Browsing by Author "Bravo, Eduardo"

Now showing 1 - 3 of 3
  • No Thumbnail Available
    Item
    Functional expression of the α7 and α4-containing nicotinic acetylcholine receptors on the neonatal rat carotid body
    (2012) Meza, Rodrigo C.; Ortiz, Fernando C.; Bravo, Eduardo; Iturriaga-Vasquez, Patricio; Eugenin, Jaime L.; Varas, Rodrigo
    The carotid bodies (CBs) are chemosensory organs that respond to hypoxemia with transmitter neurosecretion, leading to a respiratory reflex response. It has been proposed that acetylcholine is a key regulator of transmitter release through activation of presynaptic nicotinic acetylcholine receptors (nAChRs). In the present work, we studied the identity of such nAChRs and their contribution to catecholamine release from CBs.
  • No Thumbnail Available
    Item
    Neuroanatomical basis of behavioral disturbances in patients with prefrontal lesions
    (2006) Slachevsky, Andrea; Pena, Marcela; Perez, Carolina; Bravo, Eduardo; Alegria, Patricia
    The role of the frontal lobe in control of behavioral and cognitive abilities is explored in a group of 34 patients with brain lesions restricted to the prefrontal cortex. The scores in both structured behavioral questionnaires and standard neuropsychological tests were analyzed using the injured area of the frontal lobe as the independent variable. Our results show that patients with simultaneous lesions in supero- and inferomedial areas of the prefrontal cortex exhibit higher behavioral disturbances. Bilateral lesions also are associated with greater behavioral troubles. On the contrary. cognitive abilities are globally impaired in prefrontal patients. Results are discussed in relation to Current models of the organization of the prefrontal cortex and its role on behavior control.
  • Thumbnail Image
    Item
    Prenatal to Early Postnatal Nicotine Exposure Impairs Central Chemoreception and Modifies Breathing Pattern in Mouse Neonates: A Probable Link to Sudden Infant Death Syndrome
    (SOC NEUROSCIENCE, 2008) Eugenin, Jaime; Otarola, Marcelo; Bravo, Eduardo; Coddou, Claudio; Cerpa, Veronica; Reyes Parada, Miguel; Llona, Isabel; von Bernhardi, Rommy
    Nicotine is a neuroteratogen and is the likely link between maternal cigarette smoking during pregnancy and sudden infant death syndrome (SIDS). Osmotic minipumps were implanted in 5-7 d CF1 pregnant mice to deliver nicotine bitartrate (60 mg Kg(-1) day(-1)) or saline (control) solutions for up to 28 d. Prenatal to early postnatal nicotine exposure did not modify the number of newborns per litter or their postnatal growth; however, nicotine-exposed neonates hypoventilated and had reduced responses to hypercarbia (inhalation of air enriched with 10% CO2 for 20 min) and hypoxia (inhalation of 100% N-2 for 20 s) at postnatal days 0-3 (P0-P3). In contrast, at postnatal day 8, nicotine-exposed neonates were indistinguishable from controls. Isolated brainstem-spinal cord preparations obtained from P0 to P3 nicotine-exposed neonates showed fictive respiration with respiratory cycles longer and more irregular than those of controls, as indicated by high short- and long-term variability in Poincare plots. In addition, their responses to acidification were reduced, indicating compromise of central chemoreception. Furthermore, the cholinergic contribution to central chemosensory responses switched from muscarinic receptor to nicotinic receptor-based mechanisms. No significant astrogliosis was detectable in the ventral respiratory group of neurons with glial fibrillary acidic protein immunohistochemistry. These results indicate that nicotine exposure affects the respiratory rhythm pattern generator and causes a decline in central chemoreception during early postnatal life. Consequently, breathing would become highly vulnerable, failing to respond to chemosensory demands. Such impairment could be related to the ventilatory abnormalities observed in SIDS.