scholarly journals FACILITATION BY PREVIOUS ACTIVITY IN A PACINIAN CORPUSCLE

1958 ◽  
Vol 41 (4) ◽  
pp. 847-856 ◽  
Author(s):  
Werner R. Loewenstein
Keyword(s):  
Refractory Period ◽  
Recovery Time ◽  
Node Of Ranvier ◽  
Pacinian Corpuscle ◽  
Generator Potential ◽  
Relative Refractory Period ◽  
Supernormal Period ◽  
Local Potentials

A period of supernormal excitability is left by a propagated impulse in a Pacinian corpuscle. The increase in excitability is found 6 to 10 msec. after an impulse occurs in the corpuscle. Supernormality is produced by either mechanically elicited dromic impulses, or by electrically excited antidromic impulses. Generator potentials do not cause supernormality. Local potentials discharged spontaneously by the corpuscle, and which fall on the supernormal trail left by an antidromic impulse, become enhanced in amplitude, an eventually are turned into propagated dromic potentials. The supernormal period is interpreted as caused by a negative after-potential left at the first intracorpuscular node of Ranvier which outlasts both the recovery time of the firing level and that of the generator potential during the corpuscle's relative refractory period.

scholarly journals THE SITES FOR MECHANO-ELECTRIC CONVERSION IN A PACINIAN CORPUSCLE

1958 ◽  
Vol 41 (6) ◽  
pp. 1245-1265 ◽  
Author(s):  
Werner R. Loewenstein ◽  
Raquel Rathkamp ◽  
Keyword(s):  
Mechanical Stimulation ◽  
Nerve Ending ◽  
Sensory Nerve ◽  
Node Of Ranvier ◽  
Electric Activity ◽  
Myelinated Axon ◽  
Pacinian Corpuscle ◽  
Mechanical Stimuli ◽  
Myelinated Nerve ◽  
Generator Potential

The sensory nerve ending in the Pacinian corpuscle is surrounded by a non-nervous capsular structure which occupies about 99.9 per cent of the corpuscle's entire mass. After extirpation of practically all of the non-nervous structure, the sense organ's remains continue to function as a mechano-receptor, namely to produce generator and all-or-nothing potentials in response to mechanical stimuli. Compression of the first intracorpuscular node of Ranvier abolishes the production of "all-or-nothing" potentials in the corpuscle. Graded generator potentials constitute then the only response to mechanical stimulation. This reveals that the first node is the site of origin of the all-or-nothing potential and that the non-myelinated ending is incapable of producing all-or-nothing responses in response to mechanical stimulation. Compression of the entire length of non-myelinated ending suppresses the production of generator potentials. Partial compression of the ending abolishes mechano-responsiveness only of the compressed part. The intact remains of the ending continue to give generator potentials upon mechanical stimulation. This suggests that the generator potential arises at functionally independent membrane parts distributed all over the non-myelinated nerve ending. 24 to 36 hours after denervation of the corpuscle by transection of its sensory axon, no sign of electric activity is detected. Failure of mechano-reception at the nerve ending precedes that of conduction at the degenerating myelinated axon.

scholarly journals THE REFRACTORY STATE OF THE GENERATOR AND PROPAGATED POTENTIALS IN A PACINIAN CORPUSCLE

1958 ◽  
Vol 41 (4) ◽  
pp. 805-824 ◽  
Author(s):  
Werner R. Loewenstein ◽  
Rafael Altamirano-Orrego
Keyword(s):  
Time Course ◽  
Node Of Ranvier ◽  
Pacinian Corpuscle ◽  
Mechanical Stimuli ◽  
Stimulus Interval ◽  
Generator Potential ◽  
Msec Duration ◽  
Refractory State ◽  
Strength Constant ◽  
Spontaneous Fluctuations

