Trans-spinal direct current enhances corticospinal output and stimulation-evoked release of glutamate analog, D-2,3-³H-aspartic acid

Trans-spinal direct current (tsDC) stimulation is a modulator of spinal excitability and can influence cortically elicited muscle contraction in a polarity-dependent fashion. When combined with low-frequency repetitive cortical stimulation, cathodal tsDC [tsDC(-)] produces a long-term facilitation of cortically elicited muscle actions. We investigated the ability of this combined stimulation paradigm to facilitate cortically elicited muscle actions in spinal cord-injured and noninjured animals. The effect of tsDC-applied alone or in combination with repetitive spinal stimulation (rSS) on the release of the glutamate analog, D-2,3-(3)H-aspartate (D-Asp), from spinal cord preparations in vitro-was also tested. In noninjured animals, tsDC (-2 mA) reproducibly potentiated cortically elicited contractions of contralateral and ipsilateral muscles tested at various levels of baseline muscle contraction forces. Cortically elicited muscle responses in animals with contusive and hemisectioned spinal cord injuries (SCIs) were similarly potentiated. The combined paradigm of stimulation caused long-lasting potentiation of cortically elicited bilateral muscle contraction in injured and noninjured animals. Additional analysis suggests that at higher baseline forces, tsDC(-) application does not increase the rising slope of the muscle contraction but causes repeated firing of the same motor units. Both cathodal and anodal stimulations induced a significant increase of D-Asp release in vitro. The effect of the combined paradigm of stimulation (tsDC and rSS) on the concentration of extracellular D-Asp was polarity dependent. These results indicate that tsDC can powerfully modulate the responsiveness of spinal cord neurons. The results obtained from the in vitro preparation suggest that the changes in neuronal excitability were correlated with an increased concentration of extracellular glutamate. The combined paradigm of stimulation, used in our experiments, could be noninvasively applied to restore motor control in humans with SCI.     

Central excitability does not limit postfatigue voluntary activation of quadriceps femoris.

After fatigue, motor evoked potentials (MEP) elicited by transcranial magnetic stimulation and cervicomedullary evoked potentials elicited by stimulation of the corticospinal tract are depressed. These reductions in corticomotor excitability and corticospinal transmission are accompanied by voluntary activation failure, but this may not reflect a causal relationship. Our purpose was to determine whether a decline in central excitability contributes to central fatigue. We hypothesized that, if central excitability limits voluntary activation, then a caffeine-induced increase in central excitability should offset voluntary activation failure. In this repeated-measures study, eight men each attended two sessions. Baseline measures of knee extension torque, maximal voluntary activation, peripheral transmission, contractile properties, and central excitability were made before administration of caffeine (6 mg/kg) or placebo. The amplitude of vastus lateralis MEPs elicited during minimal muscle activation provided a measure of central excitability. After a 1-h rest, baseline measures were repeated before, during, and after a fatigue protocol that ended when maximal voluntary torque declined by 35% (Tlim). Increased prefatigue MEP amplitude (P=0.055) and cortically evoked twitch (P<0.05) in the caffeine trial indicate that the drug increased central excitability. In the caffeine trial, increased MEP amplitude was correlated with time to task failure (r=0.74, P<0.05). Caffeine potentiated the MEP early in the fatigue protocol (P<0.05) and offset the 40% decline in placebo MEP (P<0.05) at Tlim. However, this was not associated with enhanced maximal voluntary activation during fatigue or recovery, demonstrating that voluntary activation is not limited by central excitability.     

Alterations of neuromuscular function after an ultramarathon.

Neuromuscular fatigue of the knee extensor (KE) and plantar flexor (PF) muscles was characterized after a 65-km ultramarathon race in nine well-trained runners by stimulating the femoral and tibial nerves, respectively. One week before and immediately after the ultramarathon, maximal twitches were elicited from the relaxed KE and PF. Electrically evoked superimposed twitches of the KE were also elicited during maximal voluntary contractions (MVCs) to determine maximal voluntary activation. MVC and maximal voluntary activation decreased significantly after the ultramarathon (-30.2 +/- 18.0% and -27.7 +/- 13.0%, respectively; P < 0.001). Surprisingly, peak twitch increased after the ultramarathon from 15.8 +/- 6.3 to 19.7 +/- 3.3 N. m for PF (P < 0.01) and from 131.9 +/- 21.2 to 157.1 +/- 35.9 N for KE (P < 0.05). Also, shorter contraction and half-relaxation times were observed for both muscles. The compound muscle action potentials (M wave) were not significantly altered by the ultramarathon with the exception of the soleus, which showed a slightly higher M-wave amplitude after the running. From these results, it can be concluded that 65 km of running 1) severely depressed the maximal voluntary force capacity mainly because of a decrease in maximal voluntary activation, 2) potentiated the twitch mechanical response, and 3) did not change significantly the M-wave characteristics.     

