Basolateral Amygdala Regulates EEG Theta-activity During Rapid Eye Movement Sleep

Machida, Manabu; Sweeten, Brook L.W.; Adkins, Austin M.; Wellman, Laurie L.; Sanford, Larry D.

doi:10.1016/j.neuroscience.2021.06.018

Cited by 3 publications

(12 citation statements)

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“…In conclusion, the current study confirmed our prior finding that optogenetic activation of BLA Glu specifically during post-shock REM reduced REM-θ amplitude [22] and provided additional support for the contention that REM-θ plays a functional role in the processing of fear memory [29]. The reduction in REM-θ amplitude was associated with subsequent attenuated freezing and altered fear-conditioned REM responses, whereas fear-conditioned SIH was not significantly impacted compared to other groups receiving identical ST and stimulation during NREM.…”

Section: Discussionsupporting

confidence: 92%

“…It should be noted that the restraint and tethering required to implement optogenetic experiments can induce a stress response as indicated by SIH [16,22] which can, in turn, influence REM [43]. Indeed, we observed continued SIH and enhanced reductions in REM while mice were tethered during the post-ST REM + L and NREM + L treatment conditions.…”

Section: Discussionmentioning

confidence: 58%

“…We further found that, under baseline conditions, optogenetic inhibition of BLA Glu during naturally occurring REM enhances REM-associated-theta (θ) activity in the EEG (REM-θ), increases attempts at transitioning into REM, and thus can increase REM amount under some circumstances [16]. By comparison, optogenetic activation of BLA Glu during spontaneous REM reduces REM-θ without otherwise altering REM amounts or propensity for REM [22].…”

Section: Introductionmentioning

confidence: 74%

“…We previously found that REM-specific optogenetic activation of BLA Glu reduced REM-θ activity whereas optogenetic inhibition of BLA Glu increased REM-θ [16,22]. Generally, large-scale θ oscillations detected in the EEG are thought to be primarily produced in the hippocampus [23], and changes in power amplitude are thought to result from macroscopic changes in synchronization within local neural ensembles [58].…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, REM can be either decreased or increased following virtually identical fear-induced freezing and stress responses [19][20][21]37,44], indicating that fear memory can differentially regulate outputs across functional systems. By comparison, REM-dependent physiological events including θ coherence [61], REM-θ amplitude [22,29] and phasic pontine-waves (P-waves) [65] may be more accurate predictors of successful consolidation of fear memory than REM amount. Interestingly, both REM-θ and P-waves [66][67][68] are regulated by the amygdala, which along with the mPFC and hippocampus, exhibits coordinated θ activity associated with contextual fear conditioning [33].…”

Section: Discussionmentioning

confidence: 99%

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The Basolateral Amygdala Mediates the Role of Rapid Eye Movement Sleep in Integrating Fear Memory Responses

Machida

Sweeten

Adkins

et al. 2021

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The basolateral amygdala (BLA) mediates the effects of stress and fear on rapid eye movement sleep (REM) and on REM-related theta (θ) oscillatory activity in the electroencephalograph (EEG), which is implicated in fear memory consolidation. We used optogenetics to assess the potential role of BLA glutamate neurons (BLAGlu) in regulating behavioral, stress and sleep indices of fear memory, and their relationship to altered θ. An excitatory optogenetic construct targeting glutamatergic cells (AAV-CaMKIIα-hChR2-eYFP) was injected into the BLA of mice. Telemetry was used for real-time monitoring of EEG, activity, and body temperature to determine sleep states and stress-induced hyperthermia (SIH). For 3 h following shock training (ST: 20 footshocks, 0.5 mA, 0.5 s, 1 min interval), BLA was optogenetically stimulated only during REM (REM + L) or NREM (NREM + L). Mice were then re-exposed to the fear context at 24 h, 48 h, and 1 week after ST and assessed for behavior, SIH, sleep and θ activity. Control mice were infected with a construct without ChR2 (eYFP) and studied under the same conditions. REM + L significantly reduced freezing and facilitated immediate recovery of REM tested at 24 h and 48 h post-ST during contextual re-exposures, whereas NREM + L had no significant effect. REM + L significantly reduced post-ST REM-θ, but attenuated REM-θ reductions at 24 h compared to those found in NREM + L and control mice. Fear-conditioned SIH persisted regardless of treatment. The results demonstrate that BLAGlu activity during post-ST REM mediates the integration of behavioral and sleep indices of fear memory by processes that are associated with θ oscillations within the amygdalo-hippocampal pathway. They also demonstrate that fear memories can remain stressful (as indicated by SIH) even when fear conditioned behavior (freezing) and changes in sleep are attenuated.

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Section: Discussionsupporting

confidence: 92%