Do specialized cutaneous cold receptors exist?

The relative quantity of the cutaneous nerve unmyelinated fibers that conduct the excitation impulses from mechanoreceptors under contraction of pilomotors without and during cooling of the skin by 10 degrees C at a rate of 1 degree C per second was measured by the integrating method of colliding impulses. The same mechanoreceptors are shown to be excited by pilomotors both under skin deformation and cooling. A conclusion is made about absence of specific cold receptors in the cat skin.     

Changes of impulse activity recorded from the rat vagus nerve during short-lasting total cooling

Gradual cooling of anesthetized rats followed by a drop in rectal temperature (RT) increased the frequency of efferent impulses and decreased the frequency of afferent impulses in the vagus nerves. Preliminary short-lasting (5 h) moderate cooling of the animals in a thermochamber to +5°C (RT did not change), or intensive cooling to −20°C (RT dropped to 32°C) changed the response of efferent nerve fibers to cooling of the body. Under these conditions, a drop in RT to 29°C was followed by a significant increase in efferent discharges in the vagus nerve after additional cooling throughout the experiment, while an initial cooling phase (RT was equal to 35-30°C) was followed by some inhibitory effect. At the same time, the changes in the afferent link were different. As in the control, gradual cooling decreased frequency of afferent impulses, although the intensity of the effects was different. The involvement of the vagus nerve system in the maintenance of temperature homeostasis during body cooling has been discussed.     

Role of vagal C-fiber afferents in respiratory response to hypercapnia

The respiratory response to hypercapnia has been investigated in 10 anesthetized rabbits by use of a rebreathing technique. The responses were obtained in three situations: with one intact vagus nerve (control), during differential block of conduction, and after vagotomy. Differential block was achieved using anodal hyperpolarization by application of a direct current to the cervical vagus nerve. Great care was taken during the differential block to establish that all impulse conduction in myelinated fibers of the cervical vagus nerve was abolished but that the nonmyelinated fibers conducted normally. Additionally, in five more rabbits the nature of the differential block was confirmed from single-fiber recordings of activity in both myelinated and nonmyelinated fibers. The same increase in tidal volume in response to hypercapnia was present in all three experimental situations, indicating that it was not vagally mediated. The increase in frequency in response to hypercapnia in the control state was abolished by vagotomy but preserved when only the nonmyelinated fibers were functioning during the differential block. This increased frequency response, attributable to decreases in both inspiratory and expiratory durations, was usually enhanced during the differential block, despite the slower deeper pattern of breathing attributed to loss of activity in myelinated fibers. The implications of this reflex increase in frequency in response to hypercapnia, mediated by nonmyelinated vagal endings in the lung, are discussed.     

Immunocytological localization of the major peripheral nervous system glycoprotein P0 and the L2/HNK-1 and L3 carbohydrate structures in developing and adult mouse sciatic nerve

Immunocytological localization of the major glycoprotein of peripheral myelin P0 and its associated carbohydrate structures L2/HNK-1 and L3 was performed at the light- and electron-microscopic levels in mouse sciatic nerves at several developmental stages and in adulthood. P0 was first expressed on Schwann cells at the time that Schwann cells associated with axons on a 1:1 basis. P0 remains expressed at all times of myelin formation and in compact myelin. After cessation of myelination P0 is no longer detectable in the uncompacted parts of myelin, i.e., Schmidt-Lanterman incisures, paranodal loops, and outer and inner mesaxons. P0 is not detectable on basement membranes, interstitial collagens, and non-myelin-forming Schwann cells. The associated carbohydrate epitope L2 does not follow the expression of P0 at any developmental or adult stage. Until 21 days the L2 epitope is confined to nonmyelinated fibers. In sciatic nerves of mice older than 8 weeks, however, only a few nonmyelinated fibers remain L2-positive. L2 immunoreactivity is clearly seen in a subpopulation of compact myelin figures largely associated with motor fibers. The L3 epitope is never detectable on nonmyelinated fibers and becomes first visible when compact myelin is discerned. Unlike the L2 epitope L3 is present in most, if not all, compact myelin figures. These observations suggest that P0 may be involved in ensheathment of axons by Schwann cells at the decisive stages of initiation of myelination and later on, possibly in conjunction with the L3 carbohydrate structure, in maintenance of compact myelin. The appearance of the L2 carbohydrate epitopes in compact myelin of largely motor and fewer sensory nerve fibers at times when morphogenesis of myelin has ceased remains to be elucidated in functional terms.     

