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Rats given extended access to high-fat high-sugar food show behavioral and physiological changes that are similar to those caused by drugs of abuse. However, parallels between drug and food “addiction” should be drawn with caution.
The molecular mechanisms responsible for anxiety remain largely unresolved. A study in this issue finds that an interaction between receptors for a hormone and a neurotransmitter regulates anxiety.
Axon degeneration in the adult brain is usually pathological, but a new study finds that mis-sprouting cholinergic axons in the healthy mouse brain are eliminated by a degenerative process that is triggered by myelin via p75NTR.
A study identifies a previously unknown neuropeptide-based feedback signaling pathway in C. elegans that modulates the response of primary sensory neurons to chemical stimuli and odorant-evoked behaviors.
A new study finds causal evidence that the lateral prefrontal cortex, implicated in executive function, is critical for making decisions in which forgoing a small immediate reward can lead to a better future outcome. These results suggest that this area provides a neural signal that biases behavior in favor of delaying gratification.
Jablonska et al. find that adult mouse neural progenitors can markedly alter their fate, from olfactory bulb interneurons to oligodendroglia, in response to demyelination. The fate change is triggered by chordin, which is upregulated in the subventricular zone in this pathological condition.
The authors induce selective astrocytosis in the mouse hippocampus and examine the consequences on synaptic transmission in CA1 pyramidal neurons. They report a specific reduction in inhibitory synaptic currents mediated by downregulation of glutamine synthetase that results in hyperexcitability.
TRPV1 is a member of the family of temperature-activated transient receptor potential ion channels. This study identifies mutations in the outer pore region of TRPV1 that impair temperature activation by ablating long channel openings.
In all animals, hypoxia triggers a defensive response that is orchestrated by the conserved transcription factor HIF-1. The authors find that HIF-1 induces new serotonin synthesis in certain sensory neurons in C. elegans. This serotonin then activates a previously unknown circuitry that enhances the worms' salt sensation.
In addition to the neurotropic role of brain-derived neurotrophic factor (BNDF) in cortical circuit plasticity, there is a good positive correlation between the cortical expression level of BDNF and developmental changes in visual acuity. Here, the authors find that directly impairing BDNF signaling using transgenic methods causes visual impairment by affecting the systems level control on contrast gain.
A hallmark of Huntington's disease is the accumulation of polyglutamine-expanded huntingtin (htt) protein in striatal neurons. The removal of cytosolic mutant htt is known to be mediated by the macroautophagy-lysosomal system. Here the authors specifically identify the defective step of autophagy in Huntington's models, in which autophagosomes fail to recognize mutant htt as a cargo destined for degradation.
An et al. visualized complexin, a cytosolic protein implicated in synaptic vesicle fusion, during real-time single exocytic events in live cells. They find that complexin is recruited to a SNARE complex prior to fusion and directly regulates the dynamics of fusion pore dilation.
The authors report that inactivating the protein kinase isoform PKMζ in the amygdala impairs fear conditioning in rats and that PKMζ maintains long-term memory by trafficking GluR2-containing AMPA receptors.
