Purinergic signaling controls mammalian sperm transport.

Bone cells exposed to physiological forces release ATP through repairable membrane injury, generating an intercellular signal that conveys the destructive potential of forces and the adaptive capacity of endangered cells.

Autocrine activation of macrophages is modulated by Connexin-43-mediated ATP release in response to TLR-4 and -2 agonists in a P2Y1-dependent manner, ultimately determining sepsis survival.

Keratinocytes are critical for normal innocuous and noxious touch through their mechanically evoked ATP release and subsequent signaling to P2X4 channels on sensory neurons.

CO₂/H⁺-dependent purinergic signaling by astrocytes provides specialized control of vascular tone in a brainstem respiratory center in a manner that contributes to respiratory behavior.

Understanding how loss of CO₂/H⁺ vascular reactivity affects respiratory control may facilitate development of treatments for breathing problems in this population.

Supporting cells in the cochlea change their shape in response to purinergic receptor activation, which influences hair cell excitability by altering potassium redistribution in the extracellular space.

Apoptotic cells release molecules to recruit macrophages, but do not cause inflammation because they also secrete AMP that functions as a ‘calm down’ signal.

A genetic strategy reveals that the perisynaptic glial response to neural activity in one population of these glia regulates postsynaptic function and therefore muscle fatigue.

Novel brainstem organotypic cultures that generate rhythmic respiratory motor activity reveal the neural networks that control breathing and a new pathway in the hypercapnic response.