Effects of heating and cooling on nerve terminal impulses recorded from cold-sensitive receptors in the guinea-pig cornea

An in vitro preparation of the guinea-pig cornea was used to study the effects of changing temperature on nerve terminal impulses recorded extracellularly from cold-sensitive receptors. At a stable holding temperature (31-32.5 degrees C), cold receptors had an ongoing periodic discharge of nerve terminal impulses. This activity decreased or ceased with heating and increased with cooling. Reducing the rate of temperature change reduced the respective effects of heating and cooling on nerve terminal impulse frequency. In addition to changes in the frequency of activity, nerve terminal impulse shape also changed with heating and cooling. At the same ambient temperature, nerve terminal impulses were larger in amplitude and faster in time course during heating than those recorded during cooling. The magnitude of these effects of heating and cooling on nerve terminal impulse shape was reduced if the rate of temperature change was slowed. At 29, 31.5, and 35 degrees C, a train of 50 electrical stimuli delivered to the ciliary nerves at 10-40 Hz produced a progressive increase in the amplitude of successive nerve terminal impulses evoked during the train. Therefore, it is unlikely that the reduction in nerve terminal impulse amplitude observed during cooling is due to the activity-dependent changes in the nerve terminal produced by the concomitant increase in impulse frequency. Instead, the differences in nerve terminal impulse shape observed at the same ambient temperature during heating and cooling may reflect changes in the membrane potential of the nerve terminal associated with thermal transduction.     

Rapid shallow breathing caused by pulmonary vascular congestion in cats

The vasculature of one lung of unanesthetized spontaneously breathing decerebrate cats was isolated and congested with blood. Such pulmonary vascular congestion (PVC) consistently resulted in a shallow tachypnea associated with expiratory activation of the diaphragm and thyroarytenoid muscles, signifying augmented expiratory braking. With progressive increases in pulmonary vascular pressure, tachypnea and expiratory braking increased progressively and ultimately obscured phasic activity in the diaphragm and thyroarytenoid. Thus the apnea caused by PVC constitutes not an arrest of neural respiratory activity but rather a continuous activation of thoracic inspiratory and laryngeal adductor muscles. When capsaicin, a neurotoxin that activates nonmyelinated afferents, was injected into the pulmonary artery of the isolated lung, it produced changes in timing and distribution of respiratory motor output that resembled those with PVC but were more abrupt in onset. Capsaicin, applied perineurally to the cervical vagi, preferentially blocked the conduction of nonmyelinated afferent fibers. This procedure, which produced little degradation in Hering-Breuer reflexes, eliminated tachypnea and expiratory braking caused by PVC or capsaicin injection. The results indicate that activation of pulmonary vagal afferent fibers of C or A-delta category in unanesthetized cats reflexly modifies the respiratory motor output in a way that resembles the human response to PVC or pulmonary embolism. This is a brain stem reflex.     

