Static magnetic field influence on rat tail nerve function

746

Static Magnetic Field Influence on Rat Tail Nerve Function Chang-Zern Hong, MD, David Harmon, BS, Jen Yu, MD, PhD Department

of PM&R,

University

of California,

Irvine Medical

Center,

Orange,

CA 92668

ABSTRACT. Hong C-Z, Harmon D, Yu J: Static magnetic field influence on rat tail function. Arch Phys Med Rehabil 67:746-749, 1986. l Motor nerve conduction and excitability were measured on the tail nerve of anesthetized rats before and after the nerve was exposed perpendicularly to a static electromagnetic field of various intensities and durations. There was no significant change in either the distal latencies or the amplitudes of the compound muscle action potential (CMAP) measured from stimulating the tail nerve after it was exposed to the electromagnetic field with a density up to 1.2Tesla (T) for a duration of 60 seconds. However, the nerve excitability expressed as changes of the amplitudes of the submaximally evoked CMAP increased significantly when the tail nerve was exposed to a magnetic field with a density higher than OST for more than 30 seconds. The finding that an electromagnetic field increases motor nerve excitability suggests a possible mechanism of its therapeutic effects. KEY WORDS:

Magnetics;

Nerve fibers:

Neural

transmission:

The effects of static magnetic field on nerve function have been reported previously. Findings from earlier studies in this area are controversial. Liberman and coworkers’ ’ found no change in excitation threshold of isolated frog sciatic nerve after exposure to a static magnetic field of more than 10,000 oersteds (Oe). Vovk and Tkach17 demonstrated that the fluctuation in the threshold of direct stimulation on isolated frog muscle increased when the muscle was placed in a permanent magnetic field of 2200 Oe. Reno14 reported that a magnetic field with the intensity of 1.16Tesla (T) significantly increased the conduction velocity of the isolated frog sciatic nerve, particularly in the parallel configuration. Schwartz,‘” on the other hand, found no significant effect of a 1.2T magnetic field upon conduction velocity of the isolated nerve of the lobster in either parallel or perpendicular configurations with respect to the field. Another study, from Edelman’s group,4 demonstrated an increase in the amplitude of the compound action potential of the isolated frog sciatic nerve when it was exposed to a perpendicular magnetic field of 1850 gauss (Gi or higher. More recently. a comprehensive in vitro study on the frog sciatic nerve during exposure to static magnetic fields was reported by Gaffey and Tenforde.” The action potential amplitude, conduction velocity, and absolute and relative refractory periods of the isolated sciatic nerve were found to be unaffected by a continuous 4-hour exposure to perpendicular or parallel 2T magnetic fields. All the above were in-vitro studies. To our knowledge, there is no animal study reported on mammalian species. The present study investigated the in vivo effects of the static magnetic field on the mammalian nerve function.

MATERIALS

AND METHODS

In 113 adult Sprague-Dawley albino rats (BW 200 to 3508) the motor nerve conductivity or excitability in the tail nerve was measured before and immediately after perpendicular exposure to a constant electromagnetic field of various densities Arch Phys Med Rehabil Vol67,

October 1966

Neurophwiolo,g

and durations. The rats were anesthetized with intraperitoneal chloral hydrate (250mgikg). Ring electrodes were placed on the tail for stimulation, recording, or as ground, with a Cadwell 5200 EMG machine,” the stimulus was applied at the proximal end of the tail nerve and the response recorded from the tail muscles distally. The ground was placed on the right front foot. The duration of stimulation current was set at O.OSmsec. The distance between the stimulation and recording electrodes was maintained at 5cm. A compound muscle action potential (CMAP) with amplitude higher than 5mV is usually obtained from supramaximal stimulation. A round electromagnet (6in diameter) was positioned in contact with the dorsal part of the tail but without exerting any pressure on it, with the center of the electromagnet midway between the stimulating and recording electrodes. and connected to a rectifier controller which adjusted the density of electromagnetic field from zero to 1.2T. The intensity of the magnetic field was confirmed by the reading from a gauss meter. The room temperature was 24? 1C. and the tail skin temperature was 34 i 1C throughout the whole study. Measurement of Nerve Conduction. Nineteen rats were studied for magnetic effects of nerve conduction; 11 were exposed to the field of 1.2T for 60 seconds and 8 were exposed to the field of 1.T for 60 seconds. Each animal was subjected to one co$rol study followed by one or more experimental tests. During the control study, the electromagnet was placed on the tail (as in the experimental tests) with the magnetic field set at zero by the adjustment of the rectifier controller. The evoked CMAP was recorded with supramaximal stimulation on the proximal segment of the tail. The latencies to the onset (Lob) and to the negative peak (Lpb) of the CMAP and the amplitude (Vb) of the CMAP were measured. Then the electromagnet was turned on (with zero density) for 60 seconds. The conduction study was repeated immediately (less than lsec)

