Flash Visually Evoked Potentials in the Newborn and their Maturation During the First Six Months of Life

The aim of this paper has been to obtain normative data for the major components of the visually evoked potentials obtained by flash stimulus (F-PEV) in the newborn, and to analyse the evolution of these responses during the first 24 weeks of life. In order to do so, F-VEP were recorded in 109 normal full-term newborn infants. Fifty-five of these infants were also studied longitudinally at 4, 8, 12 and 24 weeks. We recorded responses in all newborns. A great morphological variability was observed. P2 was the only component present in all of these infants. Early components, which were always present from the fourth week of life on, were recorded in 34% of the newborns. There were significant differences according to waking/sleep state. At 24 weeks the most characteristic response was a triphasic waveform with clear negative–positive–negative components at 67.9, 110 and 158.3 ms. The morphological variability observed in the F-PEV of the newborn and the presence of early components in some cases, suggest differences in the maturation of the specific and unspecific visual system at birth. The study of these responses provides us with information about certain aspects of visual maturation. The relative stability of P2 response of the newborn and of the early negative components later on, made them the most useful components to be used in paediatric clinical work . The latency of P2 in the newborn is the parameter that showed lower variability, and therefore the most suitable one to establish normative data.     

Electrical interaction of mechanosensitive fibroblasts and myocytes in the heart

Fibroblasts in the heart can respond to mechanical deformation of the plasma membrane with characteristic changes of their membrane potential. Membrane depolarization of the fibroblasts occurs during the myocardial contractions and is caused by an influx of cations, mainly of sodium ions, into the cells. Conversely, application of mechanical stretch to the cells, i.e., during diastolic relaxation of the myocardium, will hyperpolarize the membrane potential of the fibroblasts due to reduced sodium entry. Thus, cardiac fibroblasts can function as mechano–electric transducers that are possibly involved in the mechano–electric feedback mechanism of the heart. Mechano–electric feedback refers to the phenomenon, that the cardiac mechanical environment, which depends on the variable filling pressure of the ventricles, modulates the electrical function of the heart. Increased sensitivity of the cardiac fibroblasts to mechanical forces may contribute to the electrical instability and arrhythmic disposition of the heart after myocardial infarction. Novel findings indicate that these processes involve the intercellular transfer of electrical signals between fibroblasts and cardiomyocytes via gap junctions. In this article we will discuss the recent progress in the electrophysiology of cardiac fibroblasts. The main focus will be on the intercellular pathways through which fibroblasts and cardiomyocytes communicate with each other.     

The opioid fentanyl affects light input, electrical activity and Per gene expression in the hamster suprachiasmatic nuclei

The suprachiasmatic nuclei (SCN) contain a major circadian pacemaker, which is regulated by photic and nonphotic stimuli. Although enkephalins are present in the SCN, their role in phase regulation of the pacemaker is largely unknown. The opioid agonist fentanyl, a homologue of morphine, is an addictive drug that induces phase shifts of circadian rhythms in hamsters. We observed that these phase shifts are blocked by naloxone, which is a critical test for true opioid receptor involvement, and conclude that opioid receptors are the sole mediators of the actions of fentanyl on the circadian timing system. A strong interaction between opioids and light input was shown by the ability of fentanyl and light to completely block each other's phase shifts of behavioural activity rhythms. Neuronal ensemble recordings in vitro provide first evidence that SCN cells show direct responses to fentanyl and react with a suppression of firing rate. Moreover, we show that fentanyl induces a strong attenuation of light-induced Syrian hamster Period 1 (shPer1) gene expression during the night. During the subjective day, we found no evidence for a role of shPer1 in mediation of fentanyl-induced phase shifts. Based on the present results, however, we cannot exclude the involvement of shPer2. Our data indicate that opioids can strongly modify the photic responsiveness of the circadian pacemaker and may do so via direct effects on SCN electrical activity and regulation of Per genes. This suggests that the pathways regulating addictive behaviour and the circadian clock intersect.     