Equilibria of frog nerve with different external concentrations of sodium ions

Using the ability of the nerve fibers to conduct impulses as indicator of changes in the concentration of sodium ions in the interstitial spaces of nerve an evaluation has been made of the diffusion constant of sodium ions. The calculated minimal value (0.62 x 10(-4) cm.(2)/min.) undoubtedly is much too low; nevertheless, it is still so high that as a rule the diffusion of sodium ions is far more rapid than the establishment of excitability changes; therefore, diffusion times need not be taken into account in the interpretation of ordinary experiments. By measurements of the changes in the longitudinal conductivity of nerve which result from changes in the external concentration of sodium chloride an evaluation has been made of the diffusion constant of sodium chloride in the interstitial spaces of nerve. A minimal value for this constant is 1.4 x 10(-4) cm.(2)/min. The evidence presented would be compatible with the assumption that the permeability of the connective tissue sheath for sodium ions decreases slightly after the concentration of sodium ions in the interstitial spaces of the nerve has become negligible; the evidence, however, shows that changes in the permeability of the sheath cannot play a significant role in determining the temporal courses of the development of inexcitability in a sodium-free medium and of the restoration of excitability by added sodium ions. If a decrease in the permeability of the sheath should take place in a sodium-free medium, the change would be small and would occur after the nerve fibers have become inexcitable; on the other hand the action of a moderate concentration of sodium ions would be sufficient to restore the permeability of the sheath. As measured by the recovery by A fibers of the ability to conduct impulses the restoration by 0.1 N sodium ions of nerve that has been deprived of sodium for 15 to 20 hours, i.e. for several hours after the nerve fibers have become inexcitable, begins after a significant delay, since no A fiber begins to conduct impulses in less than 8 or 10 minutes. The delay is referable to the fact that, before the A fibers can regain the ability to conduct impulses, those changes in their properties have to be reversed, which have taken place in the absence of sodium ions. Usually within 1 minute after sodium ions are made available to the nerve the polarizability of the membrane by the anodal current begins to increase; the A fibers soon begin to produce unconducted impulses in response to the break of the anodal current; then, they produce unconducted impulses in response to the closure of the cathodal current, and finally they become able to conduct impulses, although at a markedly reduced speed. The C fibers, that become inexcitable in a sodium-free medium later than the A fibers, begin to conduct impulses within 1 minute or 2 after 0.1 N sodium ions are made available to the nerve. Treatment of a nerve, that has been kept in a sodium-free medium, for 15 to 20 hours, with a moderate concentration of sodium ions (0.015, 0.02 N), acting for 1 hour or 2, is not sufficient to restore the ability to conduct impulses to more than a few A fibers, but it produces in a relatively large number of fibers a partial restoration, so that when the concentration of sodium ions outside the epineurium is increased by 0.005 or 0.01 N a significant number of A fibers begin to conduct impulses within less than 5 seconds. Initially the recovery progresses with great rapidity, but after a small number of minutes the height of the conducted spike remains practically stationary. Increase of the external concentration of sodium ions by a small amount again causes a rapid enhancement of the recovery, but once more, after a few minutes the height of the spike remains practically stationary, etc. A subnormal concentration of sodium ions may restore to all the A fibers the ability to conduct impulses, but only 0.1 N sodium ions are able to produce a complete restoration of the speed of conduction, and only after they have been allowed to act for a considerable period of time. The ability of all the C fibers to conduct impulses may be restored by relatively small concentrations of sodium ions, 0.02 to 0.025 N. Nerve fibers that have become inexcitable in a sodium-free medium and have been restored by sodium ions are far more sensitive to the effect of the lack of sodium than the fibers of untreated nerve. Repeated removal and addition of sodium ions may bring the nerve fibers, especially those of spinal roots, to a state in which the sensitivity to the lack of sodium is exceedingly great; spinal root fibers may then begin to become inexcitable in a sodium-free medium within a few seconds. Treatment of the nerve with 0.1 N sodium ions for 1 hour or 2 is sufficient to bring about a marked increase in the resistance to the lack of sodium. On the other hand keeping a nerve in Ringer's solution or in the presence of 0.04 N sodium ions does not produce a readily detectable increase in the sensitivity to the lack of sodium. Even the resistance of nerve kept in the presence of 0.025 N sodium ions for 23 hours is very high, since after 2 hours in a sodium-free medium more than two-thirds of the initially conducting fibers will be able to conduct impulses. Frog nerve reaches different states of equilibrium with different external concentrations of sodium ions. The states are characterized by the degree of effectiveness of the nerve reaction, the speed of conduction of impulses, and the number of conducting fibers. Approximately the same equilibrium state may be reached by (a) leaving the nerve for 20 to 24 hours in the presence of a subnormal concentration of sodium ions and (b) by leaving the nerve in a sodium-free medium for 15 to 20 hours, restoring it with 0.1 N sodium ions acting for a short period of time, rendering it inexcitable again in a sodium-free medium, and finally restoring it with a moderate concentration of sodium ions. If, however, the nerve that has been kept in a sodium-free medium for 15 to 20 hours is restored directly by a moderate concentration of sodium ions the state will not be reached, at least not for several hours, which corresponds to equilibrium with that concentration. The role of sodium in nerve physiology is discussed. Sodium participates in at least four processes, (a) The regulation of the concentration of water outside the nerve fibers; (b) the regulation of the total value of the membrane potential; (c) the production of the nerve impulse, and (d) the establishment of the nerve reaction. In so far as processes (c) and (d) are concerned only the sodium present inside the nerve fibers plays a role; the presence of sodium ions outside the nerve fibers is important only because in the absence of interstitial sodium ions the nerve fibers lose a part of their internal sodium content. The nerve impulse and the nerve reaction may be produced for long periods of time after the concentration of sodium ions outside the nerve fibers has become negligible. A working hypothesis is put forward according to which the internal sodium content and the interstitial concentration of sodium ions are in equilibrium in so far as a different internal sodium content corresponds to each interstitial concentration. The properties of the nerve fibers are determined by the internal sodium content. The change in properties, i.e. in the state of the nerve fibers, results from processes that take place inside the nerve fibers after the interstitial concentration of sodium ions and consequently also the internal sodium content have been changed.     