Recovery of action potentials and twitches after K-contractures in frog skeletal muscle

To give information about intracellular Ca2+ translocation during and after K-contractures in vertebrate skeletal muscle fibers, we examined recovery of action potentials and twitches after interruption and spontaneous relaxation of K-contractures at low temperature (3 degrees C) that greatly reduced the rate of Ca2+ reuptake by the sarcoplasmic reticulum. On membrane repolarization interrupting K-contractures, the amplitude of both action potentials and twitches recovered quickly, while the falling phase of action potential was markedly slowed at first to prolong its refractory period, so that repetitive stimulation (20 Hz) did not produce a complete tetanus. Meanwhile, on membrane repolarization after spontaneous relaxation of K-contractures, the action potentials were markedly reduced in amplitude and prolonged in duration at first, also resulting in prolonged refractory period. These results are discussed in connection with Ca2+ absorption to the surface and transverse tubule membranes, producing changes in action potential kinetics.     

Influence of orexin A on the mechanical activity of mouse gastric strips

The presence of orexins and orexin receptors has been revealed not only in the central nervous system but also in the gastrointestinal tract. The present study was aimed to investigate the influence of orexin A (OXA) on the mechanical activity of fundal and antral strips of the mouse stomach. In the fundus, electrical field stimulation (EFS) elicited tetrodotoxin (TTX)-sensitive, frequency-dependent contractile responses whose amplitude was markedly reduced by OXA and enhanced by the orexin-1 type receptor antagonist SB-334867. In the presence of the NO synthesis inhibitor L-N(G)-nitro arginine (L-NNA), OXA was no longer effective. Methacholine caused a sustained contracture whose amplitude was not influenced by OXA, TTX or L-NNA. In carbachol-precontracted strips, the neurally-induced relaxant responses elicited during EFS were increased in amplitude by OXA. Antral strips showed a spontaneous contractile activity that was unaffected by TTX or L-NNA and transiently depressed by EFS. OXA did not influence either the spontaneous motility or the EFS-induced effects. The results indicate that OXA exerts region-specific effects and that, in the fundus, depresses EFS-induced contractile responses by acting at the nervous level. It is likely that NO is involved in the effects of the peptide.     

Assessment of upper airway dynamics by anterior magnetic phrenic stimulation in conscious sleep apnea patients

Phrenic nerve magnetic stimulation (PNMS) performed anterolaterally at the base of the neck (BAMPS) and cervical magnetic stimulation are common techniques for assessing upper airway (UA) mechanical properties in conscious humans. We considered that if NMS performed at the sternal level (a-MS) could induce a similar percentage of flow-limited twitches as BAMPS in conscious subjects, gauging UA dynamic properties by PNMS would be simplified. Instantaneous flow, pharyngeal and esophageal pressures, as well as thoraco-abdominal motion were recorded in 10 conscious sleep apnea patients. BAMPS and a-MS were applied at end expiration. The percentage of flow-limited twitches, maximal tolerated intensity, and minimal stimulator output associated with flow-limited twitches were similar between BAMPS and a-MS. Examining the effects of stimulation site, stimulation intensity and site*intensity interaction on the characteristics of flow-limited twitches, the former was responsible for more negative peak esophageal pressure (BAMPS: -11.5 ± 0.9 cmH(2)O; a-MS: -6.5 ± 1.1 cmH(2)O; P = 0.002) and UA closing pressure (BAMPS: -7.7 ± 0.5 cmH(2)O; a-MS: -5.8 ± 0.6 cmH(2)O; P = 0.02) as well as for lower mean linear upper airway resistance (UAR) (BAMPS 3.5 ± 0.4 cmH(2)O·l(-1)·s(-1); a-MS 2.2 ± 0.4 cmH(2)O·l(-1)·s(-1); P = 0.02). a-MS systematically evoked outward/inward thoracic displacement, although this movement pattern was observed in only 50% of patients when they were subjected to BAMPS. Linear UAR of BAMPS-induced flow-limited twitches was lower in the presence of initial outward thoracic movement (2 ± 0.05 cmH(2)O·l(-1)·s(-1)) than with inward motion (4.3 ± 1.5 cmH(2)O·l(-1)·s(-1); P = 0.03). We conclude that a-MS represents a practical and functional technique to evaluate UA mechanical properties in conscious sleep apnea patients.     

