01807nas a2200229   4500008004100000022001400041245014300055210006900198260001200267300001400279490000700293520108100300653001701381653002701398653001901425653001901444653001201463100002101475700001901496700001501515856004701530       1989                        eng d  a0197-846200aChronic exposure of primates to 60-Hz electric and magnetic fields: I. Exposure system and measurements of general health and performance.0 aChronic exposure of primates to 60Hz electric and magnetic field  c01/1989  a277–2880 v103 aWe exposed pigtailed macaques (Macaca nemestrina) to electric (E) and magnetic (B) fields at strengths of 3 kV/m and 0.1 G, 10 kV/m and 0.3 G, and 30 kV/m and 0.9 G for three 21 day segments. These three exposure segments were preceded and followed by 21 day sham exposure segments. Additional animals received only sham exposure for five 21 day segments. Detailed description of the exposure chamber and field generation apparatus is given. We evaluated measures of animal well-being, including weight, blood chemistry, blood cell counts, and performance on a simple motor task, and performed postmortem examinations. Reliable and consistent results were obtained throughout data collection. None of the measures evaluated was significantly affected by E- and B-field exposures. Data obtained during actual exposure segments were not distinguishable from those obtained during the initial and final sham exposure segments, nor were they different from data obtained from the sham-exposed animals. Thus, field exposure had no apparent effects on general health or performance.10a60-Hz fields10acentral nervous system10aelectric field10amagnetic field10aprimate1 aWolpaw, Jonathan1 aSeegal, R., F.1 aDowman, R.  uhttp://www.ncbi.nlm.nih.gov/pubmed/275170202268nas a2200265   4500008004100000022001400041245010300055210006900158260001200227300001400239490000700253520148500260653003601745653001301781653002301794653002101817653001301838653001801851653001101869100001501880700002101895700001901916700002001935856004701955       1989                        eng d  a0197-846200aChronic exposure of primates to 60-Hz electric and magnetic fields: III. Neurophysiologic effects.0 aChronic exposure of primates to 60Hz electric and magnetic field  c01/1989  a303–3170 v103 aThe neurophysiologic effects of combined 60-Hz electric (E) and magnetic (B) fields, of magnitudes comparable to those produced by high-voltage powerlines, were investigated in 10 monkeys (Macaca nemestrina). Six animals (experimental group) were each exposed to three different levels of E and B fields: 3 kV/m and 0.1 G, 10 kV/m and 0.3 G, and 30 kV/m and 0.9 G. Field exposures were preceded and followed by sham exposures, during which factors of field generation were present (e.g., heat, vibration, noise, etc.) without E and B fields. Each of the five segments (i.e., the three exposure segments and the initial and final sham exposure segments) lasted 3 weeks. Animals were exposed for 18 h/day (fields on at 1600 h, off at 1000 h). Four other animals (external control group) were given sham exposure for the entire 15-week period. Auditory, visual, and somatosensory evoked potentials were recorded twice a week, during the daily 6-h field-off period. E- and B-field exposure had no effect on the early or mid-latency evoked potential components, suggesting that exposure at these levels has no effect on peripheral or central sensory afferent pathways. However, there was a statistically significant decrease in the amplitudes of late components of the somatosensory evoked potential during the 10kV/m and 0.3 G, and 30 kV/m and 0.9 G exposure levels. This result is possibly related to the opiate antagonist effect of electromagnetic field exposure reported by others.10a60-Hz electromagnetic radiation10aauditory10abrainstem auditory10aevoked potential10aprimates10asomatosensory10avisual1 aDowman, R.1 aWolpaw, Jonathan1 aSeegal, R., F.1 aSatya-Murti, S.  uhttp://www.ncbi.nlm.nih.gov/pubmed/275170302188nas a2200181   4500008004100000022001400041245009900055210006900154260001200223300001400235490000700249520162000256653002801876100001901904700002101923700001501944856004701959       1989                        eng d  a0197-846200aChronic exposure of primates to 60-Hz electric and magnetic fields: II. Neurochemical effects.0 aChronic exposure of primates to 60Hz electric and magnetic field  c01/1989  a289–3010 v103 aWe exposed Macaca nemestrina (pig-tailed macaques) to electric (E) and magnetic (B) fields ranging in intensity from 3 kV/m and 0.1 G to 30 kV/m and 0.9 G for three 21-day (d) periods. Experimental animals were exposed to sham E and B fields for two 21-d periods, one prior to and one following actual exposure to E and B fields, resulting in a total of five 21-d periods. Control animals were