Submitted I.?. 19X6.

for publication

September

I. 1985. Accepted in revised form February

747

MAGNETIC FIELD AND NERVE FUNCTION, Hong

atter the er!ectromagnet was turned off. The evoked CMAP was measured agaIn for the amplitude (Va) and the latencies to the onset I Lou I and to the peak (Lpa) of the action potential For the experimental tests. the values of Vb, Lob. and Lpb were obtained before the magnetic exposure. Then the electrcbmagnet was turned on for 60 seconds with the densities set at either 1.?_‘r or 1.T b\, the adjustment of the rectifier controller. The conduction study was repeated immediately (less than 1s~~ after the electromagnet was turned off. The values 1~1‘ Va. Loa. .md Lpa were obtained. Measuremenf oj‘ Nerve Excitability. Ninety-four rats were studied for the effects of exposure to the electromagnetic fields I)f various dcnsitle:) (0.3 to I .3T) for various durations ( IS. JO. and 60 \ec I on the nerve excitability. As in the nerve conduction ,;tudy. each animal was first subjected to a control study in which exposure to the electromagnetic field of zerc) Intensity was for 15. 30, or 60 seconds. respectively. Subsequently. one or more experimental tests at intervals of at least 5 minutes were done with the exposure to the fields of various densities (0.3 to I .7T) for 15, 30, or 60 seconds. respectively. Submaximal CMAP (SCMAP) was recorded with submaximal 4mulation to measure the change of nerve excitability. When the stnnulus evoking a SCMAP is repetitively applied at a i’onstant strength. the stability of the SCMAP amplitude as a function of time provides a sensitive index for detecting changes in rhe threshold for neural excitation.5 At the beginning ot each test. the amplitude of the SCMAP was adjusted to about 50 to hOR of the maximal CMAP from maximal stimulation. For either control or experimental test, the amplitude of SCMAP (Vb) before the magnet was turned on was measured as soon as it became stable with the intensity of the stimulation maintained constant. The amplitude of SCMAP (Va) was measured agaIn immediateI!- (kss than I set) after the magnetic exposure from the submaxlrnal exposure. For each measurement, four tracmgs from repetitive stimulation at I Hz were superimposed to confirm the consistency of the responses (Figure). The nerve excitability is considered as increased if the ratio of Va/Vb is greater than one. and as decreased if the ratio is less than one. Data Ana~y.sis. the ratio of the value before/after the magnetic exposure ~25 used as the index of magnetic effect\. Modified l-statistics based on analysis of variance (ANOVA) were applied to compare the values of the experimental and

Change of excitability of rat tail nerve after exposure to a static electromagnetic field of l.T for 60 set, measured as changes of amplitudes of submaximally evoked potentials from the same intensity of stimulation. The amplitude of evoked potential immediately after magnetic exposure (Va) is higher than that before exposure (Vb). Four tracings from repetitive stimulation at 1Hz are superimposed to confirm the consistency of the responses.

control conditions. cally significant.

