Reviews & Analysis

This review discusses what we have learned about the neural regulation of feeding from genetic studies, both from studies in mutant mice and more recent genome-wide association studies in humans.

Circuits have been described in the hypothalamus and brainstem involved in regulating feeding and energy balance. In this review, the authors discuss the many peripheral signals that influence these central circuits to affect feeding behavior and energy balance.

Energy balance is maintained by neuronal populations throughout the central nervous system, but is primarily localized in the mediobasal hypothalamus. In this review, the authors discuss recent work examining plastic changes in hypothalamic circuits in response changes in nutrient availability and long-term energy status.

Many comparisons between obesity and drug addiction have been made in recent years. In this review, the authors critically compare the behavioral responses to food and drugs of abuse, as well as the neural circuitry involved in each, pointing out key differences between the two.

NG2⁺ glia, the progenitors of myelinating oligodendrocytes, receive synaptic input, but why? A study now finds that sensory input regulates the proliferation and location of NG2⁺ glia in the mouse somatosensory cortex barrel field.

A report in this issue suggests that inhibiting histone deacetylase 2 (HDAC2) could be therapeutic in schizophrenia. Targeting chromatin remodeling in adults to treat a chronic brain disorder is not, however, likely to be easy.

Sensory deprivation can result in impaired perception in most sensory modalities owing to experience-dependent changes in neural processing. Odor perception, however, appears to be relatively immune to periods of deprivation. Work in humans now suggests that this stability may be due to robust, reversible, compensatory plasticity in cortex.

Animals often must vie with others for scarce resources, such as food, water and mates. Deciding when to engage and when to avoid such contests might critically depend on the activity of anterior cingulate cortex neurons.

Phasic bursting of dopaminergic neurons influences many behaviors. A study now finds that ATP-sensitive potassium channels mediate bursting in dopaminergic neurons of the medial substantia nigra and affect novelty-induced exploration.

This review compares and contrasts decision-making processes in adults versus adolescents, to highlight how adolescent decision-making is particularly susceptible to modulation by emotional and social factors (such as peer pressure).

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.

A study reveals that aged mice have decreased hippocampal expression of the DNA methyltransferase Dnmt3a2; re-expression in aged mice reverses memory deficits, and knockdown in young mice impairs memory formation.

Natural or artificially induced electrical activity changes can alter ion balance so as to briefly influence firing. An optogenetics study delineates one mechanism: Cl⁻ shifts causing seconds-long excitability changes after silencing.

Mice lacking NMDA receptors in the dentate gyrus and CA1 subfields of the hippocampus form spatial memories just as well as wild-type mice, but they disregard them when confounded by ambiguous local cues. Hippocampal NMDA receptors may influence spatial memory more subtly than previously thought.

Although the nervous and immune systems have been classically considered to modulate physiologically distinct functions, recent evidence points to coordinated activities during neurogenic inflammation. In this perspective, the authors examine the interactions between the peripheral nervous system and the immune response during health and disease.

Multiple sclerosis is a debilitating inflammatory demyelinating disease of the CNS. In this perspective, the author examines the strengths and weaknesses of the numerous animal models that are currently being used to analyze the pathogenesis of this disease with an eye toward the precise pathological aspect that each model recapitulates.

Neuropathic pain often results from trauma or insult to peripheral nerves. In this Perspective, the authors examine recent evidence that implicates the microglia-expressed purinergic receptor P2X4 in the induction of neuropathic pain and suggest that this pathway marks a spinal mechanism distinct from those that mediate acute or inflammatory pain.

Despite being protected by the blood-brain barrier, the CNS must constantly be monitored for insult or pathogen invasion. In this review, the authors illustrate the molecular and cellular players that preside over this surveillance of the brain and spinal cord.

Acute exposure to a variety of pathogens or inflammatory insults leads to a well-characterized set of responses in the CNS, aimed at promoting the clearance of the infecting agent. In this review, the authors examine the various symptoms of this 'sickness syndrome' and the actions of prostaglandins in linking inflammation with these CNS responses.

Immune cells participating in CNS inflammation are now known to mediate both beneficial and detrimental effects. In this review, the authors examine the recently discovered bidirectional relationship between immune cells and neural stem cells and how these interactions may influence brain repair and provide new therapeutic targets.