Central dopamine modulates anapyrexia but not  hyperventilation induced by hypoxia

Barros, Renata C.H.; Branco, Luiz G.S.

doi:10.1152/japplphysiol.00852.2001

Cited by 22 publications

(11 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Central dopamine affects thermal and metabolic responses to hypoxia without affecting hyperventilation (35), which is the opposite of the present results, i.e., L-glutamate affecting ventilation but not Tb. Therefore, dopamine and Lglutamate may control each system independently.…”

Section: Thermoregulatory Response To Hypoxiacontrasting

confidence: 99%

Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia

Paula

Branco

2004

Braz J Med Biol Res

View full text Add to dashboard Cite

The interaction between pulmonary ventilation (V E ) and body temperature (Tb) is essential for O 2 delivery to match metabolic rate under varying states of metabolic demand. Hypoxia causes hyperventilation and anapyrexia (a regulated drop in Tb), but the neurotransmitters responsible for this interaction are not well known. Since L-glutamate is released centrally in response to peripheral chemoreceptor stimulation and glutamatergic receptors are spread in the central nervous system we tested the hypothesis that central L-glutamate mediates the ventilatory and thermal responses to hypoxia. We measured V E and Tb in 40 adult male Wistar rats (270 to 300 g) before and after intracerebroventricular injection of kynurenic acid (KYN, an ionotropic glutamatergic receptor antagonist), α-methyl-4-carboxyphenylglycine (MCPG, a metabotropic glutamatergic receptor antagonist) or vehicle (saline), followed by a 1-h period of hypoxia (7% inspired O 2 ) or normoxia (humidified room air). Under normoxia, KYN (N = 5) or MCPG (N = 8) treatment did not affect V E or Tb compared to saline (N = 6). KYN and MCPG injection caused a decrease in hypoxiainduced hyperventilation (595 ± 49 for KYN, N = 7 and 525 ± 84 ml kg -1 min -1 for MCPG, N = 6; P < 0.05) but did not affect anapyrexia (35.3 ± 0.2 for KYN and 34.7 ± 0.4ºC for MCPG) compared to saline (912 ± 110 ml kg -1 min -1 and 34.8 ± 0.2ºC, N = 8). We conclude that glutamatergic receptors are involved in hypoxic hyperventilation but do not affect anapyrexia, indicating that L-glutamate is not a common mediator of this interaction.

show abstract

Section: Thermoregulatory Response To Hypoxiacontrasting

confidence: 99%

Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia

Paula

Branco

2004

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…DA‐2 receptor mRNA is expressed in the carotid body in type 1 glomus cells as well as in sensory neurons of the petrosal ganglion that innervate the carotid body (21, 22). Whether the predominant action of dopamine on DA‐2 receptors occurs presyn‐aptically or postsynaptically is unclear; however, the net effect of activation of DA‐2 receptors at the carotid body is to cause an inhibition of the tonic discharge of the sensory nerves and a reduction in respiratory frequency (10). DAT —/— mice are under the influence of high levels of dopamine throughout their development, and although mRNA and protein levels of postsynaptic DA‐1 and DA‐2 receptors are down‐regulated by 50% (14), specific populations of these receptors are supersensitive (14, 17), resulting in an overall effect of hyperdopaminergic tone.…”

Section: Discussionmentioning

confidence: 99%

A murine model of hyperdopaminergic state displays altered respiratory control

Vincent¹,

Waddell²,

Caron

et al. 2007

FASEB j.

View full text Add to dashboard Cite

The dopamine transporter (DAT) protein plays an important role in the termination of dopamine signaling. We addressed the hypothesis that loss of DAT function would result in a distinctive cardiorespiratory phenotype due to the significant role of dopamine in the control of breathing, especially with respect to chemical control, metabolism, and thermoregulation. The DAT knockout mouse (DAT-/-) displays a state of functional hyperdopaminergia characterized by marked novelty driven hyperactivity. Certain behavioral and drug responses in these mice are reminiscent of endophenotypes of individuals with attention deficit hyperactivity disorders (ADHD). We performed experiments on conscious, unrestrained DAT-/- mice (KO) and littermate DAT+/+ wild-type (WT) controls. Ventilation was measured by the barometric technique during normoxia, hypoxia, or hypercapnia. We measured core body temperature and CO2 production as an index of metabolism. DAT-/- mice displayed a significantly lower respiratory frequency than WT mice, reflecting a prolonged inspiratory time. DAT-/- mice exhibited a reduced ventilatory response to hypoxia characterized by an attenuation of both the respiratory frequency and tidal volume responses. Both groups showed similar metabolic responses to hypoxia. Circadian measurements of body temperature were significantly lower in DAT-/- mice than WT mice during inactive periods. We conclude that loss of the DAT protein in this murine model of altered dopaminergic neurotransmission results in a significant respiratory and thermal phenotype that has possible implications for understanding of conditions associated with altered dopamine regulation.

