Memory is essential in defining our identity by guiding behavior based on past experiences. However, aging leads to declining memory, disrupting older adult's lives. Memories are encoded through experience-dependent modifications of synaptic strength, which are regulated by the catecholamines dopamine and noradrenaline. While cognitive aging research demonstrates how dopaminergic neuromodulation from the substantia nigra-ventral tegmental area regulates hippocampal synaptic plasticity and memory, recent findings indicate that the noradrenergic locus coeruleus sends denser inputs to the hippocampus. The locus coeruleus produces dopamine as biosynthetic precursor of noradrenaline, and releases both to modulate hippocampal plasticity and memory. Crucially, the locus coeruleus is also the first site to accumulate Alzheimer's-related abnormal tau and severely degenerates with disease development. New in-vivo assessments of locus coeruleus integrity reveal associations with Alzheimer's markers and late-life memory impairments, which likely stem from impaired dopaminergic and noradrenergic neurotransmission. Bridging research across species, the reviewed findings suggest that degeneration of the locus coeruleus results in deficient dopaminergic and noradrenergic modulation of hippocampal plasticity and thus memory decline.
The locus coeruleus (LC) produces most of the brain's noradrenaline (NA). Among its many roles, NA is often said to be neuroprotective and important for brain upkeep. For this reason, loss of LC integrity is thought to impact brain volume and microstructure as well as plasticity broadly.
Engineering Research Center of Molecular and Neuro Imaging of the Ministry of Education, School of Life Science and Technology, Xidian University, Xi'an, Shaanxi 710126, China; Intelligent Non-invasive Neuromodulation Technology and Transformation Joint Laboratory, Xidian University, Xi'an, Shaanxi 710126, China; Guangzhou Institute of Technology, Xidian University, Xi'an, Shaanxi, China. Electronic address:
Background: In the face of inevitable declines in alertness and fatigue resulting from sleep deprivation, effective countermeasures are essential for maintaining performance. External trigeminal nerve stimulation (eTNS) presents a potential avenue for regulating alertness by activating the locus coeruleus and reticular activating system.
Methods: Here, we conducted a within-subject study with 66 habitual nappers, subjecting them to afternoon nap-deprivation and applying either 20-minute of 120 Hz eTNS or sham stimulation.
Distinct excitatory synaptic inputs to the locus coeruleus (LC) modulate behavioral flexibility. Here we identify a novel monosynaptic glutamatergic input to the LC from the ventral tegmental area (VTA). We show robust VTA axonal projections provide direct glutamatergic transmission to LC.
Background Obstructive sleep apnea (OSA) is an intermittent hypoxia disorder associated with cognitive dysfunction, including learning and memory impairments. There is evidence that alterations in protease activity and neuronal activation as associated with cognitive dysfunction, are dependent on sex, and may be brain region-specific. However, the mechanisms mediating OSA-induced cognitive impairments are unclear.
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).
