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GPR88 inhibits G-protein signaling of nearby GPCRs, and dampens b-arrestin recruitment by all GPCRs tested, likely by sequestration in intracellular compartments.

The α₁-adrenergic receptor augments the activity of the L-type Ca²⁺ channel Ca_V1.2 through PKC and the tyrosine kinases Pyk2 and Src and thereby synaptic plasticity.

Local presynaptic protein synthesis occurring at established nerve terminals in the mammalian brain provides a mechanism for rapidly controlling or restoring presynaptic proteins that affect neurotransmitter release and presynaptic efficiency.

Spatial suppression during motion perception reflects reduced neural response magnitudes in visual areas but is not primarily driven by neural inhibition.

A novel high-throughput, whole organism chemical screening platform was used to identify existing drugs that increase pancreatic beta-cell mass in zebrafish, implicating unique roles for the NF-κB and serotonergic signaling pathways in regulating pancreatic biology.

Repeatedly activating negative memory-bearing cells produces cellular and behavioral abnormalities.

Endolysosmal trafficking defects, expansion of lysosomes, elevation of ceramides, and disruption of mitochondria are root causes of INAD/PARK14.

Modulation of the aging process through cell signaling represents a recent and exciting area of study with the potential for development of therapeutics to extend human health.

There is substantial individual variation in behavioral and neural responses to acute ketamine administration in healthy controls, which emphasises the need for personalized approaches when harnessing ketamine as a treatment for depression.

The microenvironment of brain tumors can be modulated by in vivo conditions that change the brain levels of BDNF and IL-15, with effects on innate immune cell activation.