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Titolo:
Long term facilitation of phrenic motor output
Autore:
Fuller, DD; Bach, KB; Baker, TL; Kinkead, R; Mitchell, GS;
Indirizzi:
Univ Wisconsin, Dept Comparat Biosci, Madison, WI 53706 USA Univ Wisconsin Madison WI USA 53706 omparat Biosci, Madison, WI 53706 USA
Titolo Testata:
RESPIRATION PHYSIOLOGY
fascicolo: 2-3, volume: 121, anno: 2000,
pagine: 135 - 146
SICI:
0034-5687(200007)121:2-3<135:LTFOPM>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYPOXIC VENTILATORY RESPONSES; CHRONIC INTERMITTENT HYPOXIA; RAT BRAIN-STEM; INSPIRATORY DRIVE; NERVE ACTIVITY; IN-VITRO; PROLONGED STIMULATION; RESPIRATORY ACTIVITY; HYPOGLOSSAL NUCLEUS; NEONATAL RAT;
Keywords:
afferents, chemoselective neurons; control of breathing, hypoxia; hypoxia, long-term facilitation; mammals, humans, rat; mediators, serotonin; plasticity, long-term facilitation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Mitchell, GS Univ Wisconsin, Dept Comparat Biosci, 2015 Linden Dr W, Madison, WI 53706 USA Univ Wisconsin 2015 Linden Dr W Madison WI USA 53706 3706 USA
Citazione:
D.D. Fuller et al., "Long term facilitation of phrenic motor output", RESP PHYSL, 121(2-3), 2000, pp. 135-146

Abstract

Episodic hypoxia or electrical stimulation of carotid chemoafferent neurons elicits a sustained, serotonin-dependent augmentation of respiratory motor output known as long term facilitation (LTF). The primary objectives of this paper are to provide an updated review of the literature pertaining to LTF, to investigate the influence of selected variables on LTF via meta-analysis of a large data set from LTF experiments on anesthetized rats, and topropose an updated mechanism of LTF. LTF has been demonstrated in anesthetized and awake experimental preparations, and can be evoked in some human subjects during sleep. The mechanism underlying LTF requires episodic chemoafferent stimulation, and is not elicited by similar cumulative durations ofsustained hypoxia. Meta-analysis of phrenic nerve responses following episodic hypoxia in 63 experiments on anesthetized rats (conducted by four investigators over a period of several years) indicates that phrenic LTF magnitude correlates with peak phrenic responses during hypoxia and hypercapnia, but not with the level of hypoxia during episodic exposures. Potential mechanisms underlying these relationships are discussed, and currently available data are synthesized into an updated mechanistic model of LTF. In this model, we propose that LTF arises predominantly from episodic activation of serotonergic receptors on phrenic motoneurons, activating intracellular kinases and, thus, phosphorylating and potentiating ionic currents associated with the glutamate receptors that mediate respiratory drive. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 12:33:50