Inhibition of vestibular and neck reflexes in forelimb extensor muscles during the episodes of postural atonia induced by an anticholinesterase in decerebrate cat.
In precollicular decerebrate cats, the multiunit EMG activity of forelimb extensor muscles (e.g. the triceps brachii) was recorded during sinusoidal stimulation of labyrinth and neck receptors at the frequencies of 0.026-0.15 Hz, +/- 10 degrees and the resulting responses were tested during tonic activation of a cholinergic mechanism. In agreement with previous findings, the first harmonic component of the EMG responses to roll tilt of the animal leading to selective stimulation of labyrinth receptors was characterized by an increased activity during side-down tilt and a decreased activity during side-up tilt (labyrinth responses); on the other hand just the opposite changes were elicited for the same directions of neck rotation (neck responses). For the parameters of stimulation reported above, the responses were always related to position and not to velocity of displacement. Intravenous injection of an anticholinesterase (eserine sulphate, 0.10-0.15 mg/kg) which produced a state of postural atonia, associated with bursts of rapid eye movements (REM), similar to that occurring spontaneously in unrestrained cats during desynchronized sleep or REM sleep, also decreased the tonic activity of the triceps brachii and abolished the EMG responses of this muscle to sinusoidal stimulation of labyrinth and neck receptors. This suppression persisted throughout the episode of postural atonia associated with REM bursts. The abolition of the labyrinth and neck reflexes acting on forelimb muscles was not only dependent on the dose of anticholinesterase, but also on the state of the animal. In fact, somatosensory or acoustic stimuli applied during the REM episodes abolished the rhythmic oculomotor activity and determined the prompt recovery of both the decerebrate rigidity and the EMG responses of the triceps brachii to labyrinth and neck stimulation. The postural atonia as well as the tonic depression of the vestibular and neck reflexes acting on forelimb extensor muscles can in part at least be attributed to cholinergic activation of medullary reticulospinal neurons exerting a postsynaptic inhibitory influence on extensor motoneurons. However, since these inhibitory reticulospinal neurons collaborate with excitatory vestibulospinal neurons to the motoneuronal responses during stimulation of labyrinth and neck receptors, we cannot exclude that the suppression of the vestibular and neck reflexes may also depend on occlusion of the unit responses at reticular level.
D000818:Animals; D002415:Cats; D003655:Decerebrate State; D004576:Electromyography; D004585:Electrooculography; D005552:Forelimb / Q000502:physiology*; D009068:Movement; D009129:Muscle Tonus / Q000187:drug effects*; D009333:Neck / Q000502:physiology*; D010830:Physostigmine / Q000494:pharmacology*; D011187:Posture; D012018:Reflex / Q000502:physiology*; D012399:Rotation; D011984:Sensory Receptor Cells / Q000502:physiology*; D014722:Vestibule, Labyrinth / Q000502:physiology*
D010830:Physostigmine