Anoxia induced functional inactivation of neonatal respiratory neurones in vitro

Ballanyi, Klaus; Völker, Antje; Richter, Diethelm W.

doi:10.1097/00001756-199412300-00042

Cited by 44 publications

(64 citation statements)

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“…In perinatal rats in vivo, the frequency of breathing is profoundly reduced during anoxia from ~1·breath·s -1 to <1·breath·min -1 (Ballanyi, 2004). A similar persistence of respiratory activity at greatly reduced frequency for anoxia periods of up to 1·h is observed in brainstem-spinal cord preparations from newborn rats ( Fig.·7A; Ballanyi et al, 1994Ballanyi et al, , 1999Ballanyi, 2004). A series of reports on the latter preparation Brockhaus et al, 1993;Voipio and Ballanyi, 1997;Ballanyi, 2004) has led to the view that the high tolerance of the respiratory network in newborn mammals to oxygen depletion includes two cooperative processes.…”

Section: K Atp Channels In Brain Hypoxiasupporting

confidence: 59%

“…Such anoxic functional inactivation of a major portion of respiratory neurons does not reflect a pathophysiological impairment of synaptic transmission or membrane excitability. Action potentials can still be evoked in these cells while drive potentials of a different subpopulation of inspiratory VRG neurons remain vitually unaltered by anoxia ( Fig.·6B; Ballanyi et al, 1994Ballanyi et al, , 1999Ballanyi, 2004). This tolerance to anoxia of excitatory synaptic transmission in a subclass of neonatal respiratory neurons coincides with the ability of inspiratory premotoneurons and motoneurons to generate (respiratory-related) spiking as obvious from the persistence of inspiratory motor output during anoxia.…”

Section: Ballanyi K Atp Channels In Brain Hypoxiamentioning

confidence: 86%

“…The second process contributing to the anoxia tolerance of the neonatal respiratory network is constituted by downregulation of metabolic rate and demand by 'functional inactivation' of ion conductances as described for coldblooded vertebrates (Hochachka and Lutz, 2001). Most (>60%) of the respiratory neurons in neonatal rats in vitro respond with a sustained K + channel-mediated hyperpolarisation and conductance increase in response to blockade of aerobic metabolism by either anoxia or cyanide (Figs·6B,C,·7C;Ballanyi et al, 1994Ballanyi et al, , 1999. In about 50% of these cells, the anoxic hyperpolarisation coincides with suppression of respiratory-related membrane potential fluctuations (Fig.·6C).…”

Section: Ballanyi K Atp Channels In Brain Hypoxiamentioning

confidence: 96%

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Protective role of neuronal KATP channels in brain hypoxia

Ballanyi

2004

Journal of Experimental Biology

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129

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SUMMARY During severe arterial hypoxia leading to brain anoxia, most mammalian neurons undergo a massive depolarisation terminating in cell death. However,some neurons of the adult brain and most immature nervous structures tolerate extended periods of hypoxia–anoxia. An understanding of the mechanisms underlying this tolerance to oxygen depletion is pivotal for developing strategies to protect the brain from consequences of hypoxic-ischemic insults. ATP-sensitive K+ (KATP) channels are good subjects for this study as they are activated by processes associated with energy deprivation and can counteract the terminal anoxic-ischemic neuronal depolarisation. This review summarises in vitro analyses on the role of KATP channels in hypoxia–anoxia in three distinct neuronal systems of rodents. In dorsal vagal neurons, blockade of KATPchannels with sulfonylureas abolishes the hypoxic-anoxic hyperpolarisation. However, this does not affect the extreme tolerance of these neurons to oxygen depletion as evidenced by a moderate and sustained increase of intracellular Ca2+ (Cai). By contrast, a sulfonylurea-induced block of KATP channels shortens the delay of occurrence of a major Cai rise in cerebellar Purkinje neurons. In neurons of the neonatal medullary respiratory network, KATP channel blockers reverse the anoxic hyperpolarisation associated with slowing of respiratory frequency. This may constitute an adaptive mechanism for energy preservation. These studies demonstrate that KATP channels are an ubiquituous feature of mammalian neurons and may, indeed, play a protective role in brain hypoxia.

