<?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%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Anderson, R. J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Dopamine receptor-mediated depression of spinal monosynaptic transmission.</style></title><secondary-title><style face="normal" font="default" size="100%">Brain research</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">apomorphine</style></keyword><keyword><style  face="normal" font="default" size="100%">dopamine agonists</style></keyword><keyword><style  face="normal" font="default" size="100%">dopamine receptors</style></keyword><keyword><style  face="normal" font="default" size="100%">lergotrile</style></keyword><keyword><style  face="normal" font="default" size="100%">lisuride</style></keyword><keyword><style  face="normal" font="default" size="100%">monosynaptic transmission</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Cord</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%">06/1982</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/6126249</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">242</style></volume><pages><style face="normal" font="default" size="100%">247–254</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The effects of the dopamine agonists apomorphine, lisuride and lergotrile were evaluated on cat spinal cord monosynaptic transmission by stimulating the dorsal root and recording the ventral root compound action potential. All 3 agonists decreased the area of the monosynaptic response. This effect was prevented by pretreatment with the dopamine antagonists haloperidol and metoclopramide, but not with the alpha-adrenergic antagonist phentolamine. These results suggest the existence of spinal cord dopamine receptors which can modulate motor output.</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 S. Carp</style></author><author><style face="normal" font="default" size="100%">Anderson, R. J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Modification of spinal cord transmission by an interaction of chlorpromazine and phenytoin.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of pharmacology and experimental therapeutics</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Synaptic Transmission</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1981</style></year><pub-dates><date><style  face="normal" font="default" size="100%">02/1981</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/6257885</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">216</style></volume><pages><style face="normal" font="default" size="100%">270–274</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Cat spinal cord monosynaptic activity during slow repetitive stimulation (0.2 Hz) and post-tetanic potentiation was used to evaluate the combination effects of phenytoin and chlorpromazine. The drug effects were compared in anesthetized cats with either high spinal transection or intact central nervous systems to determine whether the drugs were acting segmentally or suprasegmentally. When chlorpromazine and phenytoin were given in combination to intact animals, the depressant effect on the monosynaptic response was limited to 50% of control, which was not more than the maximum effect of either drug given alone. In spinal animals, chlorpromazine reversed the phenytoin-induced depression during 0.2 Hz stimulation, whereas only the effects of phenytoin on post-tetanic potentiation were evident after the drug combination. These results show that although phenytoin and chlorpromazine each have a depressant effect on spinal cord transmission, the combined effect is limited to a 50% decrease in intact animals. It is suggested that this occlusive drug effect demonstrates that the drug combination has a limited depressant action in the intact nervous system, an action which permits the expression of the effects of these drugs on the other elements of the reflex arc. Collectively, these actions of the drug combination are consistent with their known efficacy in treating certain cases of spasticity.</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 S. Carp</style></author><author><style face="normal" font="default" size="100%">Anderson, R. J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The effects of phenytoin on motor function in awake cats.</style></title><secondary-title><style face="normal" font="default" size="100%">Archives internationales de pharmacodynamie et de thérapie</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Reflex</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1979</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/1979</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/485678</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">237</style></volume><pages><style face="normal" font="default" size="100%">139–148</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Adult cats were monitored for their performance of a variety of motor functions before and after acute administration of phenytoin (5, 10 or 20 mg/kg) in a schedule in which each animal received all drug doses. The only significant loss in motor function was balance and coordination. Half the animals could not balance or walk along a narrow-edged beam after 20 mg/kg of phenytoin although their performance was not impaired at lower drug doses or on wider surfaces. There were no effects of phenytoin on the righting reflex, flexor reflex, muscle strength, the hopping response, the blind placing response or visually aided placing. The data suggest that phenytoin has a selective effect on higher order neuronal systems involved with balance and locomotion rather than simple reflex pathways.</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 S. Carp</style></author><author><style face="normal" font="default" size="100%">Anderson, R. J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Sensorimotor deficits produced by phenytoin and chlorpromazine in unanesthetized cats.</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacology, biochemistry, and behavior</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Chlorpromazine</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenytoin</style></keyword><keyword><style  face="normal" font="default" size="100%">Sensorimotor deficits</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1979</style></year><pub-dates><date><style  face="normal" font="default" size="100%">04/1979</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/461481</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">513–520</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Unanesthetized adult cats were evaluated for suprasegmental reflex activity and motor skills before and after administration of chlorpromazine (0.0625–0.5 mg/kg) alone and in combination with phenytoin (20 mg/kg). The greatest deficits were seen in the tests of balance and corrdination in which half the animals failed to match their control responses after administration of chlorpromazine and phenytoin. The impairment was most noticeable with the most stringent test (walking a 4 cm wide beam), and the effects of the two drugs were additive. Although there was no effect of either drug on muscle strength, the two drugs in combination depressed the animals' motivational state, making them less willing to work against imposed loads. Neither drug, alone or in combination, altered responses to the flexor reflex, blind placing, the hopping response or visually aided placing. It is concluded that the effects of chlorpromazine and phenytoin on motor control are selective for the CNS loci which control balance and coordination. Although the two drugs produce additive responses, the deficits occur only at doses which are well above those needed for clinical efficacy and thus may not pose a problem in their long term clinical use.</style></abstract></record></records></xml>