Cocaine-related behaviors in mice with deficient gliotransmission.

Rationale: Astrocytes play an integral role in modulating synaptic transmission and plasticity, both key mechanisms underlying addiction. However, while astrocytes are capable of releasing chemical transmitters that can modulate neuronal function, the role of these gliotransmitters in mediating behaviors associated with drugs of abuse has been largely unexplored.

Objectives: The objective of the present study was to utilize mice with astrocytes that lack the ability to release chemical transmitters to evaluate the behavioral consequence of impaired gliotransmission on cocaine-related behaviors.

Cocaine self-administration is not dependent upon mesocortical α1 noradrenergic signaling.

The rewarding properties of psychomotor stimulants are traditionally thought to be independent of norepinephrine. Recent findings, however, suggest that local noradrenergic signaling through α1 receptors in the medial prefrontal cortex and the ventral tegmental area - brain regions critically important in natural and drug rewards - is in a position to influence stimulant reward. Despite this controversy, the contribution of this targeted signaling to stimulant self-administration has not been directly assessed.

CREB-mediated alterations in the amygdala transcriptome: coordinated regulation of immune response genes following cocaine.

The neuronal circuitry underlying stress- and drug-induced reinstatement of cocaine-seeking has been relatively well characterized; however, less is known regarding the long-term molecular changes following cocaine administration that may promote future reinstatement. The transcription factor cAMP response element-binding protein (CREB) is necessary for stress- but not cocaine-induced reinstatement of conditioned reward, suggesting that different molecular mechanisms may underlie these two types of reinstatement. To explore the relationship between this transcription factor and reinstatement, we utilized the place-conditioning paradigm to examine alterations in gene expression in the amygdala, a neural substrate critically involved in stress-induced reinstatement, following the development of cocaine reward and subsequent extinction.

Extracellular fluctuations of dopamine and glutamate in the nucleus accumbens core and shell associated with lever-pressing during cocaine self-administration, extinction, and yoked cocaine administration.

Rationale: Dopamine and glutamate in the nucleus accumbens (NAS) are differentially implicated in cocaine-directed behavior.

Objectives: We sought to compare extracellular fluctuations of dopamine and glutamate in core and shell of NAS associated with operant responding during cocaine self-administration, extinction, and yoked cocaine administration.

Methods: Rats were trained to lever-press for cocaine or saline under FR1 before undergoing microdialysis testing during cocaine self-administration, extinction, or yoked cocaine administration.

Capillary endothelial Na(+), K(+), ATPase transporter homeostasis and a new theory for migraine pathophysiology.

Background: Cerebrospinal fluid sodium concentration ([Na(+)](csf)) increases during migraine, but the cause of the increase is not known.

Objective: Analyze biochemical pathways that influence [Na(+)](csf) to identify mechanisms that are consistent with migraine.

Method: We reviewed sodium physiology and biochemistry publications for links to migraine and pain.

Control of within-binge cocaine-seeking by dopamine and glutamate in the core of nucleus accumbens.

Rationale: Dopamine and glutamate are thought to interact in the ventral striatum and to play important roles there in the cocaine-seeking of cocaine-experienced animals.

Objectives: We sought to determine the relative roles of the two transmitters in the two major zones of the nucleus accumbens (NAS), the core and shell subregