Volume 13 Issue 5, May 2010

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.

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.

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.

Luna et al. examined the strength of interneuron-to–pyramidal cell connections across the rat anterior piriform cortex. Surprisingly, they found a gradient of increasing inhibition across the rostro-caudal axis of the cortex.

A traditional way of inducing reconsolidation of associative fear memory is to present the conditioning stimulus (CS), which reactivates the memory trace. The current study shows that an unconditioned stimulus (US)—often stronger in perceptual intensity than CS—on its own can trigger memory reconsolidation that is specific for the sensory properties of the US.

Using transcranial magnetic stimulation, the authors report that the left lateral prefrontal cortex is critical for choosing between immediate and delayed rewards. As the LPFC has previously been implicated in self-control, these results suggest that self-control may be important for intertemporal choice.

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.

Silver et al. demonstrate that Magoh, a component of the RNA-binding exon junction complex (EJC), controls mouse cerebral cortical size by regulating neural stem cell division. A critical function of Magoh is controlling levels of the microcephaly-associated protein Lis1. This work shows a novel role for the EJC in neurogenesis.

The authors show that myelin, signaling through the receptor p75NTR and its downstream effectors, prevents aberrant sprouting of basal forebrain cholinergic axons in the adult mouse brain.

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 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.

Although most inhibitory synapses are homeostatically scaled down after chronic inactivity, Kim et al. report that chronic inactivity specifically strengthens a subset of hippocampal GABAergic synapses that express cannabinoid receptors. This local tuning effect is mediated by enhanced degradation of anandamide, which reduces basal cannabinoid receptor activation, augmenting GABA release probability.

Dendritic distortion is problematic for neurons using temporal coding strategies, such as medial superior olivary neurons, which encode microsecond differences in binaural auditory input. Mathews et al. find that both the specific activation properties and spatial distribution of K_v1 channels compensate for passive cable filtering, helping to preserve binaural synaptic timing.

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.

Odors, via the olfactory AWC neurons, trigger food searching in C. elegans. This study shows that the peptide NLP-1, co-released with glutamate from AWC neurons, acts to limit searching locomotion through a feedback loop that involves activation of the receptor NPR-11 on AIA interneurons and release of another peptide, INS-1, from the AIA neurons.

5-HT₂ and corticotrophin releasing factor (CRF) receptors both regulate stress responses and anxiety behavior; however, potential cross-talk between the two pathways is poorly understood. Magalhaes et al. find that CRF receptor activation causes cell-surface recruitment of constitutively internalized 5-HT₂ receptor and that this mechanism is relevant to anxiety-related behaviors.

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.

Overeating can be compulsive, resembling drug addiction. This paper reports that in rats, developing diet-induced obesity correlates with decreasing sensitivity of the brain's reward system. Knockdown of the striatal dopamine receptor D2 led to rapid loss of reward function and to compulsive overeating undeterred by conditioned aversive foot shocks.

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.