PubMed · 6779798
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W L Pak, S K Conrad, N E Kremer, D C Larrivee, R H Schinz, F Wong. 1980. Photoreceptor function.. https://doi.org/10.1007/978-1-4684-7968-3_24
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BACKGROUND: Although the relationship between cardiac wavelength (lambda) and path length importantly determines the stability of reentrant arrhythmias, the physiological determinants of lambda are poorly understood. To investigate the cellular mechanisms that control lambda during reentry, we developed an experimental system for continuously monitoring lambda within a reentrant circuit with the use of voltage-sensitive dyes and a new guinea pig model of ventricular tachycardia (VT). METHODS AND RESULTS: Action potentials were recorded simultaneously from 128 ventricular sites in Langendorff-perfused hearts (n = 15) in which propagation was confined to a two-dimensional rim of epicardium by an endocardial cryoablating procedure. The reentrant path was precisely controlled by creating an epicardial obstacle (2 x 10 mm) with an argon laser. To control for fiber orientation and rate-dependent membrane properties, lambda during reentry was compared with lambda during plane wave propagation transverse and longitudinal to cardiac fibers at a stimulus cycle length (CL) comparable to the VT CL. Reentrant VT (CL = 97.0 +/- 6.2 ms) was reproducibly induced by programmed stimulation in 93% of preparations. lambda varied considerably within the reentrant circuit (range, 10.6 to 22.5 mm), because of heterogeneities of conduction rather than action potential duration. lambda was significantly shorter during reentrant propagation (ie, with pivoting) parallel to fibers (10.6 +/- 4.2 mm) compared with plane wave propagation (ie, without pivoting) parallel to fibers (32.8 +/- 6.5 mm, P < .02), indicating that wave-front pivoting was primarily responsible for shortening of lambda during reentry. The mechanism of lambda shortening was conduction slowing from increased current load experienced by the pivoting wave front. CONCLUSIONS: We provide direct experimental evidence that multiple wavelengths are present even within a relatively simple reentrant circuit. Abrupt changes in loading during wave-front pivoting, rather than membrane ionic properties or fiber structure, were a major determinant of lambda and, therefore, may play an important role in the stability of reentry.
The free intracellular Ca2+ concentration ([Ca2+]i) is governed by the balance between the activation of Ca2+ channels and buffering and efflux processes. We tested the hypothesis that Ca2+ efflux pathways are susceptible to modulation. The whole-cell patch-clamp technique was used in combination with Indo-1-based microfluorometry to record Ca2+ current and [Ca2+]i simultaneously from single rat dorsal root ganglion (DRG) neurons grown in culture. Depolarizing test pulses (-80 to 0 mV, 100-300 msec) elicited [Ca2+]i transients that recovered to basal levels by a process best-fit with a single exponential (tau = 5.1 +/- 0.4 sec; n = 14) and were independent of Ca2+ load (40-500 pC) over this range of test pulses. [Ca2+]i transients recorded in whole-cell configuration were similar to those elicited by a brief train of action potentials in unclamped neurons. Inhibition of Ca2+ sequestration into intracellular stores with thapsigargin had no effect on the kinetics of recovery. Inhibition of plasma membrane Ca2+ ATPase (PMCA) function by including a peptide inhibitor (C28R2) in the patch pipette significantly slowed recovery to basal [Ca2+]i (tau = 9.9 +/- 0.8 sec; n = 4). Preincubation with calmidazolium, a calmodulin antagonist, produced modest slowing of Ca2+ efflux. Phorbol dibutyrate, an activator of protein kinase C (PKC), accelerated Ca2+ efflux only when the PMCA had been inhibited by C28R2. We conclude that in DRG neurons PMCAs are responsible for lowering [Ca2+]i after small Ca2+ loads and that PMCA-mediated Ca2+ efflux is modulated by calmodulin- and PKC-signaling pathways.
The effects of selective beta-adrenergic receptor agonist isoproterenol (Iso) on neuronal excitability and synaptic transmission were investigated in brain slices of rat amygdala. Iso (15 microM) produced a long-lasting enhancement of the EPSP that was not blocked by pretreatment with 20 microM D-2-amino-5-phosphonovalerate (D-APV) alone or D-APV in combination with kynuretic acid (1 mM). The sensitivity of postsynaptic neurons to the glutamate receptor agonist AMPA was unchanged by Iso pretreatment. Superfusion of Iso reversibly blocked the after-hyperpolarization (AHP) that followed a depolarizing current pulse and caused more action potential firing. Intracellular application of a selective inhibitor of the catalytic subunit of cAMP-dependent protein kinase A blocked the effect of Iso on the AHP, whereas Iso-induced potentiation was entirely normal in the same neuron. In addition, Iso decreased the magnitude of paired-pulse facilitation, which is consistent with a presynaptic mode of action. Substituting the Mg2+ for Ca2+ in the medium completely abolished the Iso-induced enhancement of the EPSP. The effect of Iso also was blocked by low concentrations of omega-agatoxin-IVA, but not by nifedipine or omega-conotoxin-GVIA. These results suggest that Iso enhances synaptic transmission in the amygdala via a presynaptic site of action: the mechanism underlying the potentiating effect likely is attributable to an increased Ca2+ influx through P- and/or Q-type Ca2+ channels.