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Leptin regulates energy balance. The authors show that Rho-kinase 1 (ROCK1) regulates leptin signaling by increasing activation of signaling molecules downstream of leptin receptor. Deletion of ROCK1 from POMC or AgRP neurons leads to obesity and reduced leptin sensitivity.
The pathology in Parkinson's disease is known to extend beyond mesencephalic dopaminergic neurons, but it is unclear why. Here the authors show that vulnerable neurons in the dorsal motor nucleus of the vagus have similar physiological features, including basal mitochondrial oxidant stress, providing an insight into the distributed disease pathology.
By examining natural behavioral variation of an outbred strain of mice on a Pavlovian-to-instrumental transfer task, the authors show that the level of polysialylated neural cell adhesion molecule (PSA-NCAM) in the ventromedial prefrontal cortex (vmPFC) can predict the extinction and cue-induced reinstatement of alcohol seeking. The study also shows that depleting endogenous PSA-NCAM in the vmPFC in mice confers resistance to the extinction of alcohol seeking.
Although it is well-known that sleep can strengthen existing memories, this study demonstrates that people can acquire completely new associations (between distinct tones and pleasant/unpleasant smells) during sleep, which are preserved during the awake state.
The authors show that traumatic brain injury can induce peroxidation of cardiolipin, leading to accumulation of numerous oxygenated species and the induction of neuronal cell death. This accumulation of cardiolipin and the associated toxicity can be ameliorated by mitochondria-targeted delivery of an electron scavenger.
In this paper, Bessereau and colleagues identify MOLO-1 as an auxiliary subunit for levamisole-sensitive acetylcholine receptors (L-AChRs) present at the neuromuscular junction of C. elegans. MOLO-1 is the first auxiliary subunit ever found for a member of the Cys-loop receptor superfamily.
The immediate-early gene Arc mediates synaptic plasticity and long-term memory formation. Whether Arc is dysregulated by amyloid-beta or in Alzheimer's disease is controversial. Here, a study used a reporter mouse line expressing destabilized fluorescent protein Venus under the control of the Arc promoter to show that Arc induction pattern, brain regional difference and precise location of active neurons with respect to senile plaque are major determinants of differential Arc response in a mouse model of Alzheimer's disease.
The authors show that K-ATP channels in dopamine (DA) neurons of the medial substantia nigra (m-SN) enable burst firing in vitro and in vivo. Silencing K-ATP channel activity in m-SN DA neurons decreases novelty-dependent exploratory behavior in mice.
In this study, the authors show that, during the development of the enteric nervous system, a subset of enteric neural crest cells migrate from midgut across the mesentery to colonize caudal hindgut. This trans-mesenteric migration requires GDNF and GFRα1 signaling.
In tasks involving goal-directed action selection, striatal neural activity has been shown to represent the value of competing actions. Here the authors show that transient optogenetic stimulation of dorsal striatal D1 and D2 receptor–expressing neurons during decision-making biases choices in a way that mimics an additive change in action value.
NG2 proteoglycan+ cells are neural and oligodendrocyte progenitors, and NG2+ cells in the developing barrel cortex receive glutamatergic thalamocortical inputs. Here, the authors show that NG2+ cells are primarily localized in barrel septa and that sensory deprivation induces NG2+ cell proliferation and differential localization in and around the barrels.
The anterior cingulate cortex is known to be involved in determining cost versus benefit, but, by recording from rats choosing to engage in competition with another rat for limited rewards, the authors found that this area is also involved in competitive effort.
The authors report that endogenous myocyte enhance factor 2 (MEF2) levels affect spatial and fear memory formation in adult mice. MEF2-induced memory disruption was rescued by interfering with AMPA receptor endocytosis.
The olfactory system is vulnerable to sensory deprivation owing to the prevalence of rhinosinusitis, but how the brain encodes and maintains odor information under such circumstances remains poorly understood. Using fMRI, the authors find evidence for transient changes in olfactory brain regions that sustain odor perception following disrupted sensory input.
The authors show that chronic treatment with antipsychotic drugs decreases expression of mGlu2 and histone acetylation at its promoter in frontal cortex. This is mediated through 5-HT2A receptor–dependent upregulation of HDAC2. HDAC inhibitors prevent this decrease in mGluR2, augmenting the behavioral effects of antipsychotics.
The Drosophila proteins Neuroligin (Nlg1) and Neurexin (Nrx-1) form a trans-synaptic complex that regulates synapse formation at the neuromuscular junction. Here the authors show that Syd-1, also known to regulate active zone formation, interacts with presynaptic Nrx-1, promoting synaptic clustering and immobilization of Nrx-1, and subsequent glutamate receptor incorporation.
Using juxtacellular recording and labeling of hippocampal interneurons in drug-free and behaving rats, the authors show that parvalbumin-expressing basket interneurons fire in a behavioral state–dependent manner, in contrast with neuropeptide Y– and nitiric oxide synthase–expressing ivy cells.
Humans and other animals can learn from errors of other individuals. Here, using two paired monkeys monitoring each other's action for their own action selection, the authors identify neurons in the medial frontal cortex (MFC) that have activity correlated with another's errors. This suggests that the MFC could contribute to monitoring others' mistakes.
The identity of the mechanosensitive channel responsible for sound transduction in the ear has remained elusive. Here the authors show, using interferometry, that the gating compliance of the fly's hearing organ is disrupted after deletion of TRPN1, identifying this channel as the sound transducer and/or its gating springs.
The authors show that spontaneous transmission from inhibitory synapses, in contrast with excitatory synapses, is triggered by voltage-dependent calcium channel activity. In addition, they find that spontaneous GABA release involves coincident opening of multiple closely packed calcium channels.