Differential modulation of thalamo-parietal interactions by varying depths of isoflurane anesthesia

Abstract

The thalamus is thought to relay peripheral sensory information to the somatosensory cortex in the parietal lobe. Long-range thalamo-parietal interactions play an important role in inducing the effect of anesthetic. However, whether these interaction changes vary with different levels of anesthesia is not known. In the present study, we investigated the influence of different levels of isoflurane-induced anesthesia on the functional connectivity between the thalamus and the parietal region. Microelectrodes were implanted in rats to record local field potentials (LFPs). The rats underwent different levels of isoflurane anesthesia [deep anesthesia: isoflurane (ISO) 2.5 vol%, light anesthesia (ISO 1 vol%), awake, and recovery state] and LFPs were recorded from four different brain areas (left parietal, right parietal, left thalamus, and right thalamus). Partial directed coherence (PDC) was calculated for these areas. With increasing depth of anesthesia, the PDC in the thalamus-to-parietal direction was significantly increased mainly in the high frequency ranges; however, in the parietal-to-thalamus direction, the increase was mainly in the low frequency band. For both directions, the PDC changes were prominent in the alpha frequency band. Functional interactions between the thalamus and parietal area are augmented proportionally to the anesthesia level. This relationship may pave the way for better understanding of the neural processing of sensory inputs from the periphery under different levels of anesthesia.

Understanding the Effects of Anesthesia on Cortical Electrophysiological Recordings: A Scoping Review

“…Conversely, higher doses of isoflurane from 1.4 to 2.2% were shown not only to reduce the number of active single units, but also to increase their response onset latency compared to the awake condition; the evoked LFPs were burst-suppressed and a typical pattern with alternating high amplitude bursts and silent periods emerged [ 100 ]. The level of isoflurane anesthesia proportionally affects the functional interaction between the cortex and the thalamus: from LFP recordings in adult Long-Evans rats chronically implanted with electrodes in the parietal lobe and thalamic region, it was shown that increasing the anesthesia level from light (1%) to deep (2.5%) caused an increase in the interactions between the two brain areas mainly in the alpha frequencies, and preferentially in the thalamus-to-cortex direction [ 101 ]. From EEG recordings on S1FL (forelimb) and S1BF (barrel field) primary somatosensory cortex areas in adult Sprague-Dawley rats, a burst suppression and a reduction in the delta (1–4 Hz) and gamma (>30 Hz) bands power appeared with deep isoflurane anesthesia concentration (1.8%), with respect to moderate and light concentrations (1.5 and 1.0%, respectively [ 102 ]).…”

How general anesthetics work: from the perspective of reorganized connections within the brain

“…Isoflurane inhibits the metabolism of the thalamus and disrupts thalamocortical connectivity. [86,87] Isoflurane also disrupts connectivity between anterior and posterior cortical areas. [88] Also, during isoflurane anesthesia, the brain tends to be in an overall state that is less complex and efficient, decreasing the sensitivity to external stimuli.…”

“…depth. [87] Given that the psychomimetic effects of ketamine seem to arise from a reorganization of sensory processing within other regions [75], it seems plausible that the alterations of sensory networks could give rise to antinociception during anesthesia. However, further studies should be performed to clarify this issue.…”

“…Although some differences have been noted, inhaled anesthetics in general act on the GABA receptor, similar to hypnotics such as propofol. Isoflurane inhibits metabolism in the thalamus and disrupts both thalamocortical connectivity [ 86 , 87 ] and connectivity between the anterior and posterior cortical areas [ 88 ]. Additionally, during isoflurane anesthesia, the brain tends to be in an overall state that is less complex and efficient, with a decreased sensitivity to external stimuli [ 78 ].…”

“…Commercially available monitors for antinociception are mainly based on changes in autonomic nervous system function due to sympathetic system inhibition. Anesthetics may affect functional connections between the thalamus and sensory cortex, which changes with anesthetic depth [ 87 ]. Given that the psychomimetic effects of ketamine seem to arise from a reorganization of sensory processing within other regions [ 75 ], it seems plausible that the alterations of sensory networks could give rise to antinociception during anesthesia.…”