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The protein composition of excitatory synapses differs in the areas of the human neocortex controlling language, emotion and other behaviors. This neocortical postsynaptic proteome data resource can be used to link genetics to brain imaging and behavior.
Humans can deliberately control the timing of their actions but the neural mechanisms underlying such control are largely unknown. In this article, Wang, Narain and their colleagues report that such flexibility emerges in rhesus monkeys from the ability of their brain to flexibly control the speed at which cortical responses unfold in time.
To decide how much we would like to eat a food item, our brain automatically decomposes it into constituent nutrients. The quantities of the different nutrients are represented in distinct parts of the lateral orbitofrontal cortex and then integrated by the medial orbitofrontal cortex to provide a global value judgment.
A leaky blood–brain barrier may contribute to neuropsychiatric disease. Chronic stress is shown to alter blood–brain barrier permeability, allowing an inflammatory response to penetrate the brain. The deficit is mostly around the nucleus accumbens, an area central to motivation. The affected animals exhibit features of depression.
Sommeijer et al. describe a previously unrecognized role of the thalamus: development of inhibition in the thalamus regulates ocular dominance plasticity, a form of critical-period plasticity regulation previously ascribed solely to the cortex.
The authors propose a new framework for the thalamus in cognition. They review findings from rodents and primates, emphasizing thalamic control of functional cortical connectivity, its putative mechanisms and role in flexible construction of task-relevant cortical networks.
Most species exhibit instinctive risk-avoidance, e.g., lab mice avoid predator smells despite having never encountered predators. Here the authors show how innate risk-avoidance arises from accumbal dopamine receptor neurons tuned by orexin signals.
Like all terrestrial mammals, humans emit body odors that subtly communicate emotions. This study suggests that adults with autism may be misreading these chemical signals and that this may explain a portion of their social difficulties.
Apicco and colleagues show that reducing TIA1 inhibits tau-mediated neurodegeneration and improves survival in a mouse model of tauopathy. This rescue occurs with a transition in tau aggregation from oligomeric to fibrillar forms of tau. These findings suggest a key role for RNA binding proteins in the pathophysiology of tau.
Experience-dependent plasticity in the visual system has widely been considered to be exclusively cortical. Using chronic two-photon Ca2+imaging of individual thalamic boutons, Jaepel et al. now report that dLGN cells projecting to mouse visual cortex show pronounced ocular dominance plasticity after monocular deprivation.
The authors show that oxytocin-receptor-expressing neurons in the parabrachial nucleus are key regulators of fluid homeostasis that suppress fluid intake when activated, but do not decrease food intake after fasting or salt intake after salt depletion.
The authors show that unlike body sensory neurons, craniofacial nociceptive neurons directly synapse with noxious-stimulus-activated lateral parabrachial neurons (PBL), which in turn project to multiple limbic centers processing emotions and affects. This monosynaptic pathway is both sufficient and necessary for craniofacial-pain-activated aversive behaviors.
The authors develop a methods suite for millisecond-precise, single-cell-resolution control of neural activity through protein engineering of novel opsin/trafficking sequence combinations, as well as optimized holographic two-photon optics.
Chronic social defeat stress induces loss of protein claudin-5, leading to abnormalities in blood vessel morphology, increased blood brain barrier permeability, infiltration of immune signals and depression-like behaviors.
Quantitative mass spectrometry was used to produce a proteomic survey of postnatal human brain regions. Compared to matched RNA-seq, protein levels showed more regional variation, especially for membrane-associated proteins in the neocortex.
The relationship of resting-state hemodynamics signals to ongoing neural activity is poorly understood. Using optical imaging, electrophysiology, and local pharmacological infusions, Winder et al. found that resting hemodynamic signals were weakly correlated with neural activity and that these hemodynamic fluctuations persisted when neural activity was silenced.
Arid1b haploinsufficiency causes autism and intellectual disability, yet the neurobiological basis of this is unknown. The authors demonstrate that Arid1b-heterozygous mice have impaired cortical interneuron development and epigenetic signatures. These mice also have cognitive and social deficits, which are reversed by treatment with a GABAA-receptor-positive allosteric modulator.
Mouse models have generally failed to recapitulate the dopaminergic neurodegeneration seen in Parkinson's disease. Expressing mutant α-synuclein in a background of elevated dopamine generates mice with nigrostriatal degeneration.