Stress and Inflammation Target Dorsolateral Prefrontal Cortex Function: Neural Mechanisms Underlying Weakened Cognitive Control

Animal models provide significant insight into the development of typical and disordered sensory processing. Such models have been established to take advantage of physical and behavioral characteristics of specific species. For example, the Mongolian gerbil is a well-established model for auditory processing, with a hearing range similar in frequency to that of humans and an easily accessible cochlea. Recently, early-life stress (ELS) has been shown to affect sensory processing in auditory, visual, and somatosensory neural regions. To understand the functional impact of ELS, it is necessary to evaluate the susceptibility of sensory perceptual abilities to this early perturbation. Yet measuring sensory perception – e.g., using operant conditioning – often concurrently involves animal behavioral elements such as attention, memory, learning, and emotion. All of these elements are well-known to be impacted by ELS, and may affect behavioral measurements in ways that could be misconstrued as sensory deficits. Thus, it is critical to characterize which behavioral elements are affected by ELS in any sensory model. Here we induced ELS during a developmental time window for maturation of the auditory cortex in Mongolian gerbils. We conducted behavioral measures in juveniles, a developmental age when ELS is known to impair the auditory pathway. ELS had no effect on overall activity but reduced anxiety-related behavior, impaired recognition memory, and improved spatial memory, with some sex-specific effects. These effects may influence the ability of gerbils to learn and retain operant training, particularly if anxiety-provoking reinforcement is used.

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Transcutaneous auricular vagus nerve stimulation as a potential therapy for attention deficit hyperactivity disorder: modulation of the noradrenergic pathway in the prefrontal lobe

Zhi,

Zhang,

Huang

et al. 2024

Front. Neurosci.

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Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by developmental impairments, inattention, motor hyperactivity, and impulsivity. Currently, there is no effective intervention that can completely cure it. One of the pathogenic mechanisms of ADHD involves abnormalities in the norepinephrine (NE) pathway within the prefrontal cortex (PFC). In recent years, transcutaneous auricular vagus nerve stimulation (taVNS), a non-invasive neuromodulation technique, has demonstrated promising potential in the treatment of neurological and psychiatric disorders. However, its application in the management of ADHD remains relatively unexplored. Previous studies have shown that taVNS exerts therapeutic effects on attention, cognition, arousal, perception, and behavioral regulation primarily through activating the vagus nerve conduction pathway, specifically targeting the nucleus tractus solitarius - locus coeruleus - NE pathway. These findings have led to the hypothesis that taVNS may be an effective intervention for ADHD, with NE and its pathway playing a pivotal role in this context. Therefore, this review comprehensively examines the correlation between NE pathway alterations in the PFC and ADHD, the mechanism of action of taVNS, and the potential role of the NE pathway in treating ADHD with taVNS, aiming to provide a theoretical foundation for clinical applications.

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Stress and Inflammation Target Dorsolateral Prefrontal Cortex Function: Neural Mechanisms Underlying Weakened Cognitive Control

Cited by 4 publications

References 132 publications

Low-frequency rTMS Plays a Neuroprotective role in Pilocarpine-induced Status Epilepticus Rat Models Through the AMPAR GluA1–STIM–Ca2+ Pathway

Low-frequency rTMS Plays a Neuroprotective role in Pilocarpine-induced Status Epilepticus Rat Models Through the AMPAR GluA1–STIM–Ca2+ Pathway

Characterizing Behavioral Effects of Early-Life Stress in an Animal Model of Auditory Processing

Transcutaneous auricular vagus nerve stimulation as a potential therapy for attention deficit hyperactivity disorder: modulation of the noradrenergic pathway in the prefrontal lobe

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