Olfaction, Emtion & the Amygdala: arousal-dependent modulation of long-term autobiographical memory and its association with olfaction

The sense of smell is set apart from other sensory modalities. Odours possess the capacity to trigger immediately strong emotional memories. Moreover, odorous stimuli provide a higher degree of memory retention than other sensory stimuli. Odour perception, even in its most elemental form - olfaction - already involves limbic structures. This early involvement is not paralleled in other sensory modalities. Bearing in mind the considerable connectivity with limbic structures, and the fact that an activation of the amygdala is capable of instantaneously evoking emotions and facilitating the encoding of memories, it is unsurprising that the sense of smell has its characteristic nature. The aim of this review is to analyse current understanding of higher olfactory information processing as it relates to the ability of odours to spontaneously cue highly vivid, affectively toned, and often very old autobiographical memories (episodes known anecdotally as Proust phenomena). Particular emphasis is placed on the diversity of functions attributed to the amygdala. Its role in modulating the encoding and retrieval of long-term memory is investigated with reference to lesion, electrophysiological, immediate early gene, and functional imaging studies in both rodents and humans. Additionally, the influence of hormonal modulation and the adrenergic system on emotional memory storage is outlined. I finish by proposing a schematic of some of the critical neural pathways that underlie the odour-associated encoding and retrieval of emotionally toned autobiographical memories

Formyl Peptide Receptor as a Novel Therapeutic Target for Anxiety-Related Disorders

Formyl peptide receptors (FPR) belong to a family of sensors of the immune system that detect microbe-associated molecules and inform various cellular and sensorial mechanisms to the presence of pathogens in the host. Here we demonstrate that Fpr2/3-deficient mice show a distinct profile of behaviour characterised by reduced anxiety in the marble burying and light-dark box paradigms, increased exploratory behaviour in an open-field, together with superior performance on a novel object recognition test. Pharmacological blockade with a formyl peptide receptor antagonist, Boc2, in wild type mice reproduced most of the behavioural changes observed in the Fpr2/3(-/-) mice, including a significant improvement in novel object discrimination and reduced anxiety in a light/dark shuttle test. These effects were associated with reduced FPR signalling in the gut as shown by the significant reduction in the levels of p-p38. Collectively, these findings suggest that homeostatic FPR signalling exerts a modulatory effect on anxiety-like behaviours. These findings thus suggest that therapies targeting FPRs may be a novel approach to ameliorate behavioural abnormalities present in neuropsychiatric disorders at the cognitive-emotional interface

Interactions between metabolic, reward and cognitive processes in appetite control:Implications for novel weight management therapies

Traditional models of appetite control have emphasised the role of parallel homeostatic and hedonic systems, but more recently the distinction between independent homeostatic and hedonic systems has been abandoned in favour of a framework that emphasises the cross talk between the neurochemical substrates of the two systems. In addition, evidence has emerged more recently, that higher level cognitive functions such as learning, memory and attention play an important role in everyday appetite control and that homeostatic signals also play a role in cognition. Here, we review this evidence and present a comprehensive model of the control of appetite that integrates cognitive, homeostatic and reward mechanisms. We discuss the implications of this model for understanding the factors that may contribute to disordered patterns of eating and suggest opportunities for developing more effective treatment approaches for eating disorders and weight management

The limbic system as a neuroanatomical link between obesity and depression. Neuroimaging findings

It has been described high comorbidity between depression, therefore, it becomes interesting to explore the activity of brain structures common to both conditions through neuroimaging studies. Objectives. First - to identify neuroimaging structures concerning to morbid obesity and mayor depression disorder. Second - to analyze the common structures to both conditions. Methodology. Articles were searched in Pubmed and Science databases with the following keywords: MRI (magnetic resonance imaging) obesity, mayor depression disorder, depression and brain activity; with publication dates from 2007 to 2021, no review articles were considered. Obesity has a very high comorbidity with depression. In both pathologies the activation of prefrontal cortex, putamen and insula is altered. These neuroanatomical structures are part of the reward system, so the response to hedonic stimuli is mediated by them and altered in obesity and depression.INSK KELLOGG COMPANY 4843/2019

