Loss of Endothelial Dysregulates Neural Function In Vivo.

Background: We recently found that loss of endothelial cell disrupts neurovascular and synaptic function. However, whether endothelial is detrimental or protective for neural function under physiological conditions is unknown. Therefore, the goal of this study was to determine the role of endothelial cell in regulating brain function in vivo.

Loss of Depalmitoylation Disrupts Homeostatic Plasticity of AMPARs in a Mouse Model of Infantile Neuronal Ceroid Lipofuscinosis.

Protein palmitoylation is the only reversible post-translational lipid modification. Palmitoylation is held in delicate balance by depalmitoylation to precisely regulate protein turnover. While over 20 palmitoylation enzymes are known, depalmitoylation is conducted by fewer enzymes.

Endothelial Cell Regulates Neurovascular, Neuronal, and Behavioral Function.

Background: Specialized brain endothelial cells and human are independently important for neurovascular function, yet whether expression by endothelial cells contributes to brain function is currently unknown. In the present study, we determined whether the loss of endothelial cell impacts brain vascular and neural function.

Methods: We developed /Cdh5(PAC)-CreERT2 () and /Cdh5(PAC)-CreERT2 (, control) mice and induced endothelial cell knockdown with tamoxifen at ≈4 to 5 weeks of age.

Synaptic Integration of Subquantal Neurotransmission by Colocalized G Protein-Coupled Receptors in Presynaptic Terminals.

In presynaptic terminals, membrane-delimited G-mediated presynaptic inhibition is ubiquitous and acts via Gβγ to inhibit Ca entry, or directly at SNARE complexes to inhibit Ca-dependent synaptotagmin-SNARE complex interactions. At CA1-subicular presynaptic terminals, 5-HT and GABA receptors colocalize. GABA receptors inhibit Ca entry, whereas 5-HT receptors target SNARE complexes.

MK-801 Exposure during Adolescence Elicits Enduring Disruption of Prefrontal E-I Balance and Its Control of Fear Extinction Behavior.

Understanding how disruption of prefrontal cortex (PFC) maturation during adolescence is crucial to reveal which neural processes could contribute to the onset of psychiatric disorders that display frontal cortical deficits. Of particular interest is the gain of GABAergic function in the PFC during adolescence and its susceptibility to the impact of transient blockade of NMDA receptor function. Here we assessed whether exposure to MK-801 during adolescence in male rats triggers a state of excitatory-inhibitory imbalance in the PFC that limits its functional capacity to regulate behavior in adulthood.