Auditory verbal hallucination and the auditory network: From molecules to connectivity. (1st July 2019)

• Record Type: Journal Article
• Authors: Huang, Jianjie; Zhuo, Chuanjun; Xu, Yong; Lin, Xiaodong
• Is Part Of: Neuroscience. Volume 410(2019)
• Page Start: 59
• Page End: 67
• Publication Date: 2019-07-01
• Subjects: auditory verbal hallucination -- schizophrenia -- functional imaging -- synaptic plasticity -- non-invasive transcranial stimulus; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2019.04.051
• Languages: English
• ISSNs: 0306-4522

Abstract

Abstract: Auditory verbal hallucinations (AVHs) frequently occur across multiple psychiatric diseases especially in schizophrenia (SCZ) patients. Functional imaging studies have revealed the hyperactivity of the auditory cortex and disrupted auditory–verbal network activity underlying AVH etiology. This review will firstly summarize major findings from both human AVH patients and animal models, with focuses on the auditory cortex and associated cortical/sub-cortical areas. Besides mesoscale connectivity or activity data, structure and functions at synaptic level will be discussed, in conjunction with molecular mechanisms. We have summarized major findings for the pathogenesis of AVH in SCZ patients, with focuses in the auditory cortex and prefrontal cortex (PFC). Those discoveries provide explanations for AVH from different perspectives including inter-regional connectivity, local activity in specific areas, structure and functions of synapse, and potentially molecular targets. Due to the uniqueness of AVH in humans, full replica using animals seems impossible. However, we can still extract useful information from animal SCZ models based on the disruption of auditory pathway during AVH episodes. Therefore, we will further interpolate the synaptic structures and molecular targets, whose dysregulation in SCZ models may be highly related with AVH episodes. As the last part, implications for future development of treatment strategies will be discussed. Highlights: AVH may be caused by dysregulated thalamocortical connectivity. Altered circuits in AVH are related with impaired synaptic plasticity. In future, one should focus on molecular mechanism and non-drug treatment of AVH.