Lesions of the Basolateral Amygdala Complex Block Propofol-induced Amnesia for Inhibitory Avoidance Learning in Rats

Alkire, Michael T.; Vazdarjanova, Almira; Dickinson-Anson, Heather; White, Nathan S.; Cahill, Larry

doi:10.1097/00000542-200109000-00025

Cited by 41 publications

(27 citation statements)

References 42 publications

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“…The vast majority of drug and hormone modulations of memory depend critically on amygdala function, and animal studies of general anesthetic-induced amnesia follow this consistent trend in the literature (1,7,9,22). This suggests studying the effects of other anesthetics on human emotional memory processing is warranted.…”

Section: Fig 3 the Pr For Recollection Memory Is Shown (Mean ϯ Sem)mentioning

confidence: 72%

Neuroimaging analysis of an anesthetic gas that blocks human emotional memory

Alkire

Gruver

Miller

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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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

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Section: Fig 3 the Pr For Recollection Memory Is Shown (Mean ϯ Sem)mentioning

confidence: 72%

Neuroimaging analysis of an anesthetic gas that blocks human emotional memory

Alkire

Gruver

Miller

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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“…Level II: Minimizing the perception: An adequate plane of anesthesia requiring the use of bispectral index [36] or other monitoring systems and use of an ideal "DFT cocktail" drug combination are areas that need further exploration. Currently used anesthetic agents like propofol [37] have minimal analgesic effects and could lead to potential "anesthesia awareness." Ketamine, an N-methyl-Daspartate (NMDA) receptor antagonist, may be one of the agents that can be evaluated in DFT testing as it shares both analgesic and amnesic properties [38].…”

Section: Possible Preventive and Therapeutic Interventionsmentioning

confidence: 99%

Phantom shocks unmasked: clinical data and proposed mechanism of memory reactivation of past traumatic shocks in patients with implantable cardioverter defibrillators

Jacob

Panaich

Zalawadiya

et al. 2011

J Interv Card Electrophysiol

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“…Lesion of the basolateral amygdala has also been demonstrated to block propofol-and benzodiazepine-induced amnesia in animals [100,101]. Although the amygdala may be one of the key structures in anesthetic-induced amnesia, general anesthetics have also been suggested to interact with other neuronal structures involved in the memory process, and a number of studies have shown that general anesthetics decrease synaptic transmission in hippocampal neurons [102][103][104].…”

Section: Amnesiamentioning

confidence: 99%

Mechanisms of anesthetic actions and the brain

Ishizawa

2007

J Anesth

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The neural mechanisms behind anesthetic-induced behavioral changes such as loss of consciousness, amnesia, and analgesia, are insufficiently understood, though general anesthesia has been of tremendous importance for the development of medicine. In this review, I summarize what is currently known about general anesthetic actions at different organizational levels and discuss current and future research, using systems neuroscience approaches such as functional neuroimaging and quantitative electrophysiology to understand anesthesia actions at the integrated brain level.

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Lesions of the Basolateral Amygdala Complex Block Propofol-induced Amnesia for Inhibitory Avoidance Learning in Rats

Abstract: Discrete BLAC lesions blocked the amnestic effect of propofol. BLAC activity appears to be a requirement for propofol-induced amnesia. This finding suggests that the BLAC is a key brain site mediating anesthetic-induced amnesia.

Cited by 41 publications

References 42 publications

Neuroimaging analysis of an anesthetic gas that blocks human emotional memory

Neuroimaging analysis of an anesthetic gas that blocks human emotional memory

Phantom shocks unmasked: clinical data and proposed mechanism of memory reactivation of past traumatic shocks in patients with implantable cardioverter defibrillators

Mechanisms of anesthetic actions and the brain

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