exposed to sham E and B fields for the entire 105-d interval. At the end of each 21-d period cerebrospinal fluid (CSF) was obtained by lumbar puncture and analyzed for concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), metabolites of dopamine and serotonin neurotransmitters, respectively, by high-performance liquid chromatography with electrochemical detection (HPLC-ECD). Results are based on an examination of six experimental and four control animals. Exposure to E and B fields at all strengths was associated with a significant decline in CSF concentrations of both HVA and 5-HIAA when statistical comparisons were made against values obtained at the end of the preexposure interval. However, HVA returned to preexposure levels during the postexposure period, while 5-HIAA did not. No significant change in the concentrations of HVA or 5-HIAA was noted in the control animals. These results strongly suggest that exposure of the nonhuman primate to E and B fields can significantly affect specific biochemical estimates of nervous system function. These effects may involve alterations either in neuronal activity or in the activity of enzymes that catabolize the neurotransmitters.10aNeurotransmitter Agents1 aSeegal, R., F.1 aWolpaw, Jonathan1 aDowman, R.  uhttp://www.ncbi.nlm.nih.gov/pubmed/247375501922nas a2200169   4500008004100000022001400041245010600055210006900161260001200230300001200242490000700254520139200261653001601653100001501669700002101684856004701705       1989                        eng d  a0013-469400aDiurnal rhythms in primate spinal reflexes and accompanying cortical somatosensory evoked potentials.0 aDiurnal rhythms in primate spinal reflexes and accompanying cort  c01/1989  a69–800 v723 aWe recorded spinal reflexes and cortical somatosensory evoked potentials (SEPs), elicited by stretching the biceps or the triceps muscle or by electrically stimulating the posterior tibial nerve, from monkeys throughout the day. Amplitudes of the spinal stretch reflex (SSR) and of its electrically evoked analogue, the H-reflex, varied diurnally: both were greatest midway through the lights-off period and smallest during the lights-on period. Stretch-evoked and electrically evoked SEP amplitudes also varied diurnally, but were out of phase with the spinal reflex rhythms. The H-reflex is elicited by direct stimulation of the nerve and thus, unlike the SSR, bypasses the muscle spindle. The H-reflex diurnal rhythm and the phase difference between the spinal reflex and SEP diurnal rhythms indicate that these rhythms are mediated at least in part by central mechanisms. Furthermore, both the spinal reflex and SEP diurnal rhythms appeared to be entrained by the light-dark cycle, which suggests that they may be coupled to the same oscillator. Besides their theoretical importance, these rhythms have important implications for experimental and clinical studies of spinal reflexes and SEPs. These rhythms are especially pertinent to the interpretation of long-term monitoring studies, as are often carried out in the Intensive Care Unit and during lengthy neurosurgical procedures.10aSpinal Cord1 aDowman, R.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/246447702050nas a2200181   4500008004100000022001400041245012100055210006900176260001200245300001400257490000800271520148300279653001101762653001201773100001501785700002101800856004701821       1988                        eng d  a0014-488600aJendrassik maneuver facilitates soleus H-reflex without change in average soleus motoneuron pool membrane potential.0 aJendrassik maneuver facilitates soleus Hreflex without change in  c08/1988  a288–3020 v1013 aFacilitation of spinal reflex amplitude by remote muscle contraction, otherwise known as the Jendrassik maneuver (JM), was first shown over 100 years ago, yet the mechanism by which this facilitation operates remains undetermined. Earlier work has eliminated participation of the muscle spindle in JM-induced spinal reflex facilitation, leaving changes in postsynaptic (e.g., change in average soleus motoneuron membrane potential) and presynaptic (e.g., inhibition of presynaptic inhibition) mechanisms as viable candidates. We recorded background EMG in the soleus muscle during JM-induced soleus H-reflex facilitation in humans. The JM in this experiment consisted of wrist muscle contraction. Soleus background EMG was maintained by the subject at either a zero level (e.g., relaxed) or a specified moderate level prior to and during the JM. The JM increased H-reflex amplitude by comparable amounts in both situations, but had no effect on soleus background EMG. Given the well-known relationship between the average motoneuron pool membrane potential and background EMG, we conclude that JM facilitation of the soleus H-reflex is not caused by an increase in background excitatory input to the soleus motoneuron pool. Remaining candidates for mediation of JM induced H-reflex facilitation include change in stimulus-evoked afferent input at some point proximal to the muscle spindle, such as reduction in presynaptic inhibition, or a change in motoneuron input resistance.10aReflex10aStretch1 aDowman, R.