Involvement of the basolateral complex and central nucleus of amygdala in the omission effects of different magnitudes of reinforcement

Single units in the central nucleus of the inferior colliculus (ICC) of unanesthetized decerebrate cats can be grouped into three distinct types (V, I, and O) according to the patterns of excitation and inhibition revealed in contralateral frequency response maps. This study extends the description of these response types by assessing their ipsilateral and binaural response map properties. Here the nature of ipsilateral inputs is evaluated directly using frequency response maps and compared with results obtained from methods that rely on sensitivity to interaural level differences (ILDs). In general, there is a one-to-one correspondence between observed ipsilateral input characteristics and those inferred from ILD manipulations. Type V units receive ipsilateral excitation and show binaural facilitation (EE properties); type I and type O units receive ipsilateral inhibition and show binaural excitatory/inhibitory (EI) interactions. Analyses of binaural frequency response maps show that these ILD effects extend over the entire receptive field of ICC units. Thus the range of frequencies that elicits excitation from type V units is expanded with increasing levels of ipsilateral stimulation, whereas the excitatory bandwidth of type I and O units decreases under the same binaural conditions. For the majority of ICC units, application of bicuculline, an antagonist for GABAA-mediated inhibition, does not alter the basic effects of binaural stimulation; rather, it primarily increases spontaneous and maximum discharge rates. These results support our previous interpretations of the putative dominant inputs to ICC response types and have important implications for midbrain processing of competing free-field sounds that reach the listener with different directional signatures.

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Understanding Emotions: Origins and Roles of the Amygdala

Biomolecules ◽

10.3390/biom11060823 ◽

2021 ◽

Vol 11 (6) ◽

pp. 823

Author(s):

Goran Šimić ◽

Mladenka Tkalčić ◽

Vana Vukić ◽

Damir Mulc ◽

Ena Španić ◽

...

Keyword(s):

Sensory Information ◽

Anterior Cingulate ◽

Central Nucleus ◽

Subcortical Structures ◽

Neuronal Populations ◽

Efferent Projections ◽

Short And Long Term ◽

Understanding Emotions ◽

Fight Or Flight Response ◽

And Behavior

Emotions arise from activations of specialized neuronal populations in several parts of the cerebral cortex, notably the anterior cingulate, insula, ventromedial prefrontal, and subcortical structures, such as the amygdala, ventral striatum, putamen, caudate nucleus, and ventral tegmental area. Feelings are conscious, emotional experiences of these activations that contribute to neuronal networks mediating thoughts, language, and behavior, thus enhancing the ability to predict, learn, and reappraise stimuli and situations in the environment based on previous experiences. Contemporary theories of emotion converge around the key role of the amygdala as the central subcortical emotional brain structure that constantly evaluates and integrates a variety of sensory information from the surroundings and assigns them appropriate values of emotional dimensions, such as valence, intensity, and approachability. The amygdala participates in the regulation of autonomic and endocrine functions, decision-making and adaptations of instinctive and motivational behaviors to changes in the environment through implicit associative learning, changes in short- and long-term synaptic plasticity, and activation of the fight-or-flight response via efferent projections from its central nucleus to cortical and subcortical structures.

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Blockade of the GLT-1 Transporter in the Central Nucleus of the Amygdala Induces both Anxiety and Depressive-Like Symptoms

Neuropsychopharmacology ◽

10.1038/npp.2015.16 ◽

2015 ◽

Vol 40 (7) ◽

pp. 1700-1708 ◽

Cited By ~ 26

Author(s):

Catherine S John ◽

Elizabeth I Sypek ◽

William A Carlezon ◽

Bruce M Cohen ◽

Dost Öngür ◽

...

Keyword(s):

Central Nucleus

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Alcohol use disorder causes global changes in splicing in the human brain

Translational Psychiatry ◽

10.1038/s41398-020-01163-z ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Derek Van Booven ◽

Mengying Li ◽

J. Sunil Rao ◽

Ilya O. Blokhin ◽

R. Dayne Mayfield ◽

...

Keyword(s):

Alcohol Use ◽

Human Brain ◽

Alcohol Use Disorder ◽

Brain Regions ◽

Gene Set Enrichment Analysis ◽

Splicing Factor ◽

Central Nucleus ◽

Global Changes ◽

Aberrant Expression ◽

Altered Expression

AbstractAlcohol use disorder (AUD) is a widespread disease leading to the deterioration of cognitive and other functions. Mechanisms by which alcohol affects the brain are not fully elucidated. Splicing constitutes a nuclear process of RNA maturation, which results in the formation of the transcriptome. We tested the hypothesis as to whether AUD impairs splicing in the superior frontal cortex (SFC), nucleus accumbens (NA), basolateral amygdala (BLA), and central nucleus of the amygdala (CNA). To evaluate splicing, bam files from STAR alignments were indexed with samtools for use by rMATS software. Computational analysis of affected pathways was performed using Gene Ontology Consortium, Gene Set Enrichment Analysis, and LncRNA Ontology databases. Surprisingly, AUD was associated with limited changes in the transcriptome: expression of 23 genes was altered in SFC, 14 in NA, 102 in BLA, and 57 in CNA. However, strikingly, mis-splicing in AUD was profound: 1421 mis-splicing events were detected in SFC, 394 in NA, 1317 in BLA, and 469 in CNA. To determine the mechanism of mis-splicing, we analyzed the elements of the spliceosome: small nuclear RNAs (snRNAs) and splicing factors. While snRNAs were not affected by alcohol, expression of splicing factor heat shock protein family A (Hsp70) member 6 (HSPA6) was drastically increased in SFC, BLA, and CNA. Also, AUD was accompanied by aberrant expression of long noncoding RNAs (lncRNAs) related to splicing. In summary, alcohol is associated with genome-wide changes in splicing in multiple human brain regions, likely due to dysregulation of splicing factor(s) and/or altered expression of splicing-related lncRNAs.

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