.4 17 value ‘: 0.05 ‘A;:\ considered

statisti-

RESUI,‘rS iVerve Conduction. Table I lists thi, I.~tenci~s measured to the onset and to the peak of the compound action potential and the amplitudes of the potentials. before and after magnetic exposure. The ratio of the response bet’oreiafter magnetic esposure was calculated individually: the+: data were pooled tcr obtain average values t-SD. One-wa;, Al\JOVA c~ompared mean r&o of the response for different ma;gnztic doses including the control (zero dose). F-ratio was ca,culated as the ratio ot the mean square between/within group\. ‘The calculated F-ratich for either latencies or amplitudes reve;,led no 4gnificant differences among the groups. The modified r-statistics compared the experimental to the control values and revealed no significant changes from magnetic exposure for either latencies or amplitudes of the action potential ho significant effects were observed of the static electromagnet!lc t’ields wirh densities up to I .ZT exposed for 60 seconds on ner1.r: conduction. .Yerve Excitability. The amplitudec 0:‘ the ~ubmaximally evoked CMAP varied from animal to ~nmlal. However. for each control test, they could be fairly L.tabilized. as the ratio ot‘ the amplitudes before/after “cxposurc ’ to [em field was very close to 1. One-way ANOVA. revealed no significant differences among these three control value>. However. ANOVA. performed separately for the three :onditlons with different duration of exposure ( 15. 70. and 60 set) revealed significant differences among the mean values from various magnetic densities (0.T to I .7T) for both 60- and 30-second exposures. but not for I Z-second exposure (table 7). Further analysis with modified t-statistic5 rcvt*aled that significant changes occurred only at magnetic densi:ies higher than 0.5T. Thereihre. there is a significant increact: elf nene excitability if the nerve is exposed to the magnetic field with a density higher than O.ST for longer than 30 ~;rconJs. This effect disappeared I minute after termination of t it- magnetic field exposure (figure)

DISCUSSION We found no change in motor ncr’vt conduc,tion time in terms of either onset-latency or peak-latency afrer the nerve was exposed to a field with a density up to 1.2T. Similar results were noted in earlier in-vitro stucllcs by Schwartz,15 who also used a I .7T magnetic field ,lnd hv Gafl‘ey and Tenfor-de.> who used a higher density field. The increase in amplitude of the submaximally evoked compound muscle action potential after exposure to a magnetic tlrld with a density higher than O.ST for longer than 3OInse: ,;uggested that the excitability of the rat tail nerve was incn:.l\ed after exposure to the magnetic field. However. the in-vitro! htudb with a similar procedure of measurement by Gaffcy and l‘enforde did not show the same finding. Presman’3 noted that entire organisms or systems may be more sensitive to electromagnetic field\ .han isolated organs or cells. An in-vivo study may uncover some effects that cannot be detected from an in-vitro study. This may explain why Arch Phys Med Rehabil Vol67,

October 1966

MAGNETIC FIELD AND NERVE FUNCTION, Hong

748

Table 1: Effects of Electromagnetic Fields of Various Intensities on Latencies and Amplitudes of Maximally Evoked Potentials Magnetic Exposure 1.2T x 60sec Number

Magnetic Exposure l.T x 60 set

11

of Subiects

ANOVA F Ratio

Control 0.T X 6Osec

10

19

Latency. Onset: Before exposure (Lob) After exposure (Loa) Los/Lob Ratio Modified f-statistics (magnet vs control)

2.91 2.94 1.01 p >

? 0.28 msec i 0.22 msec i 0.08 0.5

2.81 2.75 0.99 p >

t 0.58 msec + 0.56 msec I 0.13 0.1

2.70 -C 0.71 msec 2.77 -+ 0.70 msec 1.04 + 0.09

0.802

Latency, Peak: Before exposure (Lpbl After exposure (Lpa) LpaiLpb Ratio Modified t-statistics (magnet vs control)

4.08 4.11 1.01 p >

? 0.36 msec + 0.36 msec % 0.08 0.05

3.87 3.89 1.02 p >

t 0.77 msec t 0.64 msec t 0.11 0.05

3.79 * 0.89 msec 4.1 I 2 1.03msrc 1.09 -t 0.12

2.442

Amplitude: Before exposure (Vb) After exposure (Va) Va/Vb Ratio Modified r-statistics (magnet vs control)

