| Literature DB >> 32001274 |
Juan A Arias1, Claire Williams2, Rashmi Raghvani2, Moji Aghajani3, Sandra Baez4, Catherine Belzung5, Linda Booij6, Geraldo Busatto7, Julian Chiarella6, Cynthia Hy Fu8, Agustin Ibanez9, Belinda J Liddell10, Leroy Lowe11, Brenda W J H Penninx3, Pedro Rosa7, Andrew H Kemp12.
Abstract
Sadness is typically characterized by raised inner eyebrows, lowered corners of the mouth, reduced walking speed, and slumped posture. Ancient subcortical circuitry provides a neuroanatomical foundation, extending from dorsal periaqueductal grey to subgenual anterior cingulate, the latter of which is now a treatment target in disorders of sadness. Electrophysiological studies further emphasize a role for reduced left relative to right frontal asymmetry in sadness, underpinning interest in the transcranial stimulation of left dorsolateral prefrontal cortex as an antidepressant target. Neuroimaging studies - including meta-analyses - indicate that sadness is associated with reduced cortical activation, which may contribute to reduced parasympathetic inhibitory control over medullary cardioacceleratory circuits. Reduced cardiac control may - in part - contribute to epidemiological reports of reduced life expectancy in affective disorders, effects equivalent to heavy smoking. We suggest that the field may be moving toward a theoretical consensus, in which different models relating to basic emotion theory and psychological constructionism may be considered as complementary, working at different levels of the phylogenetic hierarchy.Entities:
Keywords: Affective neuroscience; Basic emotions; GENIAL model; Genetics; Health and wellbeing; Heart rate variability; Major depressive disorder; Neuroimaging; Psychological constructionism; Psychophysiology; Sadness; Vagal function
Mesh:
Year: 2020 PMID: 32001274 DOI: 10.1016/j.neubiorev.2020.01.006
Source DB: PubMed Journal: Neurosci Biobehav Rev ISSN: 0149-7634 Impact factor: 8.989