Effects Of Cyclobenzaprine Research Articles

P-843 - Effects of cyclobenzaprine and ketanserin on the γ-motoneuronal activity.

P-843 - Effects of cyclobenzaprine and ketanserin on the γ-motoneuronal activity.

Effects of cyclobenzaprine on spinal synaptic transmission

The effects of cyclobenzaprine on spinal synaptic transmission were studied in spinal unanesthetized cats. The drug, in cumulative doses up to 20 mg/kg, depressed monosynaptic reflexes evoked by stimulation at 0.2 Hz to a moderate degree. Polysynaptic reflexes were depressed to a similar extent. Monosynaptic reflexes evoked repeatedly at 5 and 10 Hz were depressed even after 5 mg/kg of cyclobenzaprine. Maximum potentiation of monosynaptic responses after tetanization was not affected. Neither direct postsynaptic nor recurrent inhibition was influenced by the drug. Presynaptic inhibition was slightly reduced. It is suggested that direct effects of cyclobenzaprine at the spinal level do not represent the primary site of action responsible for its antispastic activity.

Cyclobenzaprine and ethanol interaction

The effects of cyclobenzaprine, a tricyclic compound, on the central depressant action of ethanol and on hepatic ethanol metabolizing enzymes were studied in rodents. Administration of cyclobenzaprine, 5 mg/kg, IP, 30 min prior to a narcotic dose of ethanol solution, 5 g/kg, IP, enhanced ethanol-produced narcosis in mice. This effect was greater in male than in female mice. Cyclobenzaprine inhibited endogenous rat liver alcohol dehydrogenase in vitro in the concentration range between 10 −5M and 10 −6M. Cyclobenzaprine exerted little effect on hepatic aldehyde dehydrogenase in vitro. The results suggest that cyclobenzaprine possesses depressant properties and inhibition of liver alcohol dehydrogenase may underlie the observed behavioral response studied. It is concluded that alteration of endogenous liver alcohol dehydrogenase by certain tricyclic antidepressant drugs may be involved in the mechanism(s) of their toxic interaction with ethanol.

Cyclobenzaprine: Some pharmacological cardiac actions

The effects of cyclobenzaprine (CBZ) on isolated spontaneously beating rabbit atria were studied to investigate some of its pharmacological actions. At concentrations (equal to or less than 9 × 10 −7M) which are not cardiotoxic, CBZ blocks muscarinic cholinergic receptors, augments the activity of exogenously administered norepinephrine (at higher concentrations it probably also releases endogenous catecholamines) and acts as an antihistaminic. CBZ appears to be very similar in action to other tricyclic compounds, particularly the antidepressants amitriptyline and imipramine.

Effects of cyclobenzaprine on interneurones of the spinal cord

Experiments were performed on decerebrate cats to determine whether CBZ acted as a general depressant to spinal cord neurones or whether the depression was selective to certain groups of neurones. At doses which appreciably affected motoneurone pools, CBZ had no depressant effect on Renshaw or IA inhibition; most spontaneously active neurones in Rexed layers V and VI, and brainstem reticular formation cells were depressed by CBZ. These results indicate that CBZ does not have a general depressant action on spinal cord neurones. Although some direct action on the spinal cord may be present, the major effects are secondary to an apparent action on specific neurones in the brainstem.

Effects of cyclobenzaprine on brainstem motor systems

Cyclobenzaprine, a new centrally acting skeletal muscle relaxant, was compared with diazepam as to their effects on several brainstem motor systems. Precollicular decerebrate cats were used to investigate intervestibular, vestibulo-spinal and reticulo-spinal effects. Both cyclobenzaprine and diazepam were without significant effect at less than high doses on the vestibular system as assessed by the monosynaptic response recorded in the median longitudinal fasciculus to vestibular nerve stimulation. The effects on brainstem reticular formation was assessed by the vestibulo-reticulo-spinal, spinal-bulbo-spinal and reticulo-spinal responses. In every case cyclobenzaprine had a strong blocking effect on reticular-produced inhibition of the spinal cord monosynaptic reflex. Diazepam was without effect or enhanced the inhibition. The evidence supports the notion that cyclobenzaprine depresses spinal cord interneurone activity by disfacilitation from a reticulo-spinal pathway.