A propagated potential produced in the Pacinian corpuscle in response to mechanical stimuli leaves a refractory state of 7 to 10 msec. duration. The refractory state is presumably produced at the first intracorpuscular node of Ranvier. The recovery of receptor excitability for producing an all-or-none response to mechanical stimulation follows the same time course as that of the electrically excited axon. Upon progressive reduction of stimulus interval (mechanical), the propagated potential falls progressively to 75 per cent of its resting magnitude and becomes finally blocked within the corpuscle. A non-propagated all-or-none potential, presumably corresponding to activity of the first node, is then detected. The critical firing level for all-or-none potentials increases progressively during the relative refractory period of the all-or-none potential, as the stimulus interval is shortened. Thus generator potentials up to 85 per cent of a propagated potential can be produced in absence of all-or-none activity. Generator potentials show: gradual over-all increase in amplitude and rate of rise as a function of stimulus strength; constant latency; and spontaneous fluctuations in amplitude. A generator potential leaves a refractory state (presumably at the non-myelinated ending) so that the amplitude of a second generator response which falls on its refractory trail is directly related to the time elapsed after the first generator response and inversely to its amplitude. The generator potential develops independently of any refractory state left by a preceding all-or-none potential.

Anodal Excitation of Cardiac Muscle

1957 ◽  
Vol 190 (2) ◽  
pp. 383-390 ◽  
Author(s):  
Paul F. Cranefield ◽  
Brian F. Hoffman ◽  
Arthur A. Siebens
Keyword(s):  
Cardiac Muscle ◽  
Refractory Period ◽  
Ventricular Myocardium ◽  
Relative Refractory Period ◽  
Double Origin ◽  
Cathodal Stimulation

The strength-interval curve of dog ventricular myocardium has been measured with anodal and cathodal stimulation. During diastole the anodal threshold is higher than the cathodal. As anodal stimuli are applied progressively earlier the anodal threshold first rises above and then falls to levels below the anodal diastolic threshold. During most of the relative refractory period the anodal threshold is lower than the cathodal threshold. At all times during the late relative refractory period and throughout diastole excitation of double origin (anodal and cathodal) is evoked by sufficiently strong stimuli; this simultaneous origin of excitation at two points does not evoke fibrillation. During the early relative refractory period, however, only the anode is able to excite. Differences between anodal and cathodal thresholds are not attributable to asynchronous repolarization at the two electrode sites. The ‘no-response’ phenomenon occurs only when the anodal threshold is markedly lower than the cathodal.

Physiological properties of individual cerebral axons studied in vivo for as long as one year

1985 ◽  
Vol 54 (5) ◽  
pp. 1346-1362 ◽  
Author(s):  
H. A. Swadlow
Keyword(s):  
Conduction Velocity ◽  
Cortical Neurons ◽  
Refractory Period ◽  
Antidromic Activation ◽  
Conduction Velocities ◽  
Supernormal Period ◽  
Velocity Changes ◽  
The Stability ◽  
Over Time

The long-term stability of conduction velocity and recovery processes were studied in a fast-conducting (corticotectal) and in a more slowly conducting (visual callosal) axonal system. Chronic microelectrode recording methods were used in conjunction with antidromic activation via electrical stimulation at one or more axonal site. These methods enabled 54 axons to be studied for greater than 20 days and seven of these cells to be studied for 101-448 days. The conduction velocities of corticotectal axons were characteristic of myelinated axons and were very stable over time. The conduction velocities of most callosal axons were characteristic of nonmyelinated axons, and 68% of callosal axons had conduction velocities that were stable over long periods of time. Of the remaining callosal axons, approximately one third showed an increase in conduction velocity (8-14%), whereas two thirds showed a progressive and systematic decrease in conduction velocity (6-81%). These changes in conduction velocity were distributed along the callosal axon, rather than limited to a single segment of axon. Although the refractory period of callosal and corticotectal axons showed considerable variability over time, the minimal interval between two conducted impulses was stable. The stability of this property was remarkable because the minimal interspike intervals of different axons with similar conduction velocities often differed greatly. Callosal axons show a supernormal period of increased conduction velocity following the relative refractory period and a subsequent subnormal period of decreased conduction velocity following a burst of prior impulses. In different callosal axons the magnitude of the velocity changes (percent change) differs greatly, even among axons of the same conduction velocity. For a given axon, however, these properties are very stable over time. These results on axonal properties may be useful in studies requiring the examination of extracellular responses of individual neurons over long periods of time. Antidromic latency provides a useful means of identifying a cell, particularly when conduction times are long. The stability of the minimal interspike interval and the supernormal period within individual axons make them suitable as ancillary criteria in identifying individual neurons. These three measures are independent of spike amplitude and waveform, and together they provide a "signature" by which individual cortical neurons can be identified over periods that represent a significant portion of the lifespan of adult mammals.

