Neuroscience
-
Understanding the neural mechanisms of training-induced brain plasticity has significant implications for improving academic achievement. Previous studies suggest abacus-based mental calculation (AMC) training significantly improves individual's arithmetic capability, and the frontal-parietal network is suggested to be the key neural circuit underlying AMC. Yet, it remains unclear how AMC training shifts brain activation in this network and whether the training effect is transferable or not. ⋯ The control group, on the other hand, did not exhibit any pre- to post-training differences in brain activation on any of the three tasks. These findings extend the previous cross-sectional studies of AMC and suggest that AMC training induces functional changes in brain activation and such plasticity may be transferable beyond the AMC. The training effects on sustained and transient neural activity may also provide a new perspective to understand training-induced neural plasticity and related transfer effect.
-
Aging causes various functional changes, including cognitive impairment and inflammatory responses in the brain. Transient receptor potential melastatin 2 (TRPM2), a Ca2+-permeable channel expressed abundantly in immune cells, exacerbates inflammatory responses. Previously, we reported that TRPM2 on resident microglia plays a critical role in exacerbating inflammation, white matter injury, and cognitive impairment during chronic cerebral hypoperfusion; however, the physiological or pathophysiological role of TRPM2 during age-associated inflammatory responses remains unclear. ⋯ However, these characteristics were not seen in TRPM2 knockout (TRPM2-KO) mice. Consistent with the finding of cognitive impairment, aged WT mice exhibited white matter injury and hippocampal damage and an increase in the number of Iba1-positive cells and amounts of pro-inflammatory cytokines in the brain; these characteristics were not seen in TRPM2-KO mice. These findings suggest that TRPM2 plays a critical role in exacerbating inflammatory responses and cognitive dysfunction during aging.
-
Brain-derived neurotrophic factor (BDNF) is known to mediate activity-dependent changes in the developing auditory system. Its expression in the brainstem auditory nuclei, auditory cortex and hippocampus of neonatal chicks (Gallus gallus domesticus) in response to in ovo high intensity sound exposure at 110 dB (arrhythmic sound: recorded traffic noise, 30-3000 Hz with peak at 2700 Hz, rhythmic sound: sitar music, 100-4000 Hz) was examined to understand the previously reported altered volume and neuronal number in these regions. In the brainstem auditory nuclei, no mature BDNF, but proBDNF at the protein level was detected, and no change in its levels was observed after in ovo sound stimulation (music and noise). ⋯ Expression microarray analysis was performed to understand changes in gene expression in the hippocampus in response to music and noise, followed by gene ontology analysis showing enrichment of probable signaling pathways. Differentially expressed genes like CAMK1 and STAT1 were found to be involved in downstream signaling on comparing music versus noise-exposed chicks. In conclusion, we report that BDNF is differentially regulated in the auditory cortex at the transcriptional and post-translational level, and in the hippocampus at the post-translational level in response to in ovo sound stimulation.
-
Lamina X is localized in the spinal cord within the region surrounding the central canal and receives descending projections from the supraspinal nuclei. Norepinephrine (NE) is a neurotransmitter in descending pathways emanating from the brain stem; NE-containing fibers terminate in the spinal dorsal cord, particularly in the substantia gelatinosa (SG). NE enhances inhibitory synaptic transmission in SG neurons by activating presynaptic α1-receptors and hyperpolarizes the membranes of SG neurons by acting on α2-receptors; NE may thus act directly on SG neurons of the dorsal spinal cord and inhibit nociceptive transmission at the spinal level. ⋯ NE-induced enhancement of mIPSCs was blocked by α1A-receptor antagonists, and NE-induced outward current was blocked by α2-receptor antagonists. NE did not affect GABA- or glycine- induced outward currents. These findings are similar to those obtained from SG neurons: NE may act at presynaptic terminals of GABAergic and glycinergic interneurons on lamina X to facilitate inhibitory-transmitter release through α1A-receptor activation and directly induce inhibitory interneuron membrane hyperpolarization through α2-receptors activation.
-
Concussion injury results in a rapid onset of transient neurological impairment that can resolve quickly, or sometimes evolve over time, but usually resolve within seven to 10 days. However, a small but noticeable cohort (~10%) of individuals continues to experience persistent lingering effects, particularly fatigue, recognized as post-concussion symptoms (PCS). This study explored neurophysiological mechanisms in people with persistent PCS. ⋯ Somatosensory differences were observed for amplitude discrimination (F2,57 = 5.166; p = 0.009), temporal order judgment (F2,57 = 4.606; p = 0.014) and duration discrimination (F2,57 = 6.081; p = 0.004). Increased intracortical inhibition in TMS single pulse suprathreshold stimulation (110%: F2,57 = 6.842; p = 0.002; 130%: F2,57 = 4.900; p = 0.011; 150%: F2,57 = 4.638; p = 0.014; 170%: F2,57 = 9.845; p < 0.001) and paired pulse protocols was also seen (SICI: F2,57 = 23.390; p < 0.001, and LICI: F2,57 = 21.603; p < 0.001). Using non-invasive stimulation techniques, this novel study showed increased cortical inhibition and compromised central information processing, suggesting neural mechanisms underpinning ongoing fatigue, allowing for potential clinical rehabilitation strategies.