01262nas a2200241   4500008004100000022001400041245007900055210006900134260001200203300001400215490000800229520055700237653001600794653002200810653002300832653001500855653001300870653003000883653001600913100002300929700002100952856004700973       1982                        eng d  a0006-899300aDopamine receptor-mediated depression of spinal monosynaptic transmission.0 aDopamine receptormediated depression of spinal monosynaptic tran  c06/1982  a247–2540 v2423 aThe 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.10aapomorphine10adopamine agonists10adopamine receptors10alergotrile10alisuride10amonosynaptic transmission10aSpinal Cord1 aCarp, Jonathan, S.1 aAnderson, R., J.  uhttp://www.ncbi.nlm.nih.gov/pubmed/612624901958nas a2200169   4500008004100000022001400041245009600055210006900151260001200220300001400232490000800246520141700254653002601671100002301697700002101720856004701741       1981                        eng d  a0022-356500aModification of spinal cord transmission by an interaction of chlorpromazine and phenytoin.0 aModification of spinal cord transmission by an interaction of ch  c02/1981  a270–2740 v2163 aCat 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.10aSynaptic Transmission1 aCarp, Jonathan, S.1 aAnderson, R., J.  uhttp://www.ncbi.nlm.nih.gov/pubmed/625788501279nas a2200169   4500008004100000022001400041245006200055210005700117260001200174300001400186490000800200520080000208653001101008100002301019700002101042856004601063       1979                        eng d  a0003-978000aThe effects of phenytoin on motor function in awake cats.0 aeffects of phenytoin on motor function in awake cats  c01/1979  a139–1480 v2373 aAdult 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.10aReflex1 aCarp, Jonathan, S.1 aAnderson, R., J.  uhttp://www.ncbi.nlm.nih.gov/pubmed/48567801836nas a2200193   4500008004100000022001400041245009100055210006900146260001200215300001400227490000700241520124500248653001901493653001401512653002601526100002301552700002101575856004601596       1979                        eng d  a0091-305700aSensorimotor deficits produced by phenytoin and chlorpromazine in unanesthetized cats.0 aSensorimotor deficits produced by phenytoin and chlorpromazine i  c04/1979  a513–5200 v103 aUnanesthetized 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.10aChlorpromazine10aPhenytoin10aSensorimotor deficits1 aCarp, Jonathan, S.1 aAnderson, R., J.  uhttp://www.ncbi.nlm.nih.gov/pubmed/461481