Inhibitory effects of CB1 and CB2 receptor agonists on responses of DRG neurons and dorsal horn neurons in neuropathic rats

Cannabinoid 2 (CB2) receptor mediated antinociception and increased levels of spinal CB2 receptor mRNA are reported in neuropathic Sprague-Dawley rats. The aim of this study was to provide functional evidence for a role of peripheral, vs. spinal, CB2 and cannabinoid 1 (CB1) receptors in neuropathic rats. Effects of the CB2 receptor agonist, JWH-133, and the CB1 receptor agonist, arachidonyl-2-chloroethylamide (ACEA), on primary afferent fibres were determined by calcium imaging studies of adult dorsal root ganglion (DRG) neurons taken from neuropathic and sham-operated rats. Capsaicin (100 nm) increased [Ca2+]i in DRG neurons from sham and neuropathic rats. JWH-133 (3 microm) or ACEA (1 microm) significantly (P<0.001) attenuated capsaicin-evoked calcium responses in DRG neurons in neuropathic and sham-operated rats. The CB2 receptor antagonist, SR144528, (1 microm) significantly inhibited the effects of JWH-133. Effects of ACEA were significantly inhibited by the CB1 receptor antagonist SR141716A (1 microm). In vivo experiments evaluated the effects of spinal administration of JWH-133 (8-486 ng/50 microL) and ACEA (0.005-500 ng/50 microL) on mechanically evoked responses of neuropathic and sham-operated rats. Spinal JWH-133 attenuated mechanically evoked responses of spinal neurons in neuropathic, but not sham-operated rats. These inhibitory effects were blocked by SR144528 (0.001 microg/50 microL). Spinal ACEA inhibited mechanically evoked responses of neuropathic and sham-operated rats, these effects were blocked by SR141716A (0.01 microg/50 microL). Our data provide evidence for a functional role of CB2, as well as CB1 receptors on DRG neurons in sham and neuropathic rats. At the level of the spinal cord, CB2 receptors have inhibitory effects in neuropathic, but not sham-operated rats suggesting that spinal CB2 may be an important analgesic target.     

Tone responses in core versus belt auditory cortex in the developing chinchilla

Single-unit responses to tone pip stimuli were isolated from numerous microelectrode penetrations of core primary auditory cortex (AI) and a dorsocaudal (DC) belt region in the ketamine-anesthetized chinchilla (laniger). Results are reported at postnatal day 3 (P3), P15, P30, and from adult animals. The AI core could be distinguished from the DC belt on the basis of its strict tonotopic organization, evident in all chinchillas studied (including the youngest). Averaged by age group and compared to their core counterparts, belt neurons generally had similar absolute (spike rate) thresholds and onset latencies (at a given sound pressure level), but lower maximum spike rates, broader tuning bandwidths, and more complex (multipeaked) receptive fields. Most notably, the fraction of complex belt units in the near-newborn (P3) group was high (approximately 50%), and did not systematically increase with age, while that of complex core units was approximately 10% at P3 and increased steadily to about 40% in adulthood. These results provide further evidence to support the hypothesis that, at least to some extent, core and belt auditory cortex may constitute parallel processing streams which represent different aspects of complex acoustic stimuli.     

Electrophysiologic Effects of Carvedilol: Is Carvedilol an Antiarrhythmic Agent?

The cardiovascular drug carvedilol is characterized by multiple pharmacological actions, which translate into a wide-spectrum therapeutic potential. Its major molecular targets are membrane adrenoceptors, ion channels, and reactive oxygen species. Carvedilol's favorable hemodynamic effects are due to the fact that the drug competitively blocks beta(1)-, beta(2)-, and alpha(1)- adrenoceptors. Several additional properties have been documented and may be clinically important, including antioxidant, antiproliferative/antiatherogenic, anti-ischemic, and antihypertrophic effects. The antiarrhythmic action of carvedilol may be related to a combination of its beta-blocking effects with its modulating effects on a variety of ion channels and currents. Several studies suggest that the drug may be useful in reducing cardiac death in high-risk patients with prior myocardial infarction and/or heart failure, as well as for primary and secondary prevention of atrial fibrillation. This article will review experimental data available on the electrophysiologic properties of carvedilol, with a focus on their clinical relevance.     

Unusual QRS morphology on ECG: a rare condition and an interesting response to pacing

We present the interesting case of a young man with borderline wide QRS complexes noted on electrocardiogram (ECG). The diagnosis of an unusual form of preexcitation was reached using observations from intracardiac tracings at electrophysiology study. Atrial pacing consistently resulted in further widening of the first conducted QRS complex, and the physiology underlying this unusual finding is explored.     