Features of changes in bioelectric reactions of the cerebral cortex in rats with deafferentation pain syndrome]

In rats with pain syndrome after sciatic nerve section the authors studied spontaneous and evoked bioelectric activity in sensomotor cerebral cortex of both hemispheres. Electrocorticogram showed the presence of hyper-synchronic discharges and paroxysmal peak-wave (700-800 mV) activity in contralateral hemisphere. While stimulating the injured limb the threshold of evoked potentials (EP) was observed to decrease, its amplitude to increase and focus maximum EP activity to extend.     

Slowly Adapting Cutaneous Mechanoreceptor Afferent Units Associated with Merkel Cells in Frogs and Effects of Direct Currents

In the bullfrog, two types of slowly adapting (SA) cutaneous mechanoreceptor afferent units have been identified physiologically: irregularly discharging frog type I (Ft I) units in both warty and nonwarty skin, and regularly discharging frog type II (Ft II) units in the nonwarty skin. In the present study, mechanosensitive spots of Ft I units were located around the skin warts in the warty skin. The quinacrine technique (Crowe and Whitear, 1978) revealed that quinacrine-accu-mulating Merkel cells were present around the skin warts and near the orifice of skin glands that also surrounded the skin warts. Thus, a significant correlation was found between the location of Merkel cells and the receptive fields (RFs) of Ft I units in the warty skin.

Direct current (DC) stimulation was applied for 1 sec to the skin inside and outside the mechanical RFs of the two types of SA units. RFs for DC stimulation were located on those for mechanical stimulation in both types of SA units. The current threshold required to produce a single spike was lower in cathodal than in anodal pulses in both types of SA units. Greater current intensity elicited an increased number of spikes, but the effective polarity of currents was anodal for Ft I units and cathodal for Ft II units. The optimal current intensity for producing prolonged discharges ranged from +60 to +100 μA in Ft I units and from -50 to -80 μA in Ft II units. The sequence of impulses evoked was irregular in Ft I units and regular in Ft II units, as seen in mechanical responses. When current of the effective polarity for each type of unit was superimposed on the mechanical indentations, it facilitated the mechanical response. Currents of opposite polarity were not effective without mechanical indentation, but when used together, they depressed the mechanical response in both the Ft I units and the Ft II units. Thus, different polarities of DC could selectively activate two different types of SA units in bullfrogs. We consider these findings in connection with a presumed receptor structure for each type of unit; it is likely that the prolonged discharges in the Ft I unit are produced by active involvement of Merkel cells, whereas those in Ft II units are the result of a direct activation of afferent nerve terminals.     

糖尿病痛过敏大鼠尾神经中传入单位对交感传出的反应

实验观察了刺激交感神经（sympathetic stimulation,SS）、静脉注射去甲肾上素（noradrenaline,NA）和酚妥拉明对糖尿病痛过敏大鼠尾神经中各种传入单位的影响。结果发现,糖尿病痛过敏大鼠的具有自发放电的C单位和Aδ单位在SS后放电频率增加,α－受体阻断剂能消除这些自发放电活动;在无自发放电的C单位和Aδ单位中,SS能使部分C单位和Aδ单位由静息状态转入活动状态;它虽不能诱发C－机械感受单位（C mechanical receptive unit,C-M）产生传入放电,但可诱发部分C－机械热单位（C mechano-heat unit,C-MH）和C－多型单位（C polymodal unit,C-Pol）的活动;SS还能使部分Aδ－机械单位（Aδ mechanical receptive unit,Aδ-M）和Aδ－机械热单位（Aδ mechano-heat unit,Aδ-MH）产生传入放电;它所诱发的C单位和Aδ单位反应的潜伏期不等,但不短于5s;SS不能引起糖尿病痛过敏大鼠Aβ机械感受性单位和对照组大鼠各类感受性单位产生新的传入活动。静脉注射NA可诱发糖尿病痛过敏大鼠的部分C单位和Aδ单位产生新的传入活动。结果提示,交感神经末梢释放的NA对糖尿病痛过敏大鼠C单位和Aδ单位的兴奋作用是糖尿病大鼠产生痛过敏和感觉异常的外周因素。     

