Activation of Pontine Cholinergic Sites Implicated in Unconsciousness Following Cerebral Concussion in the Cat

Abstract

Low levels of cerebral concussion in the cat produce reversible behavioral suppression presumably associated with unconsciousness. This injury is also associated with increased rates of glucose utilization in regions within the dorsomedial pontine tegmentum. Microinjection of carbachol into these regions produced behavioral suppression resembling that following concussion. These data, together with previously published observations on cholinergic responses to brain injury, suggest that concussive unconsciousness may be attributable in part to activation of cholinergic pontine sites.

Brainstem node for loss of consciousness due to GABAA receptor-active anesthetics

“…Its mediation by dedicated brain circuitry therefore suggests that in clinical use GABA A -R active anesthetics substitute for the neurotransmitter GABA much as in endogenous pain control circuitry morphine substitutes for enkephalins and endorphins. It follows that the switching circuitry itself serves an adaptive functional role, presumably in the realm of natural sleep and perhaps also in the realms of syncope (fainting), anti-predator immobility and concussion (Franks, 2008;Hayes et al, 1984;Joiner et al, 2013;Sandoval-Herrera et al, 2011). If so, MPTA neurons might contribute to state switching in these functions as well.…”

Diaschisis.

“…197 Supporting this theory is the reproduction in cats of transient behavioral and EEG changes mimicking concussion following acetylcholine agonist (carbachol) infusion. An increased 2DG utilization in cholinergic neurons remote from the site of trauma was observed in a concussion model.…”

Cerebral Activity during the Anesthesia-Like State Induced by Mesopontine Microinjection of Pentobarbital

“…A competing hypothesis holds that as in sleep-wake transitions, behavioral collapse in anesthesia and the anesthesia-like states is related to activity in dedicated brainstem and diencephalic structures, some associated with the reticular formation (Magni et al, 1959;Hayes et al, 1984;Katayama et al, 1988;Alkire et al, 2000;Nelson et al, 2002;Tung and Mendelson, 2004;Lydic and Baghdoyan, 2005;Morales et al, 2006;Franks, 2008;Zecharia et al, 2009). According to this view, global metabolic suppression in the brain is secondary to network activity transmitted by specific ascending pathways.…”