Role of cAMP in activation of ischemically sensitive abdominal visceral afferents

A number of metabolites produced during abdominal ischemia can stimulate and/or sensitize visceral afferents. The precise mechanisms whereby these metabolites act are uncertain. Other studies have shown that the adenylate cyclase-cAMP system may be involved in the activation of sensory neurons. Therefore, we hypothesized that cAMP contributes to the activation of ischemically sensitive abdominal visceral afferents. Single-unit activity of abdominal visceral C fibers was recorded from the right thoracic sympathetic chain in anesthetized cats before and during 7 min of abdominal ischemia. Forty-six percent of ischemically sensitive C fibers responded to intra-arterial injection of 8-bromo-cAMP (0.35-1. 0 mg/kg), an analog of cAMP, with responses during ischemia increasing from 0.50 +/- 0.06 to 0.84 +/- 0.08 impulses/s (P < 0.05, n = 11 C fibers). Conversely, an inhibitor of adenylate cyclase, 2', 5'-dideoxyadenosine (DDA; 0.1 mg/kg iv), attenuated ischemia-induced increase in activity of afferents from 0.66 +/- 0.10 to 0.34 +/- 0. 09 impulses/s (P < 0.05; n = 8). Furthermore, whereas exogenous PGE(2) (3-4 microg/kg ia) augmented the ischemia-induced increase in activity of afferents (P < 0.05, n = 10), treatment with DDA (0.1 mg/kg iv) substantially reduced the increase in discharge activity of afferents during ischemia, which was augmented by PGE(2) (1.45 +/- 0.24 vs. 0.70 +/- 0.09 impulses/s, -DDA vs. +DDA; P < 0.05) in six fibers. A time control group (n = 4), however, demonstrated similar increases in the activity of afferents with repeated administration of PGE(2). These data suggest that cAMP contributes to the activation of abdominal visceral afferents during ischemia, particularly to the action of PGs on activation and/or sensitization of these endings.     

Effect of menthol on cold receptor activity. Analysis of receptor processes

The effect of menthol on the discharge pattern of feline nasal and lingual cold receptors was analyzed in order to elucidate the underlying sensory transducer mechanism. A repetitive beating activity and burst (grouped) discharges were observed in both cold receptor populations at constant temperatures and after rapid cooling. An analysis of the impulse activity revealed a cyclic pattern of impulse generation, which suggested the existence of an underlying receptor potential oscillation that initiates impulses in the afferent nerve when it exceeds a threshold value. The frequency and amplitude of the periodic impulse-inducing receptor processes were characterized by the burst frequency, which increased with warming, and by the average number of impulses generated during each cycle, which increased with cooling. Menthol at micromolar concentrations induced an acceleration of the burst frequency at higher temperatures, but reduced the burst frequency in the midtemperature range. At temperatures above 25 degrees C, menthol increased the number of impulses elicited during each cycle and induced bursting in previously repetitively discharging fibers. At low temperatures, menthol suppressed bursting and finally inhibited all cold receptor activity. The impulse pattern at constant temperatures and during the dynamic response to rapid cooling was comparably affected by menthol. Calcium application completely abolished the stimulating menthol effect. Since, in equal concentrations, menthol specifically impairs neuronal calcium currents, the results are consistent with the conjecture that in cold receptors, menthol reduces the activation of a calcium-stimulated outward current by an impeding effect on a calcium conductance, thereby inducing depolarization and a modification of bursting behavior. The data confirm the hypothesis of a calcium-controlled outward conductance being involved in the generation of cyclic afferent activity in cold receptors.     