Pacing-induced electrophysiological remodeling in hypertrophic obstructive cardiomyopathy--observations on cardiac memory

BACKGROUND: Hypertrophic cardiomyopathy carries an increased risk for sudden cardiac death. While pacing therapy reduces the left ventricular outflow tract gradient and improves symptoms in a subgroup of hypertrophic obstructive cardiomyopathy (HOCM) patients, its electrophysiological consequences are unknown and were therefore assessed in this prospective study. METHODS AND RESULTS: Fifteen consecutive HOCM patients were studied and compared with 14 patients without HOCM paced because of sinus bradycardia. ECG intervals were measured before pacemaker implantation and after > or =3 months of DDD pacing in HOCM patients and > or =5 weeks in controls. Both groups showed similar ECG signs of cardiac memory development. In HOCM patients, with baseline QTc 447 +/- 33 ms, cardiac memory development was not associated with any significant changes in ECG intervals. In contrast, baseline repolarization in control patients was significantly prolonged by 6% (QTc 429 +/- 33 vs 454 +/- 46 ms; P < 0.05). Furthermore, in HOCM patients repolarization was 7% shorter during DDD pacing compared to sinus rhythm (JTc 329 +/- 25 vs 353 +/- 21 ms; P < 0.05), despite a significantly prolonged ventricular activation time (QRS duration 155 +/- 16 vs 91 +/- 9 ms; P < 0.01). CONCLUSIONS: Importantly, the development of cardiac memory-induced different repolarization responses depending on baseline structure and electrophysiology. In HOCM patients repolarization was shorter during right ventricular apical pacing than during normal activation despite prolonged activation time.     

Effect of low power 655 nm diode laser irradiation on the neuromuscular junctions of the mouse diaphragm

BACKGROUND AND OBJECTIVES: Low level laser therapy (LLLT) in specific wavelengths and fluence maintains the electrophysiological activity of injured peripheral nerve in rats, preventing scar formation (at injury site) as well as degenerative changes in the corresponding motor neurons of the spinal cord, thus accelerating regeneration of the injured nerve. We studied the effect of LLLT on the neurotransmitter release in neuromuscular junctions of the mouse diaphragm. STUDY DESIGN/MATERIALS AND METHODS: Thirty-nine diaphragm muscles were studied. LLLT with GaAlAs 655 nm (1-12 J/cm(2)) was used. Neurotransmitter release was studied by conventional intracellular recording techniques on curarised or high magnesium media. Quantal content, amplitude, latency and rise time were analysed for end-plate potentials (EPPs). Frequency and amplitude were evaluated for the miniature end-plate potentials (MEPPs). Short-term plasticity of the neurotransmitter release (fast facilitation) was also evaluated by paired pulse stimulation. RESULTS AND CONCLUSIONS: This study showed that LLLT (655 nm) in these doses has no detectable physiological effect on the motor end-plate neurotransmitter release in mice.     

Neurotransmitter release changes induced by low power 830 nm diode laser irradiation on the neuromuscular junctions of the mouse

BACKGROUND AND OBJECTIVE: Treating patients with a Gallium-Aluminum-Arsenide (GaAlAs) infrared (IR) diode laser reduces muscle spasm and increases mobility in the muscles. The effect of low intensity laser irradiation on nerve function, growth, and repair mechanisms is a contentious area of research. We have addressed one aspect of this controversy by systematically examining the influence of 830 nm laser radiation on neurotransmitter release in neuromuscular junctions (NMJ) of the mouse diaphragm. STUDY DESIGN/MATERIALS AND METHODS: Thirty adult mice were studied. Diode laser GaAlAs 830 nm (4 and 12 J/cm2) was used. Neurotransmitter release was studied by conventional intracellular recording techniques on curarized muscles or high magnesium media. The quantal content, amplitude, and latency of the end-plate potentials (EPPs) were analyzed. Frequency and amplitude were evaluated for the miniature end-plate potentials (MEPPs). Facilitation of the neurotransmitter release was also evaluated by paired pulse stimulation. RESULTS AND CONCLUSIONS: The irradiated (12 J/cm2) muscles showed a significant reduction in quantal content (P = 0.01) and EPP amplitude (P = 0.04), but the latency, spontaneous transmitter release (MEPPs) and paired pulse facilitation did not change. No alterations were observed in NMJ irradiated with 4 J/cm2. We conclude that 830 nm diode laser irradiation (at a dose of 12 J/cm2) can affect the evoked neurotransmitter release in the mouse motor endplates.