Methods:Distortion product otoacoustic emissions were measured before and after decerebration in 17 guinea pigs.

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In addition, decerebration did not alter propofol requirements.

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In addition, the decerebration significantly diminished the peak pressor effects on PRN stimulation.

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Results:DPOAEs amplitude decreased significantly and rapidly after decerebration and remained at the lowest levels for 2,5,10 min. DPOAEs gradually recovered to the previous levels with time delay.

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In animals under little anesthetic influence, midcollicular decerebration significantly lowered the resting SAP, but both DM and VLM pressor responses were not significantly changed.

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The inhibitory effect of the DPN inputs on pressor response of the defence reaction was not influenced apparently after decerebration at a level rostral to the nucleus arcuatus , but was abolished by decerebration at a level caudal to the Arc or by electrolytic lesion of this nucleus.

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The activation of NRM neurons by electroaeupuncture was eliminated after decerebration at superior colliculus level, indicating that this effect of EA depends mainly on the supra-midbrain structure. Furthermore, all treatments including AR isolation, disconnection of #beta#-endorphinergic tract and micrpinjection of naloxone or anti-#beta#-endorphin serum into PAG, would make the effect of EA disappear. Thus, it is the #beta#-endorphinergic pathway between AR and PAG-NRM system that mediates the major excitatory effect of EA on NRM.

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