Blog
About

12
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Postnatal development of neural chemoafferent pathway and respiration is altered following prenatal nicotine exposure in rats

      , 2 , 2 , 2 , 2 , 1 , 2 , 1 , 2

      Respiratory Research

      BioMed Central

      Neural Control of Breathing

      1-4 September 2001

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Related collections

          Most cited references 3

          • Record: found
          • Abstract: found
          • Article: not found

          Cholinergic receptors in heart and brainstem of rats exposed to nicotine during development: implications for hypoxia tolerance and perinatal mortality.

          Cigarette smoking during pregnancy increases the incidence of perinatal mortality and Sudden Infant Death Syndrome (SIDS). We have evaluated prenatal or postnatal nicotine exposure in developing rats to examine the potential role of altered neurotransmitter receptor expression in these processes. Pregnant rats received continuous infusions of nicotine throughout gestation, at doses mimicking the plasma levels found in smokers. After birth, cardiac M2-muscarinic cholinergic receptors, which are responsible for inhibitory autonomic actions, were enhanced in the nicotine group, coincidentally with decreases in stimulatory beta-adrenergic receptors that have been demonstrated previously. Studies of adenylyl cyclase activity confirmed that the changes in receptor binding represented functional alterations: the stimulatory response to isoproterenol was obtunded by prenatal nicotine exposure, whereas the inhibitory response to carbachol was enhanced. Elevations of M2-muscarinic receptor binding were not generalized to all tissues, as the same prenatal nicotine treatment elicited a reduction in these receptors in the brainstem, an effect that has also been noted in infants who died of SIDS; we found no effects of prenatal nicotine on brainstem M1-receptor binding. Postnatal administration of nicotine produced similar brainstem receptor effects when treatment was conducted during the first postnatal week but not thereafter; postnatal nicotine treatment did not affect cardiac M2-receptor binding. Thus, during a critical developmental period, nicotine exposure produces cardiac and brainstem receptor imbalances that favor inhibitory responses, effects that can contribute to morbidity and mortality evoked by hypoxic episodes, such as those experienced during parturition, sleep apnea or airway obstruction. Copyright 1999 Elsevier Science B.V.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

            The drive on respiration mediated by the peripheral arterial chemoreceptors was assessed by the hyperoxic test in 3-day-old rat pups. They accounted for 22.5 +/- 8.8% during control conditions, but only for 6.9 +/- 10.0% after nicotine exposure, an effect counteracted by blockade of peripheral dopamine type 2 receptors (DA2Rs). Furthermore, nicotine reduced dopamine (DA) content and increased the expression of tyrosine hydroxylase (TH) in the carotid bodies, further suggesting that DA mediates the acute effect of nicotine on arterial chemoreceptor function. During postnatal development TH and DA2R mRNA levels in the carotid bodies decreased. Thus, nicotine from smoking may also interfere with the postnatal resetting of the oxygen sensitivity of the peripheral arterial chemoreceptors by increasing carotid body TH mRNA, as well as DA release in this period. Collectively these effects of nicotine on the peripheral arterial chemoreceptors may increase the vulnerability to hypoxic episodes and attenuate the protective chemoreflex response. These mechanisms may underlie the well-known relation between maternal smoking and sudden infant death syndrome.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Dynamic ventilatory responses in rats: normal development and effects of prenatal nicotine exposure.

              Infants of smoking mothers are at increased risk of SIDS, one cause of which is thought to be due to impaired ventilatory responses. We tested the hypotheses that prenatal nicotine exposure impairs the development of dynamic carotid chemoreceptor-driven ventilatory responses, and reduces the ability to lower metabolic rate in hypoxia. Osmotic minipumps were implanted into 20 pregnant rats at day 3 of gestation to deliver nicotine (6 mg/kg per day free base) or saline for 4 weeks. Minute ventilation was recorded breath by breath in rat pups at 3, 8 and 18 days (n = 6, 8 and 6) postnatal in response to 5-sec challenges of 100% O2 (Dejours test) and 5% O2 + 5% CO2. Carotid sinus nerve (CSN) responses to hypoxia and CO2 were recorded from 22 control and 17 nicotine-exposed preparations at ages between 3-20 days. Oxygen consumption (V(O)2) was measured in groups of pups at 3 days (n = 7 each for nicotine and control) and 8 days (n = 5 each for nicotine and control) in room air and 10% O2. There was no detectable effect of nicotine exposure on the development of CSN responses. Ventilatory responses to 5% O2-5% CO2 increased with age but did not differ between nicotine and control groups. Ventilatory responses to 100% O2 were unaffected by nicotine exposure at 8 and 18 days. However, the 3-day nicotine group showed no significant response to 100% O2 whereas V(E) was significantly reduced in the control group by 100% O2. There was no significant effect of nicotine exposure on the ability to reduce oxygen consumption in hypoxia at 3 or 8 days, but at 3 days, baseline (room air) variability in oxygen consumption was greater in the nicotine group. We conclude that nicotine exposure appears to result in abnormal ventilatory responses to withdrawal of baseline peripheral chemoreceptor drive during a period of early postnatal life. We speculate that a transient abnormality could contribute to a period of instability and increased vulnerability to challenges.
                Bookmark

                Author and article information

                Affiliations
                [1 ]Department of Woman and Child Health, Karolinska Institute, S17176 Stockholm, Sweden
                [2 ]Laboratoire de Physiologie, UMR CNRS 5578, 8 avenue Rockefeller, 69008 Lyon, France
                Conference
                Respir Res
                Respir. Res
                Respiratory Research
                BioMed Central
                1465-9921
                1465-993X
                2001
                17 August 2001
                : 2
                : Suppl 1
                : P16
                3402863 rr132 10.1186/rr132
                Copyright ©2001 BioMed Central Ltd
                Neural Control of Breathing
                Rotorua, New Zealand
                1-4 September 2001
                Categories
                Poster Presentation

                Respiratory medicine

                Comments

                Comment on this article