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| Qualifications |
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1953-56 Brooklyn College Chemistry Major |
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| Research Interests |
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Research Interests: Neural control of respiration; upper airway function, sleep apnea, motor control. For further details visit: Institute of Neurological Sciences Research Techniques: Extracellular and intracellular microelectrode recording, microstimulation, spike-triggered averaging, antidromic mapping, microinjection and iontophoresis, microdialysis. Research Summary: Current investigations center on the neural mechanisms underlying the obstructive apneas/hypopneas that occur during sleep, especially rapid eye movement (REM) sleep. For this, decerebrate cat and anesthetized rat models of REM sleep are used to study the changes in the control of motoneuronal activity to various respiratory muscles (both upper airway and respiratory pump muscles) that accompany the postural atonia characteristic of REM sleep. A REM sleep-like state, with full postural muscle atonia and rapid eye movements is induced by the microinjection of carbachol, a cholinergic agonist, into the dorsal pontine tegmentum. Such injections induce a profound suppression of activity in motoneurons to most respiratory muscles. There is a differential suppression of respiratory motoneuronal activity, with a pattern similar to natural REM sleep, in that phrenic motoneurons are least affected, and intercostal and hypoglossal/pharyngeal motoneurons strongly depressed. The depression of the activity of hypoglossal motoneurons, unlike the situation with lumbar (postural) motoneurons, is not due principally to a fast postsynaptic inhibition mediated by inhibitory amino acids. Rather, it is likely that the depression is caused by the removal of excitation (disfacilitation) that results from a decrease in the firing of serotonergic neurons of the medullary raphe and catecholaminergic neurons of the pons. The role of these two aminergic systems of the brainstem in the motor and reflex control of upper airway motoneurons (hypoglossal, pharyngeal, laryngeal) and the relation of these systems to the atonia of REM sleep is currently being investigated using a variety of complementary neurophysiological, neuroanatomical and neuropharmacological techniques. |
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| Selected Publications |
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| Kubin, L., H. Kimura, H. Tojima, R.O. Davies and A.I. Pack. Suppression of hypoglossal motoneurons during carbachol-induced atonia of REM sleep is not caused by fast synaptic inhibition. Brain Research, 611:300-312, 1993. Kubin, L., C. Reignier, H. Tojima, O. Taguchi, A.I. Pack and R.O. Davies. Changes in serotonin level in the hypoglossal nucleus region during carbachol-induced atonia. Brain Research, 645:291-302, 1994. Kubin, L. and R.O. Davies. Central pathways of pulmonary and airway vagal afferents. In: Regulation of Breathing. Ed. by J. Dempsey and A.I. Pack. New York: Marcel Dekker, 1995, pp. 219-284. Woch, G., R.O. Davies, A.I. Pack and L. Kubin. Behavior of raphe cells projecting to the dorsomedial medulla during carbachol-induced atonia in the cat. J. Physiol. (London)., 490:745-758, 1996. Kubin, L., H. Tojima, C. Reignier, A.I. Pack, and R.O. Davies. Interaction of serotonergic excitatory drive to hypoglossal motoneurons with carbachol-induced, REM sleep-like atonia. Sleep, 19:187-195, 1996. Fenik, V., L. Kubin, S. Okabe, A.I. Pack and R.O. Davies. Differential sensitivity of laryngeal and pharyngeal motoneurons to iontophoretic application of serotonin. Neuroscience, 81:873- 885, 1997. Pack, A.I., L. Kubin and R.O. Davies. Changes in the cardiorespiratory system during sleep. In: Fishman’s Pulmonary Diseases and Disorders, Third Edition. Ed. by A.P. Fishman. New York: McGraw-Hill, 1998, Chapter 101, pp 1607-1615. Kubin, L., R.O. Davies and A.I. Pack. Control of upper airway motoneurons during REM sleep. News Physiol. Sci., 13:91-97,1998. Fenik, V., R.O. Davies, A.I. Pack and L. Kubin. Differential suppression of upper airway motor activity during carbachol-induced, REM sleep-like atonia. Am. J. Physiol., 275 (Regulatory Integrative Comp. Physiol. 44): R1013-R1024, 1998. Woch, G., H. Ogawa, R.O. Davies and L. Kubin. Behavior of hypoglossal inspiratory premotor neurons during the carbachol-induced, REM sleep-like suppression of upper airway motoneurons. Exp. Brain Res., 130: 508-520, 2000. Kubin, L. and R.O. Davies. Mechanisms of airway hypotonia. In: Pathogenesis, Diagnosis and Treatment of Sleep Apnea. Ed. by A.I. Pack. New York: Marcel Dekker, 2002, pp. 99-154. Fenik, V. B., V. Marchenko, P. Janssen, R.O. Davies and L. Kubin. A5 cells are silenced when REM sleep-like signs are elicited by pontine carbachol. J. Appl. Physiol., 93: 1448-1456, 2002. Fenik, V., R.O. Davies and L. Kubin. Combined antagonism of aminergic and amino acid inhibitory receptors in the XII nucleus abolishes REM sleep-like depression of hypoglossal motoneuronal activity. Arch. Ital. Biol., 142: 237-249, 2004. Volgin, D.V.,V.B. Fenik, R. Fay, S. Okabe, R.O. Davies and L. Kubin. Serotonergic receptors and effects in hypoglossal and laryngeal motoneurons. In: Post-Genomic Perspectives in Modeling and Control of Breathing. Ed. by J. Champagnat, M. Denavit-Saubié, G. Fortin, A.S. Foutz and M. Thoby-Brisson. Amsterdam: Kluwer Academic/Plenum, 2004, pp. 183-188. Fenik, V., H. Ogawa, R.O. Davies and L. Kubin. Carbachol injections into the ventral pontine reticular formation activate locus coeruleus cells in urethane-anesthetized rats. Sleep, 28: 560-570, 2005. Fenik, V.B., R.O. Davies and L. Kubin. REM sleep-like atonia of hypoglossal (XII) motoneurons is caused by loss of noradrenergic and serotonergic inputs. Am. J. Respir. Crit. Care Med., 172: 1322-1330, 2005. |
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