Neuroscience
-
Brain developmental disorders such as lissencephaly can result from faulty neuronal migration and differentiation during the formation of the mammalian neocortex. The cerebral cortex is a modular structure, where developmentally, newborn neurons are generated as a neuro-epithelial sheet and subsequently differentiate, migrate and organize into their final positions in the cerebral cortical plate via a process involving both tangential and radial migration. The specific role of Mest, an imprinted gene, in neuronal migration has not been previously studied. ⋯ The differentiation and migration properties of neurons via Wnt-Akt signaling were affected by Mest changes. In addition, miR-335, encoded in a Mest gene intron, was identified as being responsible for blocking the default tangential migration of the neurons. Our results suggest that Mest and its intron product, miR-335, play important roles in neuronal migration with Mest regulating the morphological transition of primary neurons required in the formation of the mammalian neocortex.
-
The somatosensory information from the orofacial region, including the periodontal ligament (PDL), is processed in a manner that differs from that used for other body somatosensory information in the related cortices. It was reported that electrical stimulation to rat PDL elicited activation of the insular oral region (IOR) and the primary (S1) and secondary (S2) somatosensory cortices. However, the physiological relationship between S1 and S2/IOR is not well understood. ⋯ An injection of FluoroGold™ (FG) to the initial response area in S1 or the S2/IOR showed that FG-positive cells were scattered in the non-injected cortical counterpart. This morphological result demonstrated the presence of a bi-directional intracortical connection between the initial response areas in S1 and the S2/IOR. These findings suggest the presence of a mutual connection between S1 and the S2/IOR as an intracortical signal processing network for orofacial nociception.
-
Chronic psychosocial stress modulates brain antioxidant systems and causes neuroinflammation that plays a role in the pathophysiology of depression. Although the antidepressant fluoxetine (FLX) represents the first-line treatment for depression and the atypical antipsychotic clozapine (CLZ) is considered as a second-line treatment for psychotic disorders, the downstream mechanisms of action of these treatments, beyond serotonergic or dopaminergic signaling, remain elusive. We examined behavioral changes, glutathione (GSH)-dependent defense and levels of proinflammatory mediators in the prefrontal cortex (PFC) of adult male Wistar rats exposed to 21days of chronic social isolation (CSIS). ⋯ In conclusion, prefrontal cortical GSH depletion and the proinflammatory response underlying depressive- and anxiety-like states induced by CSIS were prevented by FLX. The protective effect of CLZ, which was equally effective as FLX on the behavioral level, was limited to proinflammatory components. Hence, different mechanisms underlie the protective effects of these two drugs in CSIS rats.
-
Microglia are critical for developmental pruning and immune response to injury, and are implicated in facilitating neural plasticity. The rodent gustatory system is highly plastic, particularly during development, and outcomes following nerve injury are more severe in developing animals. The mechanisms underlying developmental plasticity in the taste system are largely unknown, making microglia an attractive candidate. ⋯ Our results show that microglia density is highest during times of normal gustatory afferent pruning. Furthermore, the quantity of the microglia response is higher in the mature system than in neonates. These findings link increased microglia presence with instances of normal developmental and injury induced alterations in the rNTS.
-
In this study we tested whether a selective reward could affect the adaptation of saccadic eye movements in monkeys. We induced the adaptation of saccades by displacing the target of a horizontal saccade vertically as the eye moved toward it, thereby creating an apparent vertical dysmetria. The repeated upward target displacement caused the originally horizontal saccade to gradually deviate upward over the course of several hundred trials. ⋯ Saccades in the rewarded direction showed more rapid adaptation of their directions than did saccades in the non-rewarded direction, indicating that the selective reward increased the speed of saccade adaptation. The differences in adaptation speed were reflected in changes in saccade metrics, which were usually more noticeable in the deceleration phases of saccades than in their acceleration phases. Because previous studies have shown that the oculomotor cerebellum is involved with saccade deceleration and also participates in saccade adaptation, it is possible that selective reward could influence cerebellar plasticity.