7.22 7.10 0.98 p >

? 1.40 mV 2 1.60 mV k 0.11 0.1

8.26 7.69 0.95 p >

i- 2.45 mV i 2.41 mV -’ 0.23 0.1

7.44 2 2.39 mV 7.Sl i 2.06 mV 1.033 t 0.16

0.768

our results are different from those obtained in the in-vitro studies. However, the mechanism responsible for the difference between the two types of studies on the magnetic effect on nerve function is still unclear. The possible magnetic effects on nervous tissue have been discussed previously3-‘1~‘3~‘7. The direct effects of the static magnetic field on the action potential were attributed to either the Hall effect or the inductive effect.2~3~‘” When a magnetic field is applied at right angles to the direction of the electric current, the electrons traveling in the conductor will experience deflection. As a consequence, an electric field, or potential difference, is set up in the direction perpendicular to both magnetic and electric current (the Hall effect). The inductive effect is the generating of an electromotive force in a moving specimen exposed to a magnetic field. Mathematical analysis by Liboff12 suggests that a magnetic field on the order of Ggauss ( lo9 gauss) is required to induce the distortion of the action-potential current-pattern of squid axon based on the Hall effect, and the changes in current pattern due to inductive effects were not detected up to 0.1 M-gauss ( lo5 gauss) distributed over 5mm of the axon. Therefore, it is very unlikely that the magnetic field may cause any significant disturbance on the current pattern of the action potential directly. The changes in nerve excitability may occur as a result of the

changes in membrane properties.’ There is evidence of an anisotropic property of the molecules on the excitable membrane. ‘*s,” The magnetic susceptibilities along the different axes of the anisotropic molecules are different. The static magnetic field may induce rotation of the anisotropic molecule to the orientation of maximal susceptibility and thus change membrane permeability. This speculation may be supported by the finding that a magnetic field decreases sodium pump activity.6 The action potentials during magnetic exposure were too severely distorted to be measured. probably due to interference from the electromagnetic energy. Since the rat tail was small, both the stimulation and recording electrodes and the muscles were under the electromagnetic field. which leads to the suspicion that the excitability of the muscle or the neuromuscular junction rather than the nerve had been measured. However. since the nerve but not the muscle was stimulated and the transmission of electric impulses along the nerve fiber is allor-none and not graded, it is most likely that we were measuring nerve excitability. The findings of this study suggest that the effects of magnetic fields may be dose related. The “magnetic dose” implies both the density and the duration of magnetic exposure.’ ANOVA revealed stronger effects after the 60-second exposures

Table 2: Effects of Electromagnetic Fields of Various Intensities and Durations on Nerve Excitability Measured as Changes of Amplitudes of Submaximally Evoked Potentials (Ratio of Amplitude Before/After Magnetic Exposure (Va/Vb) Control 1.2T 1.OT 0.9T 0.8T 0.7T 0.6T 0.5T 0.4T 0.3T ANOVA:

1.051 -c 0.095

(n 31)

0.983

2 0.124

(n 32)

1.106 f 0.131 (n 31)

1.959 1.605 I.681 1.505 1.259 1.441 1.387 1.005 0.993

(n (n (n (n (n (n (n (n (n

5) 5) 6) 6) 6) 7) 6) 5) 7)

1.554 1.229 1.186 1.275 I.314 1.170 1.215 1.060 I.101

-t f 2 t 2 + 2 i +

(?I (n (n (n (n (n (n (n (n

I.161 1.166 1.013 1.033 0.986 1.008 0.984 0.944 0.980

5 0.554* t 0.140* + 0.311* 2 0.245* r+_0.246** t 0.269* c 0.244* -c 0.278 * 0.157 14.803 (p < 0.01)

F RATIO

*p < 0.05 from modified t-statistics.

Arch Phys Med Rehabil Vol67,

October

15 Set

30 Set

60 Set

Duration of Exposure

1966

0.489* 0.181* 0.253* 0.126* 0.326* 0.146* 0.239* 0.176 0.179 6.05

(p i 0.01)

7) 6) 6) 8) 9) 8) 19) 12) 8)

c 0.356 2 0.170 i 0.194 2 0.264 2 0.208 -*- 0.270 i 0.142 i 0.118 I! 0.178 1.3 (/, z 0.05)

01 (n (?I (n (n (II (n (II (n

7) 6) 6) 8) 6) 6) 7) 7) 6)

