<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of reciprocal inhibition in rat soleus muscle.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Stretch</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2006</style></year><pub-dates><date><style  face="normal" font="default" size="100%">10/2006</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16807351</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">96</style></volume><pages><style face="normal" font="default" size="100%">2144–2150</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Operant conditioning of the H-reflex, the electrical analog of the spinal stretch reflex (SSR), induces activity-dependent plasticity in the spinal cord and might be used to improve locomotion after spinal cord injury. To further assess the potential clinical significance of spinal reflex conditioning, this study asks whether another well-defined spinal reflex pathway, the disynaptic pathway underlying reciprocal inhibition (RI), can also be operantly conditioned. Sprague-Dawley rats were implanted with electromyographic (EMG) electrodes in right soleus (SOL) and tibialis anterior (TA) muscles and a stimulating cuff on the common peroneal (CP) nerve. When background EMG in both muscles remained in defined ranges, CP stimulation elicited the TA H-reflex and SOL RI. After collection of control data for 20 days, each rat was exposed for 50 days to up-conditioning (RIup mode) or down-conditioning (RIdown mode) in which food reward occurred if SOL RI evoked by CP stimulation was more (RIup mode) or less (RIdown mode) than a criterion. TA and SOL background EMG and TA M response remained stable. In every rat, RI conditioning was successful (i.e., change &gt; or =20% in the correct direction). In the RIup rats, final SOL RI averaged 171+/- 28% (mean +/- SE) of control, and final TA H-reflex averaged 114 +/- 14%. In the RIdown rats, final SOL RI averaged 37 +/- 13% of control, and final TA H-reflex averaged 60 +/- 18%. Final SOL RI and TA H-reflex sizes were significantly correlated. Thus like the SSR and the H-reflex, RI can be operantly conditioned; and conditioning one reflex can affect another reflex as well.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dowman, R.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Jendrassik maneuver facilitates soleus H-reflex without change in average soleus motoneuron pool membrane potential.</style></title><secondary-title><style face="normal" font="default" size="100%">Experimental neurology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Stretch</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1988</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/1988</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/3396646</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">101</style></volume><pages><style face="normal" font="default" size="100%">288–302</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Facilitation 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.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Change in short-latency response to limb displacement in primates.</style></title><secondary-title><style face="normal" font="default" size="100%">Federation proceedings</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword><keyword><style  face="normal" font="default" size="100%">Stretch</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1982</style></year><pub-dates><date><style  face="normal" font="default" size="100%">04/1982</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/7075789</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">41</style></volume><pages><style face="normal" font="default" size="100%">2156–2159</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">When a muscle is stretched in an awake, behaving primate the earliest electromyographic (EMG) responses of the muscle consists of several reflex components. The earliest, M1, is mediated entirely at the segmental level and is largely monosynaptic. The next M2, is at least in part the result of an oligosynaptic transcortical loop to control the M1 response remains to be established. If primates can learn to control M1 amplitude, the M1 loop, which is the simplest and most accessible stimulus-response pathway in the primate central nervous system, may serve as a model for the study of mechanisms of memory. Preliminary evidence presented here strongly suggests that primates can control M1 gain without change in prestimulus EMG activity. The mechanisms of such change remain to be determined. Possibilities include change in gamma motor neuron tone, in Ia synaptic function, and in alpha motor neuron recruitment. The usefulness of learned M1 change as a model for memory will depend to a large extent on the nature of the responsible mechanism and on demonstration that the change can eventually become resident at the segmental level, without need for continued descending input.</style></abstract></record></records></xml>