The function of groups of neurons changes from moment to moment.

Modern techniques that enable identification and targeted manipulation of neuron groups are frequently used to bolster theories that attribute specific behavioral functions to specific neuron types. These same techniques can also be used, however, to highlight limitations of such attribution, and to develop the argument that the question "what is the function of these neurons?" is ill-posed in the absence of temporal and network constraints. Here we do this, first reviewing evidence that neural responses are dynamic at multiple time scales, making the point that such changes in firing rates imply changes in what the neuron is doing.

Optogenetic perturbation of projections from thalamic nucleus reuniens to hippocampus disrupts spatial working memory retrieval more than encoding.

Background: Working memory deficits are key cognitive symptoms of schizophrenia. Elevated delta oscillations, which are uniquely associated with the presence of the illness, may be the proximal cause of these deficits. Spatial working memory (SWM) is impaired by elevated delta oscillations projecting from thalamic nucleus reuniens (RE) to the hippocampus (HPC); these findings imply a role of the RE-HPC circuit in working memory deficits in schizophrenia, but questions remain as to whether the affected process is the encoding of working memory, recall, or both.

Development of Cross-Orientation Suppression and Size Tuning and the Role of Experience.

Many sensory neural circuits exhibit response normalization, which occurs when the response of a neuron to a combination of multiple stimuli is less than the sum of the responses to the individual stimuli presented alone. In the visual cortex, normalization takes the forms of cross-orientation suppression and surround suppression. At the onset of visual experience, visual circuits are partially developed and exhibit some mature features such as orientation selectivity, but it is unknown whether cross-orientation suppression is present at the onset of visual experience or requires visual experience for its emergence.

A low cost, simplified, and scaleable pneumotachograph and face mask for neonatal mouse respiratory measurements.

Introduction: Neonatal respiratory disorders are a leading cause of perinatal mortality due to complications resulting from premature births and prenatal exposure to drugs of abuse, but optimal treatments for these symptoms are still unclear due to a variety of confounds and risk factors. Mouse models present an opportunity to study the underlying mechanisms and efficacy of potential treatments of these conditions with controlled variables. However, measuring respiration in newborn mice is difficult and commercial components are expensive and often require modification, creating a barrier and limiting our understanding of the short and long-term effects of birth complications on respiratory function.

Potential synergistic action of 19 schizophrenia risk genes in the thalamus.

A goal of current schizophrenia (SZ) research is to understand how multiple risk genes work together with environmental factors to produce the disease. In schizophrenia, there is elevated delta frequency EEG power in the awake state, an elevation that can be mimicked in rodents by N-methyl-d-aspartate receptor (NMDAR) antagonist action in the thalamus. This thalamic delta can be blocked by dopamine D2 receptor antagonists, agents known to be therapeutic in SZ.