Neuroscience
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Psychiatric disorders are fairly common comorbidities of epilepsy in humans. Following pilocarpine-induced status epilepticus (SE), experimental animals not only developed spontaneous recurrent seizures, but also exhibited significantly elevated levels of aggressive behavior. ⋯ Treatment with rapamycin, a potent mTOR (mammalian target of rapamycin pathway)-pathway inhibitor, markedly diminished aggressive behavior. Therefore, the mTOR pathway may have significance in the underlying molecular mechanism leading to aggression associated with epilepsy.
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High frequency stimulation (HFS) has the potential to interfere with learning and memory. HFS and motor skill training both lead to potentiation of the stimulated network and alter motor map expression. However, the extent to which HFS can interfere with the learning and performance of a skilled motor task and the resulting effect on the representation of movement has not been examined. ⋯ Reach training alone was associated with an up-regulation of GABA(A)α1, α2, GluR2, NR1 and NR2A compared to controls. HFS and reach-trained rats showed an up-regulation of GABA(A)α2 compared to stimulated rats that were not reach-trained. Therefore, we have shown that HFS induces significant plasticity in the motor cortex, and has the potential to disrupt performance on a skilled motor task.
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Stressors encountered during the juvenile period may have persistent effects on later behavioral and neurochemical functioning and may influence later responses to stressors. In the current investigation, we evaluated the influence of stressor exposure applied during the juvenile period (26-28 days of age) on anxiety-related behavior, plasma corticosterone and on GABA(A) α2, α3, α5 and γ2 mRNA expression within the prefrontal cortex (PFC) and amygdala measured during adulthood. These changes were monitored in the absence of a further challenge, as well as in response to either a social or a non-social psychogenic stressor administered during adulthood. ⋯ The current results suggest that juvenile and adult stressor experiences elicit variations of GABA(A) receptor subunit expression that are region-specific as well as sexually-dimorphic. Stressful events during the juvenile period may have pronounced proactive effects on anxiety-related behaviors, but linking these to specific GABA(A) subunits is made difficult by the diversity of GABA changes that are evident as well as the dimorphic nature of these variations. Nevertheless, these GABA(A) sex-specific subunit variations may be tied to the differences in anxiety in males and females.
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Inwardly rectifying potassium (Kir) channel Kir4.1 (also called Kcnj10) is expressed in various cells such as satellite glial cells. It is suggested that these cells would absorb excess accumulated K(+) from intercellular space which is surrounded by these cell membranes expressing Kir4.1. In the vestibular system, loss of Kir4.1 results in selective degeneration of type I hair cells despite normal development of type II hair cells. ⋯ On the other hand, in the vestibular sensory epithelia, Kir4.1 protein is localized at the calyx endings of vestibular afferents, which surround type I hair cells. Kir4.1 protein expression in the vestibular sensory epithelia is detected beginning after birth, and its localization gradually adopts a calyceal shape until type I hair cells are mature. Kir4.1 localized at the calyx endings may play a role in the K(+)-buffering action of vestibular afferents surrounding type I hair cells.
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The glomeruli are the first synaptic relay on the olfactory pathway and play a basic role in smell perception. Glomerular degeneration occurs in humans with age and in Alzheimer's disease (AD). The glomeruli heavily express β-amyloid precursor protein (APP), β-secretase (BACE1) and γ-secretase complex. ⋯ Reduced glomerular area was detected in 6-12-month-old 5XFAD mice relative to non-transgenic controls, and in aged humans relative to young/adult controls, more robust in AD than aged subjects without cerebral amyloid and tau pathologies. The results suggest that olfactory nerve terminals may undergo age-related dystrophic and degenerative changes in AD model mice and humans, which are associated with increased labeling for amyloidogenic proteins but not local extracellular Aβ deposition. The identified axon terminal pathology might affect neuronal signal transmission and integration at the first olfactory synaptic relay.