Stimulation of vagal pulmonary C-fibers by a single breath of cigarette smoke in dogs

Inhalation of cigarette smoke into the lower airway via a tracheostomy evokes immediate apnea, bradycardia, and systemic hypotension in dogs. These responses can still be evoked when conduction in myelinated vagal fibers is blocked preferentially by cooling but are abolished by vagotomy, suggesting that they are mediated by afferent vagal C-fibers. To examine this possibility, we recorded impulses in pulmonary C-fibers in anesthetized, open-chest dogs and delivered 120 ml cigarette smoke to the lungs in a single ventilatory cycle. Pulmonary C-fibers were stimulated within 1 or 2 s of the delivery of smoke generated by high-nicotine cigarettes, activity increasing from 0.3 +/- 0.1 to a peak of 12.6 +/- 1.3 (SE) impulses/s, (n = 60); the evoked discharge usually lasted 3-5 s. Smoke generated by low-nicotine cigarettes evoked a milder stimulation in 33% of pulmonary C-fibers but did not significantly affect the overall firing frequency (peak activity = 2.2 +/- 1.1 impulses/s, n = 36). Hexamethonium (0.7-1.2 mg/kg iv) prevented C-fiber stimulation by high-nicotine cigarette smoke (n = 12) but not stimulation by right atrial injection of capsaicin. We conclude that pulmonary C-fibers are stimulated by a single breath of cigarette smoke and that nicotine is the constituent responsible.     

Efferent system in the retina of the frog, Rana catesbiana.

Single units were recorded through glass microelectrodes placed on the optic disk or on the retina of the opened eye of the frog (Rana catesbiana). Units were classified as A-, B-, and C-fibers according to conduction velocities. By the method of collision between naturally elicited and electrically elicited impulses, many of the B-fibers and some A- and C-fibers, which showed unusual behavior to photic stimulation, were found to be efferent fibers. Retinal effects of the efferent nerves were studied by repetitive stimulation and cooling of the optic nerve. The effects were found to be both inhibitory and excitatory.     

A study of conduction velocity in nonmyelinated nerve fibers.

By treating a nonmyelinated nerve fiber as a continuous cable consisting of three distinct zones (Resting, transitional, and excited), the following mathematical expression was derived: (formula: see text) where v is the conduction velocity, d the diameter of the fiber, R the resistance of the membrane of unit area at the peak of excitation, rho the resistivity of the medium inside the fiber, and C the capacity of membrane per unit area. The validity of this expression was demonstrated by using squid giant nerve fibers intracellularly perfused with dilute salt solutions. The relationship between these results and previous theories and experiments on conduction velocity is discussed.     

Effects of cold and heat on behavior and cerebellar function in goldfish

Summary A similar sequence of behavioral effects was observed for either cooling or heating; most effects occurred on changing temperature of entire fish or of only the cerebellum. On moderate heating or cooling, fish are hyperexcitable, spontaneously hyperactive; on further heating or cooling swimming is uncoordinated; when the subcerebellar structures are heated or cooled, equilibrium is disturbed; on further heating or cooling coma and respiratory failure ensue. Critical temperatures are modifiable by acclimation. The behavioral effects of cerebellectomy are additive with temperature effects on motor centers.Electrical activity of Purkinje neurons changes in the same thermal ranges as behavior. Inhibition via cerebellar interneurons is most sensitive and can be modified by acclimation. Ongoing activity increases with warming up to a blocking temperature; interspike interval histograms show pattern changes during warming. Activation via mossy fibers-granule cells is more sensitive than that via climbing fibers, and antidromic impulses are most resistant.A neuronal model based on inhibitory actions of Purkinje neurons on motor centers and parallel feedback excitatory pathways can explain both behavioral and electrical observations.     

