Glia in Invertebrate Models: Insights from Caenorhabditis elegans.

Glial cells modulate brain development, function, and health across all bilaterian animals, and studies in the past two decades have made rapid strides to uncover the underlying molecular mechanisms of glial functions. The nervous system of the invertebrate genetic model Caenorhabditis elegans (C. elegans) has small cell numbers with invariant lineages, mapped connectome, easy genetic manipulation, and a short lifespan, and the animal is also optically transparent.

Purinergic signaling mediates neuroglial interactions to modulate sighs.

Sighs prevent the collapse of alveoli in the lungs, initiate arousal under hypoxic conditions, and are an expression of sadness and relief. Sighs are periodically superimposed on normal breaths, known as eupnea. Implicated in the generation of these rhythmic behaviors is the preBötzinger complex (preBötC).

Ampakine CX614 increases respiratory rate in a mouse model of Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra compacta (SNpc). In a mouse model of PD induced by the injection of 6-hydroxydopamine (6-OHDA) into the caudate putamen (CPu) dyspnea events are very common. Neuroanatomical and functional studies show that the number of glutamatergic neurons in the pre-Bötzinger Complex (preBötC) are reduced.

Molecular heterogeneity of glia across sexes.

A comprehensive description of nervous system function, and sex dimorphism within, is incomplete without clear assessment of the diversity of its component cell types, neurons and glia. has an invariant nervous system with the first mapped connectome of a multicellular organism and single-cell atlas of component neurons. Here we present single nuclear RNA-seq evaluation of glia across the entire adult nervous system, including both sexes.

The sigh and related behaviors.

Breathing is a critical, complex, and highly integrated behavior. Normal rhythmic breathing, also referred to as eupnea, is interspersed with different breathing related behaviors. Sighing is one of such behaviors, essential for maintaining effective gas exchange by preventing the gradual collapse of alveoli in the lungs, known as atelectasis.

The psychophysiology of the sigh: II: The sigh from the psychological perspective.

A sigh is a distinct respiratory behavior with specific psychophysiological roles. In two accompanying reviews we will discuss the physiological and psychological functions of the sigh. The present review will focus on the psychological functions of the sigh.

Inspiratory rhythm generation is stabilized by .

Cellular and network properties must be capable of generating rhythmic activity that is both flexible and stable. This is particularly important for breathing, a rhythmic behavior that dynamically adapts to environmental, behavioral, and metabolic changes from the first to the last breath. The pre-Bötzinger complex (preBötC), located within the ventral medulla, is responsible for producing rhythmic inspiration.

The psychophysiology of the sigh: I: The sigh from the physiological perspective.

Breathing is composed of multiple, distinct behaviors that are bidirectionally regulated through autonomic and voluntary mechanisms. One behavioral component is the sigh, which serves distinct physiological and psychological roles. In two accompanying reviews we will discuss these roles.

Impact of obesity and ovariectomy on respiratory function in female mice.

Obesity and the corresponding variations in female sex hormones are associated with severe lung disease. We determined the potential effects of obesity and sex hormones in female mice by investigating changes in lung structure and respiratory function in an obesity model induced by postnatal overnutrition. Obese female mice exhibited pronounced weight gain, abdominal fat accumulation and collagen type I deposition in the airways.

Neuron-astrocyte networking: astrocytes orchestrate and respond to changes in neuronal network activity across brain states and behaviors.

Astrocytes are known to play many important roles in brain function. However, research underscoring the extent to which astrocytes modulate neuronal activity is still underway. Here we review the latest evidence regarding the contribution of astrocytes to neuronal oscillations across the brain, with a specific focus on how astrocytes respond to changes in brain state (e.

A spatially dynamic network underlies the generation of inspiratory behaviors.

The ability of neuronal networks to reconfigure is a key property underlying behavioral flexibility. Networks with recurrent topology are particularly prone to reconfiguration through changes in synaptic and intrinsic properties. Here, we explore spatial reconfiguration in the reticular networks of the medulla that generate breathing.

Targeting TWIST1 through loss of function inhibits tumorigenicity of human glioblastoma.

TWIST1 (TW) is a bHLH transcription factor (TF) and master regulator of the epithelial-to-mesenchymal transition (EMT). In vitro, TW promotes mesenchymal change, invasion, and self-renewal in glioblastoma (GBM) cells. However, the potential therapeutic relevance of TW has not been established through loss-of-function studies in human GBM cell xenograft models.

Advances in cellular and integrative control of oxygen homeostasis within the central nervous system.

Mammals must continuously regulate the levels of O and CO , which is particularly important for the brain. Failure to maintain adequate O /CO homeostasis has been associated with numerous disorders including sleep apnoea, Rett syndrome and sudden infant death syndrome. But, O /CO homeostasis poses major regulatory challenges, even in the healthy brain.

Twist1 mediated regulation of glioma tumorigenicity is dependent on mode of mouse neural progenitor transformation.

Twist1 is a master regulator of epithelial mesenchymal transition and carcinoma metastasis. Twist1 has also been associated with increased malignancy of human glioma. However, the impact of inhibiting Twist1 on tumorigenicity has not been characterized in glioma models in the context of different oncogenic transformation paradigms.