We present a special focus on social neuroscience, bringing together several strands of research to highlight recent progress in the field.
How does the brain evaluate whether the benefits of a decision outweigh the costs? A study now reveals that neurons in the anterior cingulate cortex encode costs and benefits, and altering brain activity here biases choices away from negative outcomes. These results link anterior cingulate cortex with the regulation of emotional states.
In the developing cortex, spike timing–dependent long-term depression requires cannabinoid-induced glutamate release from astrocytes. Astrocytes may be integral to the coincidence detection that guides plasticity and map formation.
Tanycytes in the hypothalamic median eminence have now been found to form a metabolically sensitive neurogenic niche in the brain. In adult mice, tanycytes give rise to hypothalamic regulatory neurons in response to a high-fat diet.
Odorants are now shown to elevate mitochondrial Ca2+ in sensory neurons; moreover, blocking this Ca2+ sequestration impairs dynamic range. Acute stimulation rapidly recruits mitochondria from the soma to the dendritic knob.
This commentary reviews the neural processes underpinning the learning of social norms, as well the enforcement of these norms through second-party and third-party punishment. The authors suggest how these structures may have formed during our evolutionary history.
This review discusses how social factors modulate risks for mental disorders, and the neural systems that implement this modulation.
Although the relationship between social factors and physical health outcomes is well-recognized, the modulatory role of neural processing in this link is less well understood. This perspective describes the way in which neurophysiological processes respond to social connection and disconnection to influence health outcomes.
In this perspective, the authors critically evaluate the research on the neural systems supporting empathy.
How does the neuroendocrine system modulate social behavior? The authors review animal as well as human work that aims to answer this question, and suggest ways to advance further research.
This review describes how both negative and positive social factors, ranging from stress to meditation, affect brain structure and functioning.
This paper reports that microRNA-9 controls axonal extension and branching of cortical neurons via its actions on the MAP1B protein.
The authors describe a neurogenic niche in the postnatal hypothalamus of mice wherein β2-tanycytes generate neurons in response to high-fat diet. Blocking this neurogenesis leads to attenuated weight gain and increased activity levels.
In this study, the authors show that NgR1 and NgR3 can act as functional receptors for chondroitin sulfate proteoglycans (CSPGs), mediating inhibition of axonal growth and regeneration. This suggests a convergent mechanism for CSPG- and myelin-associated inhibitor activities after axonal injury in the CNS.
In this paper, the authors show that, in the non-diseased state, the huntingtin protein promotes homotypic interactions between neuroepithelial cells, a process that is critical for proper neurulation.
The engulfment receptor Draper is known to promote glial clearance of degenerating neurons in Drosophila, and this action of Draper is mediated by Src kinase. This study now shows that one of three Draper isoforms, namely Draper-II, negatively regulates glial clearance and acts in opposition to pro-clearance Draper-I.
Dendrites from the same neuron avoid each other through a mechanism involving cell surface proteins that trigger mutual repulsion. Here the authors show that the soluble axon guidance cue Netrin (UNC-6) drives sister dendrite self-avoidance in the PVD nociceptive neuron in C. elegans.
The authors show that the SNARE protein VAMP4 acts to maintain calcium-dependent asynchronous synaptic vesicle release. These findings suggest that VAMP4 is functionally distinct from synaptobrevin2, which primarily drives fast, synchronous release.
This study shows that spike timing–dependent depression between excitatory neurons requires endocannabinoid-mediated calcium signaling and glutamate release from nearby astrocytes, revealing that they are key elements in cortical plasticity.
Cytosolic Ca2+ is known to control the gain and sensitivity of signaling in the olfactory sensory neurons (OSNs) through several molecular mechanisms. Here the authors find that mitochondrial Ca2+ mobilization is another critical component of OSN neuronal function, ensuring a broad dynamic response range and maintaining the sensitivity of the spike generation machinery.
This study examines the phase response curves of gamma oscillations induced by carbachol or optogenetic stimulation in the hippocampal CA3 network. The authors report that distinct inputs differentially entrain the gamma oscillation in accordance with the relative drive to excitatory and inhibitory neurons in the circuit.
The authors conduct simultaneous recording and optogenetic silencing of PV or SOM interneurons in the CA1 region of the hippocampus in head-fixed mice actively moving a treadmill belt. They report that these interneurons have distinct roles in controlling the rate, burst and timing of hippocampal pyramidal cells.
In this paper, the authors present evidence for spatially overlapping populations of neurons representing positive and negative subjective value in the primate pregenual anterior cingulate cortex (pACC) during an approach-avoidance task. However, in one subzone of the pACC, negative coding predominated, and microstimulation in this subzone increased negative decision-making, a bias that was blocked by anti-anxiety drug treatment.
Using a combination of fMRI in humans and computational modeling, the authors show that different striatal nuclei encode different kinds of decision-making information. The anterior caudate nucleus encodes the value of individual steps in a decision tree, whereas the putamen encodes values learnt during extensive training.
This study describes the generation of knock-in mouse lines that express optogenetic activators or silencers in a CRE recombinase–dependent manner, and demonstrates the reliability and utility of these tools with in vivo and ex vivo light-induced activation and silencing of neuronal activity.