Genetic influences in emotional dysfunction and alcoholism-related brain damage

Alcoholism is a complex, multifactorial disorder involving problematic ethanol ingestion; it results from the interplay between genetic and environmental factors. Personality, likewise, is formed from a combination of inherited and acquired influences. Because selected dimensions of emotional temperament are associated with distinct neurochemical substrates contributing to specific personality phenotypes, certain aspects of abnormal emotional traits in alcoholics may be inherited. Emotions involve complex subjective experiences engaging multiple brain regions, most notably the cortex, limbic system, and cerebellum. Results of in vivo magnetic resonance imaging and post-mortem neuropathological studies of alcoholics indicate that the greatest cortical loss occurs in the frontal lobes, with concurrent thinning of the corpus callosum. Additional damage has been documented for the amygdala and hippocampus, as well as in the white matter of the cerebellum. All of the critical areas of alcoholism-related brain damage are important for normal emotional functioning. When changes occur in these brain regions, either as a consequence of chronic ethanol abuse or from a genetic anomaly affecting temperament and/or a vulnerability to alcoholism, corresponding changes in emotional functions are to be expected. In alcoholics, such changes have been observed in their perception and evaluation of emotional facial expressions, interpretation of emotional intonations in vocal utterances, and appreciation of the meaning of emotional materials

Olfactory Inputs Modulate Respiration-Related Activity In The Prefrontal Cortex And Fear Behavior

Voluntary control of respiration, especially via rhythmic nasal breathing, alleviates negative feelings such as fear and is used clinically to manage certain types of panic attacks. However, the neural substrates that link nasal breathing to fear circuits remains unknown. Here we show that during conditioned fear-induced freezing behavior, mice breathe at a steady rate (~4 Hz) which is strongly correlated with a predominant 4 Hz oscillation observed in the olfactory bulb and the prelimbic prefrontal cortex (plPFC), a structure critical for the expression of conditioned fear behaviors. We demonstrate anatomical and functional connectivity between the olfactory pathway and plPFC via circuit tracing and optogenetic approaches. Disrupting olfactory inputs significantly reduces the 4 Hz oscillation in the plPFC suggesting that respiration-related signals from the olfactory system play a role in entraining this fear-related signal. Surprisingly, we find that without olfactory inputs, freezing times are significantly prolonged. Collectively, our results indicate that olfactory inputs modulate rhythmic activity in fear circuits and suggest a neural pathway that may underlie the behavioral benefits of respiration-entrained olfactory signals

Stimulating the sleeping brain: Current approaches to modulating memory-related sleep physiology

Background: One of the most audacious proposals throughout the history of psychology was the potential ability to learn while we sleep. The idea penetrated culture via sci-fi movies and inspired the invention of devices that claimed to teach foreign languages, facts, and even quit smoking by simply listening to audiocassettes or other devices during sleep. However, the promises from this endeavor didn't stand up to experimental scrutiny, and the dream was shunned from the scientific community. Despite the historic evidence that the sleeping brain cannot learn new complex information (i.e., words, images, facts), a new wave of current interventions are demonstrating that sleep can be manipulated to strengthen recent memories. New method: Several recent approaches have been developed that play with the sleeping brain in order to modify ongoing memory processing. Here, we provide an overview of the available techniques to non-invasively modulate memory-related sleep physiology, including sensory, vestibular and electrical stimulation, as well as pharmacological approaches. Results: N/A. Comparison with existing methods: N/A. Conclusions: Although the results are encouraging, suggesting that in general the sleeping brain may be optimized for better memory performance, the road to bring these techniques in free-living conditions is paved with unanswered questions and technical challenges that need to be carefully addressed