show abstract

“…CB‐mediated hypoxic ventilation develops promptly, in less than five minutes. Limiting the observations to 10 min of hypoxia should avoid or minimize the unwanted complicating effects of longer hypoxic exposures such as hypothermia and hypometabolism (Nakano et al 2001; Barros & Branco 2002).…”

Section: Respiratory Frequency Responses To Hypoxia In Freely Moving mentioning

confidence: 99%

Ventilatory responses and carotid body function in adult rats perinatally exposed to hyperoxia

Prieto‐Lloret

Caceres

Obeso

et al. 2003

The Journal of Physiology

View full text Add to dashboard Cite

Hypoxia increases the release of neurotransmitters from chemoreceptor cells of the carotid body (CB) and the activity in the carotid sinus nerve (CSN) sensory fibers, elevating ventilatory drive. According to previous reports, perinatal hyperoxia causes CSN hypotrophy and varied diminishment of CB function and the hypoxic ventilatory response. The present study aimed to characterize the presumptive hyperoxic damage. Hyperoxic rats were born and reared for 28 days in 55%-60% O 2 ; subsequent growth (to 3.5-4.5 months) was in a normal atmosphere. The parenchyma of the carotid body (CB) is formed by chemoreceptor and sustentacular cells organized in clusters surrounded by a dense network of capillaries. Sensory nerve terminals of the carotid sinus nerve (CSN) penetrate the clusters to synapse with chemoreceptor cells (Verna, 1997). Functionally, chemoreceptor cells are activated by hypoxia and hypercapnia, and they respond with an increased release of neurotransmitters that activate the sensory nerve endings of the CSN and produce an increase in the action potential frequency in the CSN. Central projections of the CSN produce a ventilatory response, which facilitates homeostasis of blood O 2 and CO 2 levels. Catecholamines (CA) are the most abundant neurotransmitters present in chemoreceptor cells. Many groups have demonstrated that CA metabolism, including rate of synthesis and release, parallel the level of CB stimulation and action potential frequency in the CSN (Gonzalez et al. , 1994 and references therein). In adult mammals the CB is responsible for the entire hyperventilation evoked by hypoxia and for about 30-50% of the hyperventilation triggered by hypercapnia and acidosis (Cherniack & Altose 1997;Gonzalez et al. 2002a). In the intact animal a decrease in arterial P O 2 from 100 to about 75 mmHg produces only minor changes in the basal level of CSN activity or ventilation. At P O 2 below the apparent threshold of 75 mmHg there is an almost exponential increase in either response. CSN activity and ventilation double at about 50-55 mmHg, and increase by a factor of four near 40 mmHg. In the case of CO 2 the activity in the CSN and the ventilation mediated by the CB increase linearly with the P CO 2 , doubling every 15-20 mmHg (Gonzalez et al. 1994). In neonatal animals, the apparent threshold for the hypoxic response is set at a much lower P O 2 , in the range of 20-25 mmHg, i.e. at P O 2 comparable to that found in utero. At lower P O 2 , the hypoxic response increases with a lower slope than in adults. In response to elevated CO 2 there is a comparable hyposensitivity in newborn animals (Hanson & Kumar 1994;Donnelly, 1997). Functional maturation of the CB during postnatal life occurs in the first few weeks after birth, with some differences among species. In the rat, at four weeks of age the responses are fully developed (Eden & Hanson 1987a;Donnelly & Doyle 1994;Rigual et al. 2000;Donnelly, 1997). Maturation of CB function is greatly affected by the ambient P O 2 in the perinatal period. Thus, if animals ...

show abstract

Central dopamine modulates anapyrexia but not hyperventilation induced by hypoxia

Cited by 22 publications

References 34 publications

Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia

Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia

A murine model of hyperdopaminergic state displays altered respiratory control

Ventilatory responses and carotid body function in adult rats perinatally exposed to hyperoxia

Contact Info

Product

Resources

About