Effects of chronic cardiac decentralization on functional properties of canine intracardiac neurons in vitro.

Effects of chronic cardiac decentralization on functional properties of canine intracardiac neurons in vitro.
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DOI:
10.1152/ajpregu.2001.281.5.r1474
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发表时间:
2001-11
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
Frank M. Smith;A. S. McGuirt;J. Leger;John A Armour;J. Ardell
Frank M. Smith;A. S. McGuirt;J. Leger;John A Armour;J. Ardell
中科院分区:
其他
文献类型:
--
作者:
Frank M. Smith;A. S. McGuirt;J. Leger;John A Armour;J. Ardell

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Although intrinsic cardiac neurons display ongoing activity after chronic interruption of extrinsic autonomic inputs to the heart, the effects of decentralization on individual neurons remain unknown. The objective of this study was to determine the effects of chronic (3-4 wk) surgical decentralization on intracellular properties of, and neurotransmission among, neurons contained within the canine intrinsic right atrial ganglionated plexus in vitro. Properties of neurons from decentralized hearts were compared with those of neurons from sham-operated hearts (controls). Two populations of neurons were identified by their firing behavior in response to intracellular current injection. Fifty-nine percent of control neurons and 72% of decentralized neurons were phasic (discharged one action potential on excitation). Forty-one percent of control neurons and 27% of decentralized neurons were accommodating (multiple discharge with decrementing frequency). After chronic decentralization, input resistance of phasic neurons increased, whereas the duration of afterhyperpolarization of accommodating neurons decreased. Postsynaptic responses to interganglionic nerve stimulation were evoked in 89% of control neurons and 83% of decentralized neurons; the majority of these responses involved nicotinic receptors. These results show that, after chronic decentralization, intrinsic cardiac neurons 1) undergo changes in membrane properties that may lead to increased excitability while 2) maintaining synaptic neurotransmission within the intrinsic cardiac ganglionated plexus.