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Activation of putative aldosterone-sensitive neurons in the hindbrain drives mice to drink sodium solutions, and this appetite is distinct from thirst and hunger. These neurons are critical for animals to fully develop a sodium appetite following sodium depletion, although there is likely redundant circuitry.

The authors show that oxytocin-receptor-expressing neurons in the parabrachial nucleus are key regulators of fluid homeostasis that suppress fluid intake when activated, but do not decrease food intake after fasting or salt intake after salt depletion.

The genetic identity of taste-responsive neurons has not been determined. The authors describe neurons in the gustatory region of the parabrachial nucleus that express the transcription factor Satb2, project to taste-associated regions, and modulate taste preferences.

Advances in wireless technologies have enabled internalisation of light sources, but organ specific illumination is challenging. Here, the authors present a durable, multimodal, wireless system enabling optogenetic stimulation of peripheral neurons within organs.

Hypothalamic neurons that express agouti-related protein have been thought to regulate appetite by counteracting the melanocortin signaling pathway. Evidence now indicates that these neurons can also modulate dopamine signaling.

Single-cell recordings show that CGRP-expressing neurons in the parabrachial nucleus in mice respond to both noxious stimuli and signals of feeding satiety.

Nociceptin is an opioid peptide regulating important brain functions, including motivation and 2stress responses. Here, the authors develop and validate a genetically encoded sensor as a tool for high-resolution detection of endogenous nociceptin in living animals.

The glycoprotein lipocalin 2 is released from the bones of mice in a nutrient-dependent manner and binds to receptors in the brain to suppress appetite. This is the first example of bone-derived signals mediating hunger. See Article p.385

Starving animals are less likely to defend their home territory and more likely to engage in risky foraging behaviors. This work describes a circuit involving hypothalamic AgRP neurons projecting to neurons in the medial nucleus of the amygdala and their projections to the bed nucleus of the stria terminalis, which, when activated, mimics these behaviors in mice that are well fed.

Recent studies reveal several groups of neurons that become activated upon anticipation or consumption of meals. These neurons constitute key components of the complex feedback system that prevents continuous feeding by mice.

GPR88 is an orphan G protein–coupled receptor expressed in striatal medium spiny neurons (MSNs). The authors show that deletion of Gpr88 in mice leads to hyperactivity, poor motor coordination and impaired cue-based learning. MSNs lacking GPR88 show increased excitation and reduced inhibition in vitro, and enhanced firing rates in vivo.

Dissection of the neuronal circuit driving feeding behaviour in mice shows that suppression of the parabrachial nucleus protects against aphagia and promotes weight gain, and also that the parabrachial nucleus is an integration hub that bidirectionally modulates feeding and body weight.

Two populations of neurons with distinct anatomy and receptor expression that convey information from the spinal cord to the brain have different functional properties with respect to touch and pain.

Distinct clusters of inhibitory neurons in the mouse amygdala perform opposing roles in fear extinction.

Most cancer patients experience loss of appetite and feelings of illness, which contribute to cancer-related deaths and morbidity. The authors demonstrate that, in mice, activation of a subset of neurons in the parabrachial nucleus mediate cancer-induced anorexia and associated sickness behaviors.

Osteoblast-derived LCN2 activates the melanocortin 4 receptor in neurons of the paraventricular nucleus of the hypothalamus to suppress appetite, regulates insulin secretion and increases insulin sensitivity and glucose tolerance.

Inhibiting projections from the paraventricular nucleus of the thalamus to a specific division of the amygdala prevents fear conditioning in mice, indicating an important role for the thalamus–amygdala circuit in establishing and maintaining fear responses.

This Resource paper describes a set of five new reporter mice, derived from Rosa26, driving Cre-dependent strong and ubiquitous expression of fluorescent proteins. In particular, the new mice show clear and specific expression patterns in the adult brain. The mice are available through Jackson Laboratories, and growing expression datasets can be accessed at http://transgenicmouse.alleninstitute.org/.

All retinal neurons are generated from multipotent progenitor cells through a step-wise process that increasingly restricts lineage choices. Swaroop and colleagues discuss our current understanding of the transcription factors and gene-regulatory networks involved in photoreceptor subtype specification and photoreceptor development.

Recent methodological progress has greatly facilitated the determination of the connectivity and functional characterization of complex neural circuits. In this Review, Tovote, Fadok and Lüthi examine studies that have adopted circuit-based approaches to gain insight into how the brain governs fear and anxiety.