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Understanding Brain Function and Nervous System Disease: Amygdala as a...
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Understanding Brain Function and Nervous System Disease: Amygdala as a Nodal Point

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 3300

Special Issue Editors

Dr. Xian Zhang

E-Mail Website1 Website2
Guest Editor
1. Bioscience and Biomedical Engineering Thrust, Systems Hub, Hong Kong University of Science and Technology (Guangzhou), Guangzhou, China
2. Division of the Life Science, Hong Kong University of Science and Technology, Kowloon, Hong Kong, China
Interests: amygdala; fear; emotion; motivated behaviors; stress; anxiety; depression; neural circuits; neurotransmitter
Dr. Yiran Gu

E-Mail Website
Guest Editor
Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Brain Functional Genomics, East China Normal University, Shanghai 200062, China
Interests: amygdala & learning and memory; associative learning; post-traumatic stress disorder; norepinephrine; chandelier cells

Special Issue Information

Dear Colleagues,

The amygdala is part of the limbic system and has been regarded as the integrative center for regulating emotion and motivation. It is primarily well known for its involvement in fear learning and memory and later has been documented to be involved in a wide array of functions, including positive and negative valence, predatory behavior, food consumption, pain, addiction and sleep. Particularly, the amygdala participates in the regulation of neuroendocrine and autonomic responses, as well as the “fight-or-flight” response via efferent projections from its subregions to other brain areas. However, abnormal activity and altered structure, circuits and function in the amygdala have been implicated in a variety of neurodevelopmental and neuropsychiatric disorders, including anxiety, depression, posttraumatic stress disorder, insomnia, and autism. Despite these advances in understanding, they are still many questions regarding the amygdala’s function remain.

This Specific Issue will focus on all aspects of amygdala function in the regulation of emotion, motivated behaviors, as well as nervous system disease. We are pleased to invite basic and clinical research in the amygdala at molecular, cellular, circuitry, systems and behavioral levels, as well as reviews that address the neural mechanisms of emotional information processing.

Dr. Xian Zhang
Dr. Yiran Gu
Guest Editors

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Keywords

  • amygdala
  • fear
  • emotion
  • motivated behaviors
  • stress
  • anxiety
  • depression
  • neural circuits
  • neurotransmitter

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Published Papers (1 paper)

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Research

15 pages, 4978 KiB  
Article
In Vivo Ultrafast Doppler Imaging Combined with Confocal Microscopy and Behavioral Approaches to Gain Insight into the Central Expression of Peripheral Neuropathy in Trembler-J Mice
by Mariana Martínez Barreiro, Lucia Vázquez Alberdi, Lucila De León, Guadalupe Avellanal, Andrea Duarte, Maximiliano Anzibar Fialho, Jérôme Baranger, Miguel Calero, Nicolás Rubido, Mickael Tanter, Carlos Negreira, Javier Brum, Juan Pablo Damián and Alejandra Kun
Biology 2023, 12(10), 1324; https://doi.org/10.3390/biology12101324 - 10 Oct 2023
Cited by 1 | Viewed by 2492
Abstract
The main human hereditary peripheral neuropathy (Charcot-Marie-Tooth, CMT), manifests in progressive sensory and motor deficits. Mutations in the compact myelin protein gene pmp22 cause more than 50% of all CMTs. CMT1E is a subtype of CMT1 myelinopathy carrying micro-mutations in pmp22. The Trembler-J [...] Read more.
The main human hereditary peripheral neuropathy (Charcot-Marie-Tooth, CMT), manifests in progressive sensory and motor deficits. Mutations in the compact myelin protein gene pmp22 cause more than 50% of all CMTs. CMT1E is a subtype of CMT1 myelinopathy carrying micro-mutations in pmp22. The Trembler-J mice have a spontaneous mutation in pmp22 identical to that present in CMT1E human patients. PMP22 is mainly (but not exclusively) expressed in Schwann cells. Some studies have found the presence of pmp22 together with some anomalies in the CNS of CMT patients. Recently, we identified the presence of higher hippocampal pmp22 expression and elevated levels of anxious behavior in TrJ/+ compared to those observed in wt. In the present paper, we delve deeper into the central expression of the neuropathy modeled in Trembler-J analyzing in vivo the cerebrovascular component by Ultrafast Doppler, exploring the vascular structure by scanning laser confocal microscopy, and analyzing the behavioral profile by anxiety and motor difficulty tests. We have found that TrJ/+ hippocampi have increased blood flow and a higher vessel volume compared with the wild type. Together with this, we found an anxiety-like profile in TrJ/+ and the motor difficulties described earlier. We demonstrate that there are specific cerebrovascular hemodynamics associated with a vascular structure and anxious behavior associated with the TrJ/+ clinical phenotype, a model of the human CMT1E disease. Full article
(This article belongs to the Special Issue Understanding Brain Function and Nervous System Disease: Amygdala as a Nodal Point)
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