Suppression of the hindlimb flexor reflex by stimulation of the medial hypothalamus and thalamus in the rat.
Pentobarbital-anesthetized rats received electrical hindpaw stimulation every 10 s to elicit a maximal hindlimb withdrawal reflex. The integrated EMG response in the ipsilateral tibialis anterior was sampled by a computer which also controlled the timing of electrical stimuli applied to the brain. A suppression of the evoked flexor activity was obtained with currents below 0.05 mA for stimuli applied in the medial hypothalamic region. A second effective site was located in the paraventricular area of the thalamus. The suppression had an onset latency of 30 ms, increased over a period of 500 ms and was followed by a postinhibitory facilitation (rebound). When the noxious electrical shocks were given over prolonged periods (140 s) the suppression of the flexor reflex was seen to outlast the central stimulation by more than 100 s. Intravenous injection of naloxone or methysergide failed to reverse the effects of the brain stimuli. It is suggested that the hypothalamic induced inhibition of withdrawal reflexes is functionally meaningful in view of the incompatibility between these reflexes and the locomotor behavior which is part of the behavioral responses (i.e. fight or flight) controlled by this area.
Duysens
J
J
Department of Medical Physics and Biophysics, University of Nijmegen, (The Netherlands).
Dom
R
R
Gybels
J
J
D000698:Analgesia; D000818:Animals; D004525:Efferent Pathways / Q000502:physiology; D004558:Electric Stimulation; D006614:Hindlimb / Q000294:innervation* / Q000502:physiology; D007033:Hypothalamus, Middle / Q000503:physiopathology*; D010146:Pain / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012018:Reflex; D013788:Thalamus / Q000503:physiopathology*