RESUMO
Experiments were conducted to study the effect of altering external potassium on in vitro induction of myotonia in rat diaphragm using 2,4-dichlorophenoxy acetate (2,4-D). An increase in external potassium inhibited, while a decrease enhanced, the myotonic response. However, in preparations which have undergone prior denervation, there was no myotonic response to 2,4-D, even when the external potassium was lowered. The experiments also support the existence of neural factors influencing the resting ionic conductance of the muscle membrane.
Assuntos
Miotonia/fisiopatologia , Ácido 2,4-Diclorofenoxiacético/farmacologia , Animais , Diafragma/efeitos dos fármacos , Diafragma/fisiopatologia , Contração Muscular/efeitos dos fármacos , Miotonia/induzido quimicamente , Potássio/farmacologia , RatosAssuntos
Colinesterases/metabolismo , Denervação Muscular , Músculos/enzimologia , Nervos Periféricos/enzimologia , Animais , Inibidores da Colinesterase , Masculino , Músculos/efeitos dos fármacos , Paraoxon/farmacologia , Nervos Periféricos/efeitos dos fármacos , Ratos , Nervo Isquiático/enzimologia , Fatores de Tempo , Degeneração Walleriana/efeitos dos fármacosRESUMO
In order to study the influence of innervation on myotonia, an attempt was made to induce myotonia in previously denervated rat hemidiaphragm preparations in vitro with use of 2,4-dichlorophenoxy acetic acid (2,4-D) and low chloride solutions. Prior denervation prevented the onset of myotonia in both media except during the first 24 hours after nerve section. On the basis of already available data, we propose that the reduced potassium conductance accompanying denervation may be the main factor preventing induciton of myotonia in denervated muscle.
Assuntos
Denervação Muscular , Miotonia/induzido quimicamente , Ácido 2,4-Diclorofenoxiacético , Animais , Cloretos/farmacologia , Diafragma/inervação , Diafragma/fisiopatologia , Potenciais Evocados , Técnicas In Vitro , Miotonia/fisiopatologia , Nervo Frênico/fisiopatologia , RatosRESUMO
Squirrel monkeys were trained to perform ballistically initiated flexion movements of the forearm. It is shown that the motor output to agonist and antagonist subsequent to the onset of the movement depends continuously on the movement's parameters, primarily the velocity, as in man. The contribution of cerebellar activities to maintain this relationship was investigated by means of discrete lesions of the cerebellum and inferior olive. After lesions of the cerebellar nuclei, EMG activity of agonist and antagonist is no longer precisely structured. This result implies that activity of the cerebellar nuclei is necessary to maintain the gain and timing of the relationship between sensory inputs and motor outputs. Participation of the inferior olive is also required, since lesions of this structure mimic the effect of destruction of the cerebellar nuclei. Lesions of the cerebellar cortex, instead, affect mainly the timing of the motor output.
