Neuroimaging analysis of an anesthetic gas that blocks human emotional memory

Abstract

It is hypothesized that emotional arousal modulates long-term memory consolidation through the amygdala. Gaseous anesthetic agents are among the most potent drugs that cause temporary amnesia, yet the effects of inhalational anesthesia on human emotional memory processing remain unknown. To study this, two experiments were performed with the commonly used inhalational anesthetic sevoflurane. In experiment 1, volunteers responded to a series of emotional and neutral slides while under various subanesthetic doses of sevoflurane or placebo (no anesthesia). One week later, a mnemonic boost for emotionally arousing stimuli was evident in the placebo, 0.1%, and 0.2% sevoflurane groups, as measured with a recognition test. However, the mnemonic boost was absent in subjects who received 0.25% sevoflurane. Subsequently, in experiment 2, glucose PET assessed brain-state-related activity of subjects exposed to 0.25% sevoflurane. Structural equation modeling of the PET data revealed that 0.25% sevoflurane suppressed amygdala to hippocampal effective connectivity. The behavioral results show that 0.25% sevoflurane blocks emotional memory, and connectivity results demonstrate that this dose of sevoflurane suppresses the effective influence of the amygdala. Collectively, the findings support the hypothesis that the amygdala mediates memory modulation by demonstrating that suppressed amygdala effectiveness equates with a loss of emotional memory.amygdala ͉ anesthesia ͉ brain imaging ͉ cerebral metabolism ͉ sevoflurane

From high anxiety trait to depression: a neurocognitive hypothesis

“…This 'emotional tag' will strengthen synapses that have just been activated in another brain-memory system that is engaged in the learning situation eventually leading to the reinforcement of consolidation of that event [47,48]. In support of this view, recent work has shown that suppression of the amygdala to hippocampal effective connectivity blocks the emotion-induced memory-enhancing effect [49].…”

Influence of anesthesia on cerebral blood flow, cerebral metabolic rate, and brain functional connectivity

“…Higher-order association areas are more sensitive to hypnotic agents than lower-order processing regions [29,40,41]. At low concentrations, hypnotic agents reduce but do not abolish connectivity and anticorrelation of DMN and ECN [42 ,43 ,44 ], and of other higher-order networks including emotional and memory networks [45], while connectivity is preserved or even increased in lower-order sensory and motor networks [46]. An impairment of sub-cortical thalamoregulatory systems has also been reported at low concentrations that could account for an altered cortical integration of information [47 ], despite preserved activation of the thalamus by external stimuli.…”

Inhibition of learning and memory by general anesthetics

“…56 Memory for emotional encounters was blocked by sub-anesthetic concentrations of sevoflurane (0.25%), desflurane (1.5-2 times MAC-awake), and propofol (1.5-2 times MAC-awake). 57,58 At MAC-equivalent concentrations, some anesthetics are more effective than others at preventing memory. For example, both isoflurane and nitrous oxide suppressed memory in a dose-dependent manner, although isoflurane was more effective than MAC-equivalent concentrations of nitrous oxide.…”