of CO(2) activated neurons within the nTS and in the parapyramidal and midline regions of the ventral aspect of the medulla oblongata express the PPT-A gene, suggesting that these are substance P- or neurokinin A-containing neurons. Furthermore, these peptides may play a role in modulation of respiratory and cardiovascular responses to changes in CO(2)/H(+) content of the extracellular fluid.

Animals↗
PubMed2002

Differential CO(2)-induced c-fos gene expression in the nucleus tractus solitarii of inbred mouse strains.

Genetic determinants confer variation between inbred mouse strains with respect to the magnitude and pattern of ventilation during hypercapnic challenge. Specifically, inheritance patterns derived from low-responsive C3H/HeJ (C3) and high-responsive C57BL/6J (B6) mouse strains suggest that differential hypercapnic ventilatory sensitivity (HCVS) is controlled by two independent genes. The present study also tests whether differential neuronal activity in respiratory control regions of the brain is positively associated with strain variation in HCVS. With the use of whole body plethysmography, ventilation was assessed in C3 and B6 strains at baseline and during 30 min of hypercapnia (inspired CO(2) fraction = 0.15, inspired O(2) fraction = 0.21 in N(2)). Subsequently, in situ hybridization histochemistry was performed to determine changes in c-fos gene expression in the commissural subnucleus of the nucleus tractus solitarius (NTS). During hypercapnia, breathing frequency and tidal volume were significantly (P < 0.01) different between strains: C3 mice showed a slow, deep-breathing pattern relative to a rapid, shallow phenotype of B6 mice. CO(2)-induced increase in c-fos gene expression was significantly (P < 0.01) greater in NTS regions of B6 compared with C3 mice. In this genetic model of differential HCVS, the results suggest that a genomic basis for varied hypercapnic chemoreception or transduction confers greater afferent neuronal activity in the caudal NTS for high-responsive B6 mice compared with low-responsive C3 mice.

Animals↗
PubMedDate not supplied

Ontogeny of retrograde labeled chemoafferent neurons in the newborn rat nodose-petrosal ganglion complex: an ex vivo preparation.

Hypoxic chemosensitivity of the peripheral arterial chemoreceptors in the carotid body is developmentally regulated. Essential neural elements of the chemotransducing unit in the carotid body consist of the Type I cell that depolarizes and releases neurotransmitters in response to hypoxemia and the chemoafferent fibers which form synapses with Type I cells, contain postsynaptic receptors and have cell bodies in the petrosal ganglion. While many properties of the Type I cells have been characterized during postnatal development, less is known about the effect of development on the number and properties of the chemoafferents since localization of the cell bodies of chemoafferents are intermingled with the cell bodies of other sensory neurons that innervate the upper airway. Here, we describe a novel ex vivo preparation that we have developed to retrogradely label cell bodies of chemoafferents in the petrosal ganglion with rhodamine dextran. With this technique, in newborn rats, we show that there is a three-fold increase in retrogradely labeled neurons in the nodose-petrosal ganglion complex from postnatal day (PND) 3-7 with a three-fold decrease by PND 14 (P < 0.001, ANOVA). Furthermore, greater than 85% of these retrogradely labeled neurons co-express TH mRNA in all age groups. This novel ex vivo technique circumvents many of the technical difficulties encountered with retrogradely labeling chemoafferents in small newborn animals in vivo, and provides a method to identify and characterize essential neural components of the chemotranductive unit of the peripheral arterial chemoreceptors.

Age Factors↗