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

Abstract

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.

Aging and magnetism: Presenting a possible new holistic paradigm for ameliorating the aging process and the effects thereof, through externally applied physiologic PicoTesla magnetic fields

“…Low-level vagal nerve stimulation markedly attenuated the hyperactive state of the GP, thereby suppressing AF. In a recent experimental study, we recorded the neural activity of the GP and found that several hours of induced AF caused a significant increase in the amplitude and frequency, whereas low level vagal nerve stimulation not only suppressed AF propensity but also the increased amplitude and frequency of the hyperactive GP [92]. A recent clinical report from our group has confirmed that low-level vagal nerve stimulation can mitigate AF in patients with the paroxysmal form of this arrhythmia [88].…”

“…Subsequently, a series of experimental studies have been published [87][88][89][90][91] in which we used low-level vagosympathetic trunk electrical stimulation at levels 10% and 50% which did not slow the heart rate or slow atrio ventricular conduction (AVC). In an experimental model of induced AF, we found that the nerve clusters called ganglionated plexi (GP) found in specific vulnerable sites in the atria became hyperactive under the influence of excessive release of cholinergic (parasympathetic) and adrenergic (sympathetic) neurotransmitters [92]. In this regard, Smith et al [92] tested the function of the GP, weeks after separation of the vagal and sympathetic nerves from the aforementioned structures.…”

“…In an experimental model of induced AF, we found that the nerve clusters called ganglionated plexi (GP) found in specific vulnerable sites in the atria became hyperactive under the influence of excessive release of cholinergic (parasympathetic) and adrenergic (sympathetic) neurotransmitters [92]. In this regard, Smith et al [92] tested the function of the GP, weeks after separation of the vagal and sympathetic nerves from the aforementioned structures. Not only did the intrinsic GP neurons remain viable but their responsiveness was enhanced.…”

A quantum theory of disease, including cancer and aging

“…In an experimental model of induced AF, it was found that the nerve clusters called ganglionated plexi (GP) found in specific vulnerable sites in the atria became hyperactive under the influence of excessive release of cholinergic (parasympathetic) and adrenergic (sympathetic) neurotransmitters. In this regard, Smith et al [85] tested the function of the GP, weeks after separation of the vagal and sympathetic nerves from the aforementioned structures. Not only did the intrinsic GP neurons remain viable but their responsiveness was enhanced.…”

Identification and detection of the isolated sinus venosus from the Asian toad

“…Acetylcholine (Ach) released by vagal nerve may cause hyperpolarization and a bradycardia by activating a subset of muscarinic receptors . As the sinus venosus possesses plenty of adrenergic and muscarinic receptors, the influence of vagal input on pacemaking activity could be observed much distinctively . In recent years, high frequency (HF) and low frequency (LF) spectra of the HRV have been employed to study the dynamic regulation of pacemaking activity …”