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Section: K Atp Channels In Brain Hypoxiasupporting

confidence: 59%

Section: Ballanyi K Atp Channels In Brain Hypoxiamentioning

confidence: 86%

Section: Ballanyi K Atp Channels In Brain Hypoxiamentioning

confidence: 96%

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Protective role of neuronal KATP channels in brain hypoxia

Ballanyi

2004

Journal of Experimental Biology

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129

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“…Biphasic expiratory neurones (biphasic E) are characterized by preand post-inspiratory excitation and inspiratory-related inhibition (Onimaru et al 1990). Inspiratory neurones were further classified into three subtypes according to previous classifications performed with this preparation (Onimaru et al 1996(Onimaru et al , 1997 (Vm) were not corrected for liquid junction potentials, determined to be û −10 mV, in order to facilitate comparisons with earlier studies performed with this preparation Ballanyi et al 1994;Kawai et al 1996;Onimaru et al 1996Onimaru et al , 1997. The current-voltage (I-V) relationship was determined by injection of an inward current (0·02-0·08 nA, duration 100 ms) during silent phases between bursts in the expiratory phase of the respiratory cycle, or during negative holding potentials (−50 mV) in the case of certain expiratory neurones.…”

Section: Recordingsmentioning

confidence: 99%

Adenosinergic modulation of respiratory neurones in the neonatal rat brainstem in vitro

Herlenius

Lagercrantz

1999

The Journal of Physiology

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Neuronal networks in the medulla oblongata generate respiratory rhythm in mammals. The pre-B otzinger complex (Smith et al. 1991) in the rostral ventrolateral medulla oblongata (RVL) (Onimaru et al. 1988) has been proposed to be the crucial site of this rhythmogenesis, but the detailed organization of this noed vitale is still unknown. The unique patterns of receptors and membrane channels expressed by specific types of neurones, and interaction between these neurones, maintains the central pattern generator for respiration. Thus it is important to increase our understanding of the receptors and membrane channels in each type of cell in this neuronal network. One of the central modulators of respiration is adenosine, whose action is especially important around the time of birth (Runold et al. 1986; Irestedt et al. 1989;Herlenius et al. 1997). Adenosine has been proposed to be involved in the suppression of fetal and neonatal breathing (Lagercrantz et al. 1984;Bissonnette et al. 1991;Herlenius et al. 1997), particularly during hypoxia when extracellular levels of this nucleoside rapidly increase (Winn et al. 1981). Furthermore, blocking A1-receptors with xanthine derivatives abolishes or attenuates hypoxia-induced depression of breathing in newborn mammals (Runold et al. 1989;Neylon & Marshall 1991;Kawai et al. 1995). Thus blocking the action of endogenous adenosine is probably the mechanism by which theophylline exerts its clinical effects in the treatment of apnoea of prematurity. Adenosine plays multiple roles throughout the nervous system (Brundege & Dunwiddie, 1997), e.g. inhibiting excitatory postsynaptic currents in hippocampal neurones (Katchman & Hershkowitz, 1993) and decreasing neurotransmitter release in prejunctional motoneurones (Mynlieff & Beam, 1994). As recently reported, stimulation of brainstem adenosine A1-receptors depresses the activity of

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“…The first involves a generalized reduction of inhibitory synaptic transmission Lieske et al 2000), the second involves the shutdown of most of the non-pacemaker neurons (Ballanyi et al, 1994;, and the third involves a differential effect of hypoxia on pacemaker neurons. Type II (or Cd 2+ -sensitive) pacemaker neurons cease to produce rhythmic bursting activity in hypoxic conditions, whereas a major subset of type I (or Cd 2+ -insensitive) pacemaker neurons maintain their bursting activity in hypoxia Tryba et al 2006; Table 1).…”

Section: Role Of Pacemaker Neurons In Respiratory Rhythm Generation Imentioning

confidence: 99%

Possible Role or Respiratory Pacemaker Neurons in the Generation of Different Breathing Patterns

Peña‐Ortega¹

2011

Modern Pacemakers - Present and Future

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Anoxia induced functional inactivation of neonatal respiratory neurones in vitro

Cited by 44 publications

References 0 publications

Protective role of neuronal KATP channels in brain hypoxia

Protective role of neuronal KATP channels in brain hypoxia

Adenosinergic modulation of respiratory neurones in the neonatal rat brainstem in vitro

Possible Role or Respiratory Pacemaker Neurons in the Generation of Different Breathing Patterns

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