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/339664601400nas a2200253   4500008004100000022001400041245007800055210006900133260001200202300001400214490000700228520067600235653002200911653001300933653001300946653001100959653002500970653001500995653003501010653001801045100002101063700001501084856004701099       1988                        eng d  a0013-469400aOperant conditioning of primate spinal reflexes: effect on cortical SEPs.0 aOperant conditioning of primate spinal reflexes effect on cortic  c04/1988  a398–4010 v693 aPrevious studies have demonstrated operant conditioning of the primate spinal stretch reflex (SSR) and of its electrical analog, the H-reflex. We studied the evoked potential recorded over primary somatosensory cortex (SEP) which accompanies the H-reflex to determine whether the initial cortical response changes in the course of conditioned H-reflex change. When H-reflex amplitude changed, SEP amplitude also changed, but only half as much as the H-reflex. The results indicate that, while operant conditioning of the H-reflex has its largest effect on the spinal pathway of the reflex, it also has some effect on supraspinal pathways of the initial cortical response.10acortical response10aH-Reflex10aLearning10aMemory10aoperant conditioning10aplasticity10asomatosensory evoked potential10aspinal reflex1 aWolpaw, Jonathan1 aDowman, R.  uhttp://www.ncbi.nlm.nih.gov/pubmed/245073901345nas a2200229   4500008004100000022001400041245011800055210006900173260001200242300001400254490000700268520062900275653001900904653001200923653002500935653003500960653001800995653001901013100002101032700001501053856004701068       1988                        eng d  a0013-469400aSpinal stretch reflex and cortical evoked potential amplitudes versus muscle stretch amplitude in the monkey arm.0 aSpinal stretch reflex and cortical evoked potential amplitudes v  c04/1988  a394–3970 v693 aWhile investigating operant conditioning of the primate spinal stretch reflex (SSR), we studied SSR amplitude and cortical somatosensory evoked potential (SEP) amplitude as stretch amplitude changed in the monkey arm. Initial muscle length and background EMG activity remained constant. With change in stretch amplitude (and proportional change in stretch velocity and acceleration), changes in SSR and SEP amplitudes were respectively 0.75 and 0.66 as great. The lesser change in SSR amplitude may reflect saturation of Ia afferents, while that in SEP amplitude may also reflect participation of other peripheral receptors.10amuscle stretch10aprimate10aSomatosensory Cortex10asomatosensory evoked potential10aspinal reflex10astretch reflex1 aWolpaw, Jonathan1 aDowman, R.  uhttp://www.ncbi.nlm.nih.gov/pubmed/245073801766nas a2200181   4500008004100000022001400041245007000055210006800125260001200193300001400205490000700219520123300226653001801459100002401477700001501501700002101516856004701537       1988                        eng d  a0378-595500aT complex hemispheric asymmetries: effects of stimulus intensity.0 aT complex hemispheric asymmetries effects of stimulus intensity  c08/1988  a225–2320 v343 aThe T complex component of the human auditory evoked potential (AEP) is thought to be produced in auditory cortex, on the posterior lateral surface of the temporal lobe. Recorded over temporal scalp, it consists of an 80-90 ms positive peak, Ta, and a 120-140 negative peak, Tb. As part of an effort to develop the clinical usefulness of the T complex in assessing auditory cortical function, we studied the effects of change in monaural stimulus intensity (20-80 dB SL) on T complex latency, amplitude, and hemispheric differences in normal adults. Ta and Tb peak latencies decreased as stimulus intensity increased. These latency changes were not dependent on ear or hemisphere. Right hemisphere Ta latency was shorter with contralateral than with ipsilateral stimulation; while left hemisphere Ta latency was not dependent on the ear stimulated. Tb latency was shorter over the left hemisphere, and over the contralateral hemisphere. Ta-b amplitude increased as stimulus intensity increased. This amplitude change was not dependent on ear or hemisphere. Ta-b amplitudes were larger over the right hemisphere and over the contralateral hemisphere. Hemispheric asymmetries were not significantly affected by stimulus intensity.10aReaction Time1 aCacace, Anthony, T.1 aDowman, R.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/3170365