Electrophysiology of the Insect Dorsal Ocellus : I. Origin of the components of the electroretinogram

Dorsal ocelli are small cup-like organs containing a layer of photoreceptor cells, the short axons of which synapse at the base of the cup with dendritic terminals of ocellar nerve fibers. The ocellar ERG of dragonflies, recorded from the surface of the receptor cell layer and from the long lateral ocellar nerve, contains four components. Component 1 is a depolarizing sensory generator potential which originates in the distal ends of the receptor cells and evokes component 2. Component 2 is believed to be a depolarizing response of the receptor axons. It evokes a hyperpolarizing postsynaptic potential, component 3, which originates in the dendritic terminals of the ocellar nerve fibers. Ocellar nerve fibers in dragonflies are spontaneously active, discharging afferent nerve impulses (component 4) in the dark-adapted state. Component 3 inhibits this discharge. The ERG of the cockroach ocellus is similar. The main differences are that component 3 is not as conspicuous as in the dragonflies and that in most cases ocellar nerve impulses appear only as a brief burst at "off." In one preparation a spontaneous discharge of nerve impulses was observed. As in the dragonflies, this was inhibited by illumination.     

Alveolar hypercapnia augments pulmonary C-fiber responses to chemical stimulants: role of hydrogen ion.

To determine whether the excitabilities of pulmonary C fibers to chemical and mechanical stimuli are altered by CO(2)-induced acidosis, single-unit pulmonary C-fiber activity was recorded in anesthetized, open-chest rats. Transient alveolar hypercapnia (HPC) was induced by administering CO(2)-enriched gas mixture (15% CO(2), balance air) via the respirator inlet for 30 s, which rapidly lowered the arterial blood pH from a baseline of 7.40 +/- 0.01 to 7.17 +/- 0.02. Alveolar HPC markedly increased the responses of these C-fiber afferents to several chemical stimulants. For example, the C-fiber response to right atrial injection of the same dose of capsaicin (0.25-1.0 microg/kg) was significantly increased from 3.07 +/- 0.70 impulses/s at control to 8.48 +/- 1.52 impulses/s during HPC (n = 27; P < 0.05), and this enhanced response returned to control within approximately 10 min after termination of HPC. Similarly, alveolar HPC also induced significant increases in the C-fiber responses to right atrial injections of phenylbiguanide (4-8 microg/kg) and adenosine (0.2 mg/kg). In contrast, HPC did not change the response of pulmonary C fibers to lung inflation. Furthermore, the peak response of these C fibers to capsaicin during HPC was greatly attenuated when the HPC-induced acidosis was buffered by infusion of bicarbonate (1.36-1.82 mmol. kg(-1). min(-1) for 35 s). In conclusion, alveolar HPC augments the responses of these afferents to various chemical stimulants, and this potentiating effect of CO(2) is mediated through the action of hydrogen ions on the C-fiber sensory terminals.     

Conduction in bundles of demyelinated nerve fibers: computer simulation

This study presents a model of action potential propagation in bundles of myelinated nerve fibers. The model combines the single-cable formulation of Goldman and Albus (1967) with a basic representation of the ephaptic interaction among the fibers. We analyze first the behavior of the conduction velocity (CV) under the change of the various conductance parameters and temperature. The main parameter influencing the CV is the fast sodium conductance, and the dependence of CV on the temperature is linear up to 30 degrees C. The increase of myelin thickness above its normal value (5 microm) gives a slight increase in CV. The CV of the single fiber decreases monotonically with the disruption of myelin, but the breakdown is abrupt. There is always conduction until the thickness is larger than 2% of its original value, at which with at this point a sharp transition of CV to zero occurs. Also, the increase of temperature can block conduction. At 5% of the original thickness there is still spike propagation, but an increase of 2 degrees C causes conduction block. These results are consistent with clinical observations. Computer simulations are performed to show how the CV is affected by local damage to the myelin sheath, temperature alterations, and increased ephaptic coupling (i.e., coupling of electrical origin due to the electric neutrality of all the nerve) in the case of fiber bundles. The ephaptic interaction is included in the model. Synchronous impulse transmission and the formation of "condensed" pulse states are found. Electric impulses with a delay of 0.5 ms are presented to the system, and the numerical results show that, for increasing coupling, the impulses tend to adjust their speed and become synchronized. Other interesting phenomena are that spurious spikes are likely to be generated when ephaptic interaction is raised and that damaged axons suffering conduction block can be brought into conduction by the normal functioning fibers surrounding them. This is seen also in the case of a large number of fibers (N=500). When all the fibers are stimulated simultaneously, the conduction velocity is found to be strongly dependent on the level of ephaptic coupling and a sensible reduction is observed with respect to the propagation along an isolated axon even for low coupling level. As in the case of three fibers, spikes tend to lock and form collective impulses that propagate slowly in the nerve. On the other hand, if only 10% of fibers are stimulated by an external input, the conduction velocity is only 2% less than that along a single axon. We found a threshold value for the ephaptic coupling such that for lower values it is impossible to recruit the damaged fibers into conduction, for values of the coupling equal to this threshold only one fiber can be restored by the nondamaged fibers, and for values larger than the threshold an increasing number of fibers can return to normal functioning. We get values of the ephaptic coupling such that 25% of axons can be damaged without change of the collective conduction.     

