02268nas 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/275170301807nas 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/275170202188nas 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/247375501682nas a2200181   4500008004100000022001400041245010400055210006900159260001200228300001600240490000700256520111400263653001601377100002101393700001901414700002001433856004701453       1983                        eng d  a0022-307700aAdaptive plasticity in primate spinal stretch reflex: behavior of synergist and antagonist muscles.0 aAdaptive plasticity in primate spinal stretch reflex behavior of  c12/1983  a1312–13190 v503 aMonkeys can gradually change the amplitude of the biceps spinal stretch reflex (SSR) without change in initial muscle length or biceps background electromyographic activity (EMG) (17). We investigated the concurrent behavior of synergist (brachialis and brachioradialis) and antagonist (triceps) muscles. Synergist background EMG remained stable while marked change occurred in biceps SSR amplitude. Triceps background EMG was minimal under all conditions. Thus biceps SSR amplitude change was not due to change in the background activity of closely related muscles. When biceps SSR amplitude changed, synergist SSR amplitude changed similarly but to a lesser extent. Brachialis change averaged 72% of biceps change, while brachioradialis change averaged 33%. By indicating that SSR amplitude change is relatively specific to the agonist muscle, this finding eliminates a number of nonspecific mechanisms as possible origins of SSR amplitude change. Thus it supports the potential value of the SSR as a system for studying the neuronal and synaptic bases of memory in the primate central nervous system (CNS).10aSpinal Cord1 aWolpaw, Jonathan1 aSeegal, R., F.1 aO'Keefe, J., A.  uhttp://www.ncbi.nlm.nih.gov/pubmed/666332802956nas a2200181   4500008004100000022001400041245007900055210006900134260001200203300001600215490000700231520241200238653001602650100002102666700002102687700001902708856004702727       1983                        eng d  a0022-307700aAdaptive plasticity in primate spinal stretch reflex: initial development.0 aAdaptive plasticity in primate spinal stretch reflex initial dev  c12/1983  a1296–13110 v503 aDescription of the neuronal and synaptic bases of memory in the vertebrate central nervous system (CNS) requires a CNS stimulus-response pathway that is defined and accessible, has the capacity for adaptive change, and clearly contains the responsible substrates. This study was an attempt to determine whether the spinal stretch reflex (SSR), the initial, purely spinal, portion of the muscle stretch response, which satisfies the first requirement, also satisfies the second, capacity for adaptive change. Monkeys prepared with chronic fine-wire biceps electromyographic (EMG) electrodes were trained to maintain elbow position and a given level of biceps background EMG activity against constant extension torque. At random times, a brief additional extension torque pulse extended the elbow and elicited the biceps SSR. Under the control mode, reward always followed. Under the SSR increases or SSR decreases mode, reward followed only if the absolute value of biceps EMG from 14 to 24 ms after stretch onset (the SSR interval) was above or below a set value. Animals performed 3,000-6,000 trials/day over data-collection periods of up to 15 mo. Background EMG and the initial 30 ms of pulse-induced extension remained stable throughout data collection. Under the SSR increases or SSR decreases mode, SSR amplitude (EMG amplitude in the SSR interval minus background EMG amplitude) changed appropriately. Change was evident in 5-10 days and progressed over at least 4 wk. The SSR increased (SSR increases) to 140-190% control amplitude or decreased (SSR decreases) to 22-79%. SSR change did not regress over 12-day gaps in task performance. A second pair of biceps electrodes, monitored simultaneously, supplied comparable data, indicating that SSR amplitude change occurred throughout the muscle. Beyond 40 ms after pulse onset, elbow extension was inversely correlated with SSR amplitude. The delay between the SSR and its apparent effect on movement is consistent with expected motor-unit contraction time. The data demonstrate that the SSR is capable of adaptive change. At present the most likely site(s) of the mechanism of SSR amplitude change are the Ia synapse and/or the muscle spindle. Available related evidence suggests persistent segmental change may in fact come to mediate SSR amplitude change. If so, such segmental change would constitute a technically accessible fragment of a memory.10aSpinal Cord1 aWolpaw, Jonathan1 aBraitman, D., J.1 aSeegal, R., F.  uhttp://www.ncbi.nlm.nih.gov/pubmed/666332701114nas a2200265   4500008004100000022001400041245005400055210005300109260001200162300001400174490000800188520041600196653001300612653001100625653001500636653001200651653001800663653001900681100002100700700002000721700001900741700002100760700002000781856004700801       1983                        eng d  a0006-899300aAdaptive plasticity in the spinal stretch reflex.0 aAdaptive plasticity in the spinal stretch reflex  c05/1983  a196–2000 v2673 aMonkeys can change the amplitude of the spinal stretch reflex without change in initial alpha motor neuron tone, as measured by EMG, or in initial muscle length. Change is apparent in 5-10 days, continues to develop over weeks, and persists during inactive periods. Spinal stretch reflex change may be a valuable system for studying the neuronal and synaptic bases of an adaptive change in primate CNS function.10aLearning10aMemory10aplasticity10aprimate10aspinal reflex10astretch reflex1 aWolpaw, Jonathan1 aKieffer, V., A.1 aSeegal, R., F.1 aBraitman, D., J.1 aSanders, M., G.  uhttp://www.ncbi.nlm.nih.gov/pubmed/686094801145nas a2200229   4500008004100000022001400041245004900055210004800104260001200152300001400164490000800178520053400186653002100720653001900741653001900760653001200779653001800791653001900809100002100828700001900849856004700868       1982                        eng d  a0006-899300aDiurnal rhythm in the spinal stretch reflex.0 aDiurnal rhythm in the spinal stretch reflex  c07/1982  a365–3690 v2443 aWe studied primate spinal stretch reflex (SSR) amplitude as a function of time of day. SSR amplitude was greatest around midnight and smallest around noon. The diurnal rhythm was not simply a function of number of trials, or of the lighting cycle. This rhythm offers an opportunity to study the neuronal and synaptic mechanisms producing a diurnal change in CNS function. Its existence indicates that the CNS response to a given limb disturbance, and thus the CNS activity underlying a given performance, varies with time of day.10acircadian rhythm10adiurnal rhythm10amuscle stretch10aprimate10aspinal reflex10astretch reflex1 aWolpaw, Jonathan1 aSeegal, R., F.  uhttp://www.ncbi.nlm.nih.gov/pubmed/6889452