Neuroscience
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Comparative Study
Sex differences in social interaction behaviors in rats are mediated by extracellular signal-regulated kinase 2 expression in the medial prefrontal cortex.
Considerable sex differences occur in the incidence and prevalence of anxiety disorders where women are more anxious than men, particularly in situations where social interaction is required. In preclinical studies, the social interaction test represents a valid animal model to study sex differences in social anxiety. ⋯ Indeed, female rats' had lower ERK2 expression compared to male rats, and overexpression of ERK2 in the mPFC increases their social interaction to the level seen in their male counterparts. These data indicate that the sexually dimorphic expression of ERK2 mediates social anxiety-like behaviors.
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Meta Analysis
The human vestibular cortex revealed by coordinate-based activation likelihood estimation meta-analysis.
The vestibular system contributes to the control of posture and eye movements and is also involved in various cognitive functions including spatial navigation and memory. These functions are subtended by projections to a vestibular cortex, whose exact location in the human brain is still a matter of debate (Lopez and Blanke, 2011). The vestibular cortex can be defined as the network of all cortical areas receiving inputs from the vestibular system, including areas where vestibular signals influence the processing of other sensory (e.g. somatosensory and visual) and motor signals. ⋯ The only area of convergence between all three methods of stimulation was located in Ri. The data indicate that Ri, parietal operculum and posterior insula are vestibular regions where afferents converge from otoliths and semicircular canals, and may thus be involved in the processing of signals informing about body rotations, translations and tilts. Results from the meta-analysis are in agreement with electrophysiological recordings in monkeys showing main vestibular projections in the transitional zone between Ri, the insular granular field (Ig), and SII.
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Elucidation of the 'fear circuit' has opened exciting avenues for understanding and treating human anxiety disorders. However, the translation of rodent to human studies, and vice versa, depends on understanding the homology in relevant circuits across species. Although abundant evidence indicates that the hippocampal-amygdala circuit mediates contextual fear learning, previous studies indicate that this pathway is more restricted in primates than in rodents. ⋯ Immature neurons are prominent in the PL and CTA, and are overlapped by anterogradely labeled fibers from CA1', particularly in the medial PL and CTA. Hippocampal inputs to the amygdala are more focused in higher primates compared to rodents, supporting previous anatomic studies and recent data from human functional imaging studies of contextual fear. At the cellular level, a hippocampal interaction with immature neurons in the amygdala suggests a novel substrate for cellular plasticity, with implications for mechanisms underlying contextual learning and emotional memory processes.
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Postsynaptic densities (PSDs) are responsible for organizing receptors and signaling proteins that regulate excitatory transmission in the mammalian brain. To better understand the assembly and 3D organization of this synaptic structure, we employed electron cryotomography to visualize general and fine structural details of PSDs isolated from P2, P14, P21 and adult forebrain in the absence of fixatives and stains. PSDs at P2 are a loose mesh of filamentous and globular proteins and during development additional protein complexes are recruited onto the mesh. ⋯ One striking morphological feature is the appearance of lipid raft-like structures, first evident in PSDs from 14 day old animals. These detergent-resistant membranes stain for GM1 ganglioside and their terminations can be clearly seen embedded in protein "bowls" within the PSD complex. In total, these results lead to the conclusion that the PSD is assembled by the gradual recruitment and stabilization of proteins within an initial mesh that systematically adds complexity to the structure.
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Brain-derived neurotrophic factor (BDNF) plays important roles in the development, maintenance, and plasticity of the mammalian forebrain. These functions include regulation of neuronal maturation and survival, axonal and dendritic arborization, synaptic efficacy, and modulation of complex behaviors including depression and spatial learning. Although analysis of mutant mice has helped establish essential developmental functions for BDNF, its requirement in the adult is less well documented. ⋯ To identify an anatomical correlate of the abnormal behavior, we quantified dendritic spines in cortical neurons. The spine density of CaMK-BDNF(KO) mice was normal at P35, but by P84, there was a 30% reduction in spine density. The strong similarities we find between early- and late-onset BDNF knockouts suggest that BDNF signaling is required continuously in the CNS for the maintenance of some forebrain circuitry also affected by developmental BDNF depletion.