749

MAGNETIC FIELD AND NERVE FUNCTION, Hong than after rhe Wsecond exposures for the densities of 1.2, 1.. 0 9, 0.8. and D.hT. However, it seems that the density of the magnetic field IS a more important factor than the duration of exposure. Exposure of the tail to a magnetic field of less than 0.5T for longer than 5 minutes revealed no significant changes in the excitability r)f the nerve. The finding that an electromagnetic field increases motor nerve excitability suggests a possible mechanism of its therapeutic effects. For example. electromagnetic applications may relieve pain by selectively increasing the excitability of large nerve fibers and thus. according to the gate control theory, block the gate for pain. Further studies are required to understand the mechanism of magnetotherapy and to develop an optimal therapeutic approach. ADDRESS REPRINT REQCIESTS TO: Chanp-Zwn Hc)ng. Ml) I:nlvcr\~ty of (‘alifomn Irvme MedIcal Center I>epartment of PhysIcal Mrdicuw and Rehabilitation 1~11The (‘itv Drlvc oranpr. (‘4 ‘J:hhK

References

Aceto H, ‘i’ob~asCA. Silver IL: Some studies on biological cffccts of magnetic fields. IEEE Tram Magnet& 6:36X-373, 1970 Bamothy JM: Introduction. In Bamothy MF fed): Biological Effacts ot’ Magnk Field>. New York. Plenum Prchs. 1964. Part I, pp 3-X Becker RC): BIological effects of magnetic fields-survey. Med Electron Biol Eng 1:293-303. 1963 Edelman A. Tculon J. Puchalska IS: lnfluencc of magneticfields on frog sciatic nerve. Biochem Biophys Res Commun 91:118I??, 1979 Gaffey C7, Tcnforde TS: Bioelectric properties of t’rog sciatic nerves during exposure to stationary magnetic field>. Radiat Environ Biophvs 22:6-73. 1983

6. Gualticrotti T: Decrease of sodmn-1 pump activity in frog skin (rr; steady magnetic field (abstract ). Physiologist 7: 150. 1964 7. Hong C-Z. Lin JC. Bender LF. Schaeffcr JN. Meltzer RJ. Causrn P: Magnetic necklace: its therapeutic eftectiveness on neck and shoulder pain. Arch Phys Med Rehabll 63:467-466. 1982 8. Hong FT. Mauzerall D. Mauro A: Magnetic anisotropy and or1 entation of retinal rods in homogeneous magnetic field (theoretlcal retinal rod orientation). Proc Nat! Acad Sti USA 68:128?1’85. 1971 9. Kolta P: Strong and permanent lr,tersctmn between peripheral nerve and constant inhomogeneous magnetic field. Acta Physiol Acad Sci Hung 43:89-94. 1973 IO. Labes MM: Possible explanation for effec,t of mqnetic fields 01 biological systems. Naturr 2ll:‘~hX. I%(~ II. L.iberman EA. Vaintsvaig MN. Tsofina 1,M: Elfect of constam magnetic field on excitation threhhohj ,,f isolated frog nerve. Biofiziks 4:505-506. 1959 13. Liboff RL.: Neuromagnetic thrcchol& ) ‘1 hcor BIOI 83:J?7436. 1980 13. Presman AS: Introduction. In Brown I-A (cd): Electromagnetic Fleldh and Life. New York, Plenum PrczL. 1970. pp I-Ii 1-t. Renn VR: Conduction velocity in nerve exposed to high magnetic field. NASA Report NAMI-10X9. Pensacola. FL. October. 1969 15. Schwartz J-L: Influence of constant magnetic field on nerve tlssuc:h: I nerve conduction velocity \ludit:!, IEEE Trans Biometl Eng BME-25:367-473. 197X 16. Schwartz J-L,: Influence of constant magnetic fitId on nervous tissue.s: II voltage-clamp studie\. IEEE Trans Blorned Eng BME

26:13X-743. 17

a

1979

Vovk MI. Tkach VK: Influence of permanent magnetic field on fluctuation in threshold of stimulation ~>t’tsolatcd skeletal muscle Biofizika 16:X33-836. 1971

Cadwcll 99336

Lahoratorics.

Suppliers Inc.. 1021 ‘\1 Ke,lo>:g.

Arch Phys Med Rehabil

Kenncwich.

Vol67,

October

WA

1996