Chronic, Multi-Site Recordings Supported by Two Low-Cost, Stationary Probe Designs Optimized to Capture Either Single Unit or Local Field Potential Activity in Behaving Rats.

Rodent models of cognitive behavior have greatly contributed to our understanding of human neuropsychiatric disorders. However, to elucidate the neurobiological underpinnings of such disorders or impairments, animal models are more useful when paired with methods for measuring brain function in awake, behaving animals. Standard tools used for systems-neuroscience level investigations are not optimized for large-scale and high-throughput behavioral battery testing due to various factors including cost, time, poor longevity, and selective targeting limited to measuring only a few brain regions at a time.

Electrophysiological Correlates of Rodent Default-Mode Network Suppression Revealed by Large-Scale Local Field Potential Recordings.

Unlabelled: The default-mode network (DMN) in humans consists of a set of brain regions that, as measured with functional magnetic resonance imaging (fMRI), show both intrinsic correlations with each other and suppression during externally oriented tasks. Resting-state fMRI studies have previously identified similar patterns of intrinsic correlations in overlapping brain regions in rodents (A29C/posterior cingulate cortex, parietal cortex, and medial temporal lobe structures). However, due to challenges with performing rodent behavior in an MRI machine, it is still unclear whether activity in rodent DMN regions are suppressed during externally oriented visual tasks.

SimBSI: An open-source Simulink library for developing closed-loop brain signal interfaces in animals and humans.

Objective: A promising application of BCI technology is in the development of personalized therapies that can target neural circuits linked to mental or physical disabilities. Typical BCIs, however, offer limited value due to simplistic designs and poor understanding of the conditions being treated. Building BCIs on more solid grounds may require the characterization of the brain dynamics supporting cognition and behavior at multiple scales, from single-cell and local field potential (LFP) recordings in animals to non-invasive electroencephalography (EEG) in humans.

Acute effects of partial-body vibration in sitting position.

Aim: To investigate the acute effects of sinusoidal and stochastic resonance partial-body vibration in sitting position, including muscle activity, heart rate variability, balance and flexibility.

Methods: Fifty healthy participants were assigned randomly to two training conditions: A sinusoidal partial-body vibration (SIN, 8 Hz) or a stochastic resonance partial-body vibration (STOCH, 8 ± 2 Hz). For baseline assessment participants sat on the vibration platform without vibration.

Neuronal overexpression of Ube3a isoform 2 causes behavioral impairments and neuroanatomical pathology relevant to 15q11.2-q13.3 duplication syndrome.

Maternally derived copy number gains of human chromosome 15q11.2-q13.3 (Dup15q syndrome or Dup15q) cause intellectual disability, epilepsy, developmental delay, hypotonia, speech impairments, and minor dysmorphic features.

Evaluating aged mice in three touchscreen tests that differ in visual demands: Impaired cognitive function and impaired visual abilities.

Normal aging is often accompanied by reductions in cognitive abilities as well as impairments in visual acuity in men and mice. In preclinical models of human cognition this concomitance can make it difficult to assess the relative contributions of declined vision and cognitive ability on behavioral measures of cognition. To assess the influence of age on cognition and the impact of visual decline on the performance of touchscreen-based behavioral paradigms in mice, aged (11, 12, 16, 17, 19 and 21 months old) male C57BL/6J mice were compared to young (3 or 4 months old) male C57BL/6J mice using three tests of cognition as well as an assessment of visual acuity.

Touchscreen learning deficits and normal social approach behavior in the Shank3B model of Phelan-McDermid Syndrome and autism.

SHANK3 is a synaptic scaffolding protein localized in the postsynaptic density and has a crucial role in synaptogenesis and neural physiology. Deletions and point mutations in SHANK3 cause Phelan-McDermid Syndrome (PMS), and have also been implicated in autism spectrum disorder (ASD) and intellectual disabilities, leading to the hypothesis that reduced SHANK3 expression impairs basic brain functions that are important for social communication and cognition. Several mouse models of Shank3 deletions have been generated, varying in the specific domain deleted.