Spontaneous Ca2+ release from the sarcoplasmic reticulum limits Ca2+- dependent twitch potentiation in individual cardiac myocytes. A mechanism for maximum inotropy in the myocardium

We hypothesized that the occurrence of spontaneous Ca2+ release from the sarcoplasmic reticulum (SR), in diastole, might be a mechanism for the saturation of twitch potentiation common to a variety of inotropic perturbations that increase the total cell Ca. We used a videomicroscopic technique in single cardiac myocytes to quantify the amplitude of electrically stimulated twitches and to monitor the occurrence of the mechanical manifestation of spontaneous SR Ca2+ release, i.e., the spontaneous contractile wave. In rat myocytes exposed to increasing bathing [Ca2+] (Cao) from 0.25 to 10 mM, the Cao at which the peak twitch amplitude occurred in a given cell was not unique but varied with the rate of stimulation or the presence of drugs: in cells stimulated at 0.2 Hz in the absence of drugs, the maximum twitch amplitude occurred in 2 mM Cao; a brief exposure to 50 nM ryanodine before stimulation at 0.2 Hz shifted the Cao of the maximum twitch amplitude to 7 mM. In cells stimulated at 1 Hz in the absence of drugs, the maximum twitch amplitude occurred in 4 mM Cao; 1 microM isoproterenol shifted the Cao of the maximum twitch amplitude to 3 mM. Regardless of the drug or the stimulation frequency, the Cao at which the twitch amplitude saturated varied linearly with the Cao at which spontaneous Ca2+ release first occurred, and this relationship conformed to a line of identity (r = 0.90, p = less than 0.001, n = 25). The average peak twitch amplitude did not differ among these groups of cells. In other experiments, (a) the extent of rest potentiation of the twitch amplitude in rat myocytes was also limited by the occurrence of spontaneous Ca2+ release, and (b) in both rat and rabbit myocytes continuously stimulated in a given Cao, the twitch amplitude after the addition of ouabain saturated when spontaneous contractile waves first appeared between stimulated twitches. A mathematical model that incorporates this interaction between action potential-mediated SR Ca2+ release and the occurrence of spontaneous Ca2+ release in individual cells predicted the shape of the Cao-twitch relationship observed in other studies in intact muscle. Thus, the occurrence of spontaneous SR Ca2+ release is a plausible mechanism for the saturation of the inotropic response to Ca2+ in the intact myocardium.     

兔孤束核腹外侧区微量注射谷氨酸钠及甘氨酸对弓状核诱发电位的影响

实验在６６只麻醉、制动,断双侧颈迷走神经和人工通气的家兔上进行。通过微量注射神经元胞体兴奋剂谷氨酸钠和神经元胞体抑制剂甘氨酸,改变孤束核腹外侧区神经元兴奋活动,探讨对下丘脑弓状核诱发电位的影响及其可能的机制和意义。实验结果如下：（１）孤束核腹外侧区微量注射谷氨酸钠,可使膈神经放电显著增加和使弓状核诱发电位Ｐ２及Ｎ２波幅显著降低;而微量注射甘氨酸则使膈神经放电显著减少和使弓状核诱发电位Ｐ２及Ｎ２波幅显著增大。（２）静脉注射纳洛酮对谷氨酸钠引起的膈神经放电兴奋效应无明显影响,但能翻转谷氨酸钠对弓状核诱发电位Ｐ２及Ｎ２波幅的抑制效应。提示：孤束核腹外侧区呼吸神经元的兴奋活动可扩散至弓状核,并对弓状核诱发电位产生影响,此影响可能是由内源性阿片系统参与而实现的。     

Electromyographic activity and noradrenaline content of the rabbit oviduct under different hormonal states

