This review presents an analysis of the sensory and motor mechanisms as they are now understood that cause the immobility reflex (IR). Of the sensory systems that conceivably could trigger and sustain the IR, as commonly induced experimentally by inversion and manual restraint, evidence has been presented to eliminate some senses (vestibular, vision, sound, many visceral sensations, olfaction, taste, temperature), while incriminating tactile and proprioceptive influences.
We previously found that the center of animal hypnosis production in the rabbit is located around the locus ceruleus and brachium conjunctivum (LC-BC) of the brainstem. The involvement of serotonergic neurons in this area of animal hypnosis was investigated by microinjection of serotonin into these regions. The duration of animal hypnosis (DAH) induced by inversion was diminished to about 65% of the controls by serotonin microinjection into the LC-BC and microinjection of methysergide prolonged the DAH to 3.2 times that of the controls.
The notion of consciousness is at the core of an ongoing debate on the existence and nature of hypnotic states. Previously, we have described changes in brain activity associated with hypnosis (Rainville, Hofbauer, Paus, Duncan, Bushnell, & Price, 1999). Here, we replicate and extend those findings using positron emission tomography (PET) in 10 normal volunteers.
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience
General anesthetics cause sedation, hypnosis, and immobilization via CNS mechanisms that remain incompletely understood; contributions of particular anesthetic targets in specific neural pathways remain largely unexplored. Among potential molecular targets for mediating anesthetic actions, members of the TASK subgroup [TASK-1 (K2P3.1) and TASK-3 (K2P9.1)] of background K(+) channels are appealing candidates since they are expressed in CNS sites relevant to anesthetic actions and activated by clinically relevant concentrations of inhaled anesthetics.