Relative Refractory Period

2005 ◽  
Vol 14 (3) ◽  
pp. 249-250
Author(s):  
Mary G. Adams ◽  
Michele M. Pelter
Keyword(s):  
Refractory Period ◽  
Relative Refractory Period

The Repetitive Responses of Isolated Axons from the Crab, Carcinus Maenas

1966 ◽  
Vol 45 (3) ◽  
pp. 475-488
Author(s):  
R. A. CHAPMAN
Keyword(s):  
Refractory Period ◽  
Carcinus Maenas ◽  
Membrane Resistance ◽  
Physiological Solution ◽  
Response Frequency ◽  
Electrical Currents ◽  
Slowing Down ◽  
Relative Refractory Period ◽  
Repolarization Phase ◽  
Cathodal Current

1. A method is described that enables the electrical responses of motor axons isolated from the leg nerve of the crab Carcinus to be studied close to or at the site of imposed electrical currents, while this area is continuously bathed by physiological solution. 2. The three classes of repetitive responses originally described by Hodgkin (1948) have occurred during the present work and additional features of these responses have been described. 3. The results support Hodgkin's original thesis that the development of the spike generating mechanisms determine the response frequency during a repetitive response, but a progressive lengthening of the relative refractory period occurs during this response and is considered to be the agency that causes the gradual slowing down of the response frequency, i.e. the adaption. 4. The processes of membrane restoration (repolarization and recovery) have been shown to be sensitive to applied currents; anodal current hastening and cathodal current slowing it. These phenomena provide a basis for interpreting the change in the duration of the relative refractory period observed during the repetitive response. 5. The differences between the form of the repetitive response in the crab axon and the predictions of the Hodgkin-Huxley equations is discussed and it seems likely that the rapid recovery of the membrane resistance during the repolarization phase of the crab axon action potential underlies this difference.

Refractory period response of cardiac Purkinje tissue to alpha 1- and alpha 2-adrenergic influences

1994 ◽  
Vol 267 (1) ◽  
pp. H376-H382 ◽  
Author(s):  
D. G. Cable ◽  
T. E. Rath ◽  
E. R. Dreyer ◽  
J. B. Martins
Keyword(s):  
Mean Arterial Pressure ◽  
Cell Membrane ◽  
Arterial Pressure ◽  
Refractory Period ◽  
Adrenergic Stimulation ◽  
Relative Refractory Period ◽  
Wb 4101 ◽  
Adrenergic Antagonists

Our purpose was to characterize Purkinje responses in vivo to alpha 1- and alpha 2-adrenergic stimulation in sinoaortically denervated and vagotomized dogs pretreated with metoprolol (1 mg/kg). We measured Purkinje relative refractory period (PRRP) responses to norepinephrine (NE) and phenylephrine (PE) with prazosin and/or yohimbine, WB-4101, and chloralethylclonidine (CEC) in varying doses. Results were as follows: PE infusion (25 micrograms.kg-1.min-1) prolonged PRRP (9.6 +/- 1.4 ms; a 4.1 +/- 0.4% change). Prazosin blocked PRRP prolongation with PE at 7 x 10(-8) M/kg (P < 0.05). Yohimbine did not attenuate PRRP prolongation with PE either alone or in combination with prazosin. NE infusion (0.8 micrograms.kg-1.min-1) also prolonged PRRP (9.2 +/- 2.3 ms; a 4.8 +/- 1.0% change). In contrast neither prazosin nor yohimbine at any dose (up to 10(-6) M/kg) totally blocked the prolongation with NE infusion. However, with prazosin (2 x 10(-7) M/kg) pretreatment, yohimbine blocked PRRP prolongation, significant at 7 x 10(-8) M/kg (P < 0.05). In separate experiments with yohimbine pretreatment at 7 x 10(-8) M/kg, PRRP prolongation with either PE or NE infusion was blocked equipotently with WB-4101 and CEC at 7 x 10(-8) M/kg. However, CEC did not block mean arterial pressure (MAP) responses to PE or NE infusion unlike WB-4101. We concluded that both subclasses of alpha 1-adrenergic antagonists equipotently block PRRP prolongation by alpha-agonists despite different effects on MAP. Purkinje refractoriness is also prolonged by alpha 2-adrenergic stimulation acting at the cell membrane.

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