Spontaneous electromyographic (EMG) activity of the oviduct recorded in vivo in untreated, estrogen-treated, and progesterone-treated castrated rabbits was found to exhibit two main patterns: short spike bursts lasting 1-10 s and long trains of action potentials lasting several minutes, which constituted the major component of EMG activity. After estrogen treatment, both wet weight and noradrenaline (NA) content of the castrated rabbit oviduct were enhanced mainly at the ampullary-isthmic junction; long trains of discharges were significantly shorter (2.0-2.7 min vs 3.6-4.6 min) and appeared at more frequent intervals (9.8-12.2 min vs 14.2-22.6 min). After progesterone treatment, spontaneous EMG activity was not significantly different from that in untreated castrated rabbits (as was the NA content) except at the ampullary-isthmic junction. NA injection elicited a stimulatory response of the oviduct lasting 1-7 min in the three hormonal states. Phentolamine strongly depressed spontaneous EMG activity but the inhibition was more transient in castrated rabbits than in estrogen-treated and progesterone-treated animals. Propranolol had no effect on spontaneous EMG activity. These data and the high NA concentrations found in all parts of the isthmus support the hypothesis that adrenergic innervation plays a role in the organization of oviductal motility in the rabbit.     

Failure of monocytes of trauma patients to convert to immature dendritic cells is related to preferential macrophage-colony-stimulating factor-driven macrophage differentiation

Following trauma, increased inflammatory monokine activation and depressed APC function can occur simultaneously. These contradictory monocyte (Mphi) dysfunctions could result if postinjury Mphi differentiation preferentially favored inflammatory macrophage (Mac) differentiation over development into the most potent APC, dendritic cells (DC). In this report, Mphi of trauma patients with a depressed MLR induction capacity are, for the first time, shown to be unable to differentiate in vitro to immature CD1a(+) DC under the influence of GM-CSF and IL-4. Trauma patient Mphi that retained MLR-inducing capacity had a nonsignificant reduction in DC differentiation capacity. Only patient Mphi populations with depressed differentiation to immature DC (iDC) demonstrated depressed IL-12 and IL-15 production and a continued reduced MLR induction capacity. Neither increased IL-10 production nor decreased CD11c(+) DC precursor numbers correlated with depressed Mphi-to-DC differentiation. Instead, these patients' APC-dysfunctional Mphi populations had increased expression of inflammatory Mac phenotypes (CD64(+), CD86(low), HLA-DR(low)) and up-regulated secretion of M-CSF. M-CSF combined with IL-6 inhibits Mphi-to-iDC differentiation and promotes Mphi-to-Mac differentiation by down-regulating GM-CSFR expression and increasing DC apoptosis. Both depressed GM-CSFR expression and increased Mphi iDC apoptosis, as well as increased expression of CD126 (IL-6R) and CD115 (M-CSFR), were detected in APC-defective patient Mphi. In vitro addition of anti-M-CSF enhanced the IL-4 plus GM-CSF-induced Mphi-to-DC differentiation of these patients. This suggests that, in trauma patients, enhanced Mphi-to-Mac differentiation with concomitant inhibited iDC development is partially due to increased circulating Mphi sensitivity to and production of M-CSF and contributes to postinjury immunoaberrations.     

Lidocaine suppresses subthreshold oscillations by inhibiting persistent Na(+) current in injured dorsal root ganglion neurons

The aim of this study was to determine the effect and mechanism of low concentration of lidocaine on subthreshold membrane potential oscillations (SMPO) and burst discharges in chronically compressed dorsal root ganglion (DRG) neurons. DRG neurons were isolated by enzymatic dissociation method. SMPO, burst discharges and single spike were elicited by whole cell patch-clamp technique in current clamp mode. Persistent Na(+) current (I(NaP)) and transient Na(+) current (I(NaT)) were elicited in voltage clamp mode. The results showed that SMPO was suppressed and burst discharges were eliminated by tetrodotoxin (TTX, 0.2 micromol/l) in current clamp mode, I(NaP) was blocked by 0.2 micromol/l TTX in voltage clamp mode. SMPO, burst discharges and I(NaP) were also suppressed by low concentration of lidocaine (10 micromol/l) respectively. However, single spike and I(NaT) could only be blocked by high concentration of lidocaine (5 mmol/l). From these results, it is suggested that I(NaP) mediates the generation of SMPO in injured DRG neurons. Low concentration of lidocaine (10 micromol/l) suppresses SMPO by selectively inhibiting I(NaP), but not I(NaT), in chronically compressed DRG neurons.     

