Norepinephrine ignites local hotspots of neuronal excitation: How arousal amplifies selectivity in perception and memory

Abstract

Long Abstract Existing brain-based emotion-cognition theories fail to explain arousal’s ability to both enhance and impair cognitive processing. In the Glutamate Amplifies Noradrenergic Effects (GANE) model outlined in this paper, we propose that arousal-induced norepinephrine (NE) released from the locus coeruleus (LC) biases perception and memory in favor of salient, high priority representations at the expense of lower priority representations. This increase in gain under phasic arousal occurs via synaptic self-regulation of NE based on glutamate levels. When the LC is phasically active, elevated levels of glutamate at the site of prioritized representations increase local NE release, creating “NE hot spots.” At these local hot spots, glutamate and NE release are mutually enhancing and amplify activation of prioritized representations. This excitatory effect contrasts with widespread NE suppression of weaker representations via lateral and auto-inhibitory processes. On a broader scale, hot spots increase oscillatory synchronization across neural ensembles transmitting high priority information. Furthermore, key brain structures that detect or pre-determine stimulus priority interact with phasic NE release to preferentially route such information through large-scale functional brain networks. A surge of NE before, during or after encoding enhances synaptic plasticity at sites of high glutamate activity, triggering local protein synthesis processes that enhance selective memory consolidation. Together, these noradrenergic mechanisms increase perceptual and memory selectivity under arousal. Beyond explaining discrepancies in the emotion-cognition literature, GANE reconciles and extends previous influential theories of LC neuromodulation by highlighting how NE can produce such different outcomes in processing based on priority.

Physical Exercise Performed Four Hours after Learning Improves Memory Retention and Increases Hippocampal Pattern Similarity during Retrieval

“…One possibility is that the release of PRPs at a time where naturally lower levels of PRPs would be available (i.e., several hours after learning) could have mediated the facilitation of memory retention in our study. Alternatively, exercise-dependent release of dopamine and noradrenaline could have facilitated consolidation similar to previously described effects of novelty and arousal [4,5,7,14,24,27,28].…”

“…Based on previous research demonstrating the relevance of consistent neural processing (i.e., pattern similarity) for memory retention and its reported utility in investigating differences in neural representations between experimental conditions and groups, we then conducted a hippocampal pattern similarity analysis [18][19][20][21][22]. We speculated that exercise-related physiological effects (e.g., dopamine and/or noradrenaline) could have neuromodulatory effects and thus alter the neural representations of recently encoded memories [23,24]. In this way, exercise might produce differences in the neural response patterns observed during recall instead of differences in regional BOLD amplitude.…”

Emotional arousal and recognition memory are differentially reflected in pupil diameter responses during emotional memory for negative events in younger and older adults

“…The effect was considerably weaker for negative stimuli, suggesting that on trials with greater stimulus capture, subsequent memory is less driven by temporal fluctuations in attentional states. A recent theory suggests that the effects of noradrenergic modulation on incidental memory should be examined in a context of an interaction of attentional focus on the one hand and temporal modulations of tonic levels on the other hand (Mather et al, 2015;Sakaki et al, 2014). Future studies should address this assumption in more detail by introducing an additional modulation in attentional focus during stimulus encoding combined with PD measurements in the emotional memory task (Sakaki et al, 2014).…”

Influence of reward motivation on human declarative memory

“…In humans, the effects of arousal on memory are selective and are mediated by ␤-adrenoreceptors in the amygdala which purportedly helps detect salient information and recruits the LC when activated (Mather et al, 2015). Like dopamine, noradrenaline modulates memory formation by promoting long-term potentiation (LTP) through these receptors in the amygdala and the hippocampus (Mather et al, 2015;Sara, 2009).…”

“…Like dopamine, noradrenaline modulates memory formation by promoting long-term potentiation (LTP) through these receptors in the amygdala and the hippocampus (Mather et al, 2015;Sara, 2009). Noradrenaline release could thus influence hippocampus-dependent forms of memory during a limited post-learning time window (including slow-wave sleep) (Tully and Bolshakov, 2010).…”