神经退变和再生的构筑变化

将夹伤的大鼠坐骨神经分离成单根纤维,观察98d内轴突和许旺细胞的构筑变化过程发现,损伤既使轴浆转运阻断、积累的细胞器退变,也使髓鞘板层,特别是斯兰氏切迹撕裂、变形或侵入轴突。轴突或髓鞘虽可各呈单一的退变,但以两者并存多见。伤后1d即出现富含微管的再生芽,它被增殖的许旺细胞突起及其基底膜包绕,并逐步发育成熟。根据再生的特征性构筑变化,提出了再生芽、无髓和有髓纤维、斯兰氏切迹、朗氏结与神经小束的初见、发育和成熟高峰期的时间顺序。无髓纤维的发育成熟早于有髓纤维。     

刺猬胸前神经传入活动的来源及皮层代表区分布

为探讨冬眠刺猬皮肌的紧张性控制,本工作研究了支配皮肌的胸前神经(VTN)的传入活动的来源和皮层代表区的分布。VTN的传入冲动来自皮肌本体感受器,传入纤维径C_6—T_2背根入脊髓,与同部位的皮肤感觉相分离,后者经相应节段的皮神经传入。电刺激VTN引起的皮层诱发电位反应位于新皮层外侧面的中间部,相当于Woolsey的S-Ⅱ区内,与桡神经和坐骨神经的代表区有重叠,而在S-Ⅰ区没有记录到反应。     

ELECTRICAL RESPONSES FROM THE LATERAL-LINE NERVES OF FISHES : IV. THE REPETITIVE DISCHARGE

The spontaneous discharge of impulses from the lateral-line nerves of trout and catfish has been examined. 1. Broken endings of nerve fibers supplying receptors of the lateral-lines of trout and catfish may be the source of a repetitive discharge of nerve impulses. 2. This injury discharge occurs more frequently in trout and may mask the spontaneous discharge from the receptor cells. Experiments indicate that the latter discharge is not the result of injury. 3. The injury discharge ceases in from 10 to 15 minutes. The spontaneous receptor discharge in trout may continue for an hour if the circulation remains intact. The receptor response also fails in from 10 to 15 minutes after failure of the circulation. 4. The receptor discharge, the injury discharge, or the summed discharges frequently become synchronized. The excitability of the fibers of the nerve trunk appears to vary synchronously, so that nerve impulses initiated in fibers from tactile receptors not contributing to the spontaneous discharge can be conducted only during the part of the cycle occupied by the spontaneous discharge.     

Interneuronal contacts and propagation mechanism in paired receptors of the propo-dactylopodite organ of the crayfish Astacus leptodactylis]

In recordings of biopotentials from the propo-dactylopodite-organ (the PD-organ) nerve, repetitive pairs of impulses are frequently observed, which presumably reflect paired structure of receptor elements where two sensory neurons are morphologically linked by non-polarized interdendritic ephapse. It is suggested that propagation via the ephapse out to be bilateral and that each of the postephaptic fibers transmits impulses from both of the cilia of the paired receptor. However, identical impulses from different cilia reach the central nervous system at different time, this mechanisms being presumably employed for differentiation of information on each of the cilia. One of the postephaptic fibers passes, seemingly, to the right, whereas the other one - to the left half of the first thoracic ganglion.