Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Opioids are commonly thought of as compounds that alleviate pain. A new study finds that elevated levels of the opioid dynorphin can unexpectedly activate bradykinin receptors, contributing to the maintenance of neuropathic pain.
Exogenous cannabinoid receptor agonists impair hippocampus-dependent learning and decrease the power of hippocampal electroencephalographic activity. A new paper shows that cannabinoids desynchronize neuronal assemblies without affecting average firing rates, and that this effect correlates with memory deficits in individuals.
Microglia, the brain's intrinsic immune cells, rapidly sense brain injury and help clear cellular debris. Haynes et al. now show that P2Y12 receptors are critical for activating microglia and directing them to the site of injury.
Sensory systems are thought to use an internal copy of motor commands to determine which sensations are caused by the self versus the world. A new paper proves that an identified pathway performs this function for eye movements.
Multiple local motions must be combined to determine the direction of object motion, which is harder than it seems. A new paper proposes an elegant and simple solution to this problem, eminently realizable in feed-forward circuits.
An inhibitor of glycolysis is shown to have antiepileptic effects in the rat kindling model, possibly through NADH-dependent regulation of gene expression. This may explain how the 'ketogenic diet' treatment works.
How do neurons combine separate pieces of information that are only partially reliable? Surprisingly, their noise properties may simplify the underlying computations while allowing them to maintain optimal performance.
Glutamate transporters have long been thought to help terminate the synaptic response through neurotransmitter binding and reuptake, but a new report in this issue identifies a role for their anionic current in information transmission in the retina.
Most early-onset familial Alzheimer disease is caused by presenilin mutations. A recent paper reports that the presenilins act as calcium leak channels in the endoplasmic reticulum and thus may regulate intracellular calcium homeostasis.
Transmission of sensory information through the rhinal cortices is essential for hippocampus-dependent learning. In this issue Paz et al. show that amygdala activity elicited by an unexpected reward facilitates communication from perirhinal to entorhinal cortex, providing a physiological mechanism for emotional modulation of memory.
Axon guidance requires local protein synthesis at the growth cone. Two new studies show that guidance cues induce asymmetric targeting and translation of β-actin (Actb) mRNA. Such asymmetry may be the mechanism that underlies growth cone turning.
Synapse formation requires adhesive interactions between pre- and postsynaptic membranes. A new study reports that netrin-G2 ligand (NGL-2) interactions with netrin-G2 induces excitatory synapses, expanding the range of known synapse-inducing signals.
A new paper demonstrates that polyglutamine pathogenesis in spinocerebellar ataxia need not be cell autonomous. Mutant ataxin-7 expression restricted to Bergmann glia was sufficient to cause Purkinje cell degeneration and neuronal pathology.
Categorization of objects has been considered a function of the temporal 'what' pathway, but a new paper shows that neurons in the lateral intraparietal area of the 'where' pathway show learned responses based on category boundaries.