Factors affecting central inspiratory modulation of hypoglossal motoneuron activity in newborn pigs

In newborn pigs (4-6 days old), recordings of efferent whole hypoglossal and phrenic nerve discharges were obtained during hyperoxia (or normoxia) and during hypoxia, before and after bilateral vagotomy. With intact vagi, spontaneous hypoglossal inspiratory activity was not observed and was not elicited by either spontaneous changes of electroencephalogram (EEG) or hypoxic stimulation (15% O2 in N2). After bilateral vagotomy, some animals had episodes of spontaneous hypoglossal inspiratory activity; power spectral analysis of EEG demonstrated that this inspiratory activity appeared synchronously with shifts of major peaks in EEG spectra from the delta band (0.5-3.5 Hz) to the theta band (3.5-7.0 Hz). Hypoglossal inspiratory discharges were also elicited by hypoxic stimulation and usually had a decrementing discharge pattern; in some cases, this activity had an augmenting discharge pattern. Our results suggest that hypoglossal motoneurons are poorly modulated by central inspiratory drive, requiring additional facilitatory influences, i.e. corticobulbar, intra-bulbar, chemical drive, before such modulation is observed.     

Effects of different ions on resting polarization and on the mass receptor potential of carotid body chemosensors

The carotid body and its own nerve were removed from cats anesthetized with sodium pentobarbital and placed in an air gap system; the carotid body was bathed in modified Locke's solution equilibrated with 50% O₂ in N₂, pH 7.43 at 35°C. The sensory discharges, changes in “resting” receptor polarization and the mass receptor potential evoked by ACh or NaCN were recorded with nonpolarizable electrodes placed across the gap. Receptor potentials and sensory discharges evoked by ACh showed an appreciable increase in amplitude and frequency when the preparation was bathed in eserinized Locke. Eserine did not change appreciably the responses evoked by NaCN. Excessive depolarization elicited by either ACh or NaCN was accompanied by sensory discharge block. Removal of K⁺ ions from the bathing solution induced receptor hyperpolarization and an increase in the amplitude of the evoked receptor potentials. An increase of K⁺ concentration had the opposite effect. Reduction of Na⁺ or NaCl to one half, or total removal of this salt, induced an initial reduction and later disappearance of the sensory discharges, some receptor hyperpolarization and a reduction in the amplitude of the evoked receptor potentials. Reduction or removal of Ca⁺⁺ produced receptor depolarization, a marked depression of the evoked receptor potentials, an increase in the frequency of the sensory discharges and a reduction in the amplitude of the nerve action potentials. High Ca⁺⁺ or Mg⁺⁺ had little or no effect on action potential amplitude or resting polarization, but decreased sensory discharge frequency and the evoked receptor potentials. Total or partial replacement of Ca⁺⁺ with Mg⁺⁺ induced complex effects: (1) receptor depolarization which occurred in low Ca⁺⁺, was prevented by addition of Mg⁺⁺ ions; (2) the amplitude of the evoked receptor potentials was depressed; (3) the nerve discharge frequency was reduced as it was in high Mg⁺⁺ solutions; and (4) the amplitude of the nerve action potentials was reduced as it was in low Ca⁺⁺ solutions. Temperature had a marked effect on the chemoreceptors since a t high temperatures the receptors were depolarized and the discharge frequency increased. The baseline discharge and responses evoked by ACh or NaCN were depressed at low temperatures. The results are discussed in terms of possible receptor mechanisms influenced by the different ions.     

Electric discharges and electrogenesis peculiarity in two African upside-down catfishes, <Emphasis Type="Italic">Synodontis caudovittatus</Emphasis> and <Emphasis Type="Italic">S. eupterus</Emphasis> (Mochokidae,Siluriformes)

The paper reports spontaneous generation of weak electric discharges with an amplitude of 0.4–1.0 mV and a frequency of 3–9 min^–1 by solitary Synodontis caudovittatus fish. When fish individuals were tested in pairs, their aggressive–defense interactions were associated with an increase in the amplitude of the discharges (up to 30–45 mV) compared to the discharges of individual fish, while the duration of the pulses increased up to 20–25 ms due to the prolongation of the second phase. In S. eupterus, electric activity was recorded only in the course of aggression–defense interactions, while spontaneous generation of discharges was not observed at all. The paper discusses the different aspects of electrocummunication between the catfish including the role of the reversion of polarity of the merged summated discharges with increased duration.     

