Effects of 1,3-dimethyl-5-aminoadamantane hydrochloride (DMAA) on the stretch-induced reflex tension of flexor muscles and the excitability of the gamma-loop in decerebrate and spinal cats.
The effects of 10 mg/kg i.v. 1,3-dimethyl-5-aminoadamantane hydrochloride (memantine, DMAA) on the stretch-induced reflex tension of flexor muscles extensor digitorum longus and tibialis anterior (EDL/TA) and on the excitability of the neurons relaying transmission in the gamma-loop have been investigated in decerebrate and spinal cats. DMAA essentially reduced the relfex excitability of flexors EDL/TA induced by fusimotor activity in the decerebrate preparation. The drug did not stimulate the reflex activity in acute spinal cats. In the concentration used, DMAA suppressed largely the transmission of the fusimotor reflex in the decerebrate as well as in the spinal preparation, although in spinal cats DMAA increased the average firing rate of muscle spindle primaries originating from EDL/TA muscles. The possible mechanism of action of the compound on dopaminergic and serotonergic systems as well as its basic effects on neuronal membranes is discussed.
D000547:Amantadine / Q000031:analogs & derivatives*; D000818:Animals; D002415:Cats; D003655:Decerebrate State / Q000503:physiopathology; D005260:Female; D008297:Male; D008559:Memantine / Q000494:pharmacology*; D009046:Motor Neurons / Q000187:drug effects*; D009129:Muscle Tonus / Q000187:drug effects*; D009475:Neurons, Afferent / Q000502:physiology; D012018:Reflex / Q000187:drug effects*; D013116:Spinal Cord / Q000502:physiology
D000547:Amantadine; D008559:Memantine