Optogenetic insights on the relationship between anxiety-related behaviors and social deficits

被引:122
作者
Allsop, Stephen A. [1 ,2 ]
Vander Weele, Caitlin M. [1 ]
Wichmann, Romy [1 ]
Tye, Kay M. [1 ]
机构
[1] MIT, Dept Brain & Cognit Sci, Picower Inst Learning & Memory, Cambridge, MA 02139 USA
[2] Harvard Univ, Sch Med, Boston, MA USA
关键词
social deficits; optogenetics; basolateral maygdala; ventral hippocampus; mouse models of affective disorders; social interaction; autism; PARTNER-PREFERENCE FORMATION; NUCLEUS-ACCUMBENS DOPAMINE; ANIMAL-MODELS; NEURAL CIRCUITS; PRIMARY-CARE; COGNITIVE NEUROSCIENCE; INDIVIDUAL-DIFFERENCES; HIPPOCAMPAL-FORMATION; BASOLATERAL AMYGDALA; PAROXETINE TREATMENT;
D O I
10.3389/fnbeh.2014.00241
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
010107 [宗教学]; 030301 [社会学]; 070906 [古生物学及地层学(含古人类学)];
摘要
Many psychiatric illnesses are characterized by deficits in the social domain. For example, there is a high rate of co-morbidity between autism spectrum disorders and anxiety disorders. However, the common neural circuit mechanisms by which social deficits and other psychiatric disease states, such as anxiety, are co-expressed remains unclear. Here, we review optogenetic investigations of neural circuits in animal models of anxiety-related behaviors and social behaviors and discuss the important role of the amygdala in mediating aspects of these behaviors. In particular, we focus on recent evidence that projections from the basolateral amygdala (BLA) to the ventral hippocampus (vHPC) modulate anxiety-related behaviors and also alter social interaction. Understanding how this circuit influences both social behavior and anxiety may provide a mechanistic explanation for the pathogenesis of social anxiety disorder, as well as the prevalence of patients co-diagnosed with autism spectrum disorders and anxiety disorders. Furthermore, elucidating how circuits that modulate social behavior also mediate other complex emotional states will lead to a better understanding of the underlying mechanisms by which social deficits are expressed in psychiatric disease.
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页数:14
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共 241 条
[1]
Cognitive neuroscience of human social behaviour [J].
Adolphs, R .
NATURE REVIEWS NEUROSCIENCE, 2003, 4 (03) :165-178
[2]
IMPAIRED RECOGNITION OF EMOTION IN FACIAL EXPRESSIONS FOLLOWING BILATERAL DAMAGE TO THE HUMAN AMYGDALA [J].
ADOLPHS, R ;
TRANEL, D ;
DAMASIO, H ;
DAMASIO, A .
NATURE, 1994, 372 (6507) :669-672
[3]
What does the amygdala contribute to social cognition? [J].
Adolphs, Ralph .
YEAR IN COGNITIVE NEUROSCIENCE 2010, 2010, 1191 :42-61
[4]
The Social Brain: Neural Basis of Social Knowledge [J].
Adolphs, Ralph .
ANNUAL REVIEW OF PSYCHOLOGY, 2009, 60 :693-716
[5]
The Serotonin-1A Receptor in Anxiety Disorders [J].
Akimova, Elena ;
Lanzenberger, Rupert ;
Kasper, Siegfried .
BIOLOGICAL PSYCHIATRY, 2009, 66 (07) :627-635
[6]
The primate amygdala and the neurobiology of social behavior: Implications for understanding social anxiety [J].
Amaral, DG .
BIOLOGICAL PSYCHIATRY, 2002, 51 (01) :11-17
[7]
The amygdala: is it an essential component of the neural network for social cognition? [J].
Amaral, DG ;
Capitanio, JP ;
Jourdain, M ;
Mason, WA ;
Mendoza, SP ;
Prather, M .
NEUROPSYCHOLOGIA, 2003, 41 (02) :235-240
[8]
American Psychiatric Association, 2013, Diagnostic and statistical manual of mental disorders, DOI 10.1176/appi.books.9780890425596
[9]
Anxiety and stress responses in female oxytocin deficient mice [J].
Amico, JA ;
Mantella, RC ;
Vollmer, RR ;
Li, X .
JOURNAL OF NEUROENDOCRINOLOGY, 2004, 16 (04) :319-324
[10]
Anxiety: at the intersection of genes and experience [J].
Anagnostaras, SG ;
Craske, MG ;
Fanselow, MS .
NATURE NEUROSCIENCE, 1999, 2 (09) :780-782