Selective depressant action of antidromic impulses on gustatory nerve signals

The depressant action of antidromic volleys of impulses on gustatory nerve signals from the tongues of bullfrogs was studied. Electrical stimulation of the glossopharyngeal nerve at a rate of 100 Hz for 10 s and at supramaximal intensity slightly depressed the integrated glossopharyngeal nerve responses to quinine and to mechanical taps to the tongue. The same antidromic stimuli resulted in a 30-40% reduction in the responses to salt, acid, water, and warmed saline, but depressed greater than 80% of the afferent impulses firing spontaneously. The magnitude of responses to quinine and NaCl and the number of spontaneous discharges decreased gradually with an increase in either the frequency or the duration of antidromic stimuli. Similar results were obtained with intensities above the threshold for exciting gustatory and slowly adapting mechanosensitive fibers. The time required to recover from termination of the antidromic stimuli to two-thirds of the maximal amount of depression ranged between 6 and 7 min, with no significant differences among the depressions. The possible mechanisms involved in the antidromic depression of gustatory nerve signals are discussed.     

The effects of glycerol and urea on the ultrastructure and contractility of fast and slow rat skeletal muscles

The influence of the influx and efflux of glycerol and urea (400 mmol/l) on the amplitude of isometric twitches and the ultrastructure of isolated fast (EDL) and slow (SOL) muscles of young rats was studied. The influx of non-electrolytes was accompanied by a temporary decrease in the twitch tension. The removal of non-electrolytes resulted in a stable reduction of twitches. Both effects were less pronounced in glycerol experiments on slow muscles. The inhibition of twitches after the removal of non-electrolytes was associated with selective alterations of the T-system: swelling, vacuolation, and lysis of T-tubules. Quantitative analysis of the T-system showed that the extent of these changes may vary for different fibres, and the intensity of morphological alteration of the T-system generally correlated with the degree of twitch inhibition. Reloading of muscles with non-electrolytes tended to improve the T-system structure in some fibres and led to a partial restoration of the amplitude of twitches.     

Differential effect of central command on aortic and carotid sinus baroreceptor-heart rate reflexes at the onset of spontaneous, fictive motor activity

Our laboratory has reported that central command blunts the sensitivity of the aortic baroreceptor-heart rate (HR) reflex at the onset of voluntary static exercise in conscious cats and spontaneous contraction in decerebrate cats. The purpose of this study was to examine whether central command attenuates the sensitivity of the carotid sinus baroreceptor-HR reflex at the onset of spontaneous, fictive motor activity in paralyzed, decerebrate cats. We confirmed that aortic nerve (AN)-stimulation-induced bradycardia was markedly blunted to 26 ± 4.4% of the control (21 ± 1.3 beats/min) at the onset of spontaneous motor activity. Although the baroreflex bradycardia by electrical stimulation of the carotid sinus nerve (CSN) was suppressed (P < 0.05) to 86 ± 5.6% of the control (38 ± 1.2 beats/min), the inhibitory effect of spontaneous motor activity was much weaker (P < 0.05) with CSN stimulation than with AN stimulation. The baroreflex bradycardia elicited by brief occlusion of the abdominal aorta was blunted to 36% of the control (36 ± 1.6 beats/min) during spontaneous motor activity, suggesting that central command is able to inhibit the cardiomotor sensitivity of arterial baroreflexes as the net effect. Mechanical stretch of the triceps surae muscle never affected the baroreflex bradycardia elicited by AN or CSN stimulation and by aortic occlusion, suggesting that muscle mechanoreflex did not modify the cardiomotor sensitivity of aortic and carotid sinus baroreflex. Since the inhibitory effect of central command on the carotid baroreflex pathway, associated with spontaneous motor activity, was much weaker compared with the aortic baroreflex pathway, it is concluded that central command does not force a generalized modulation on the whole pathways of arterial baroreflexes but provides selective inhibition for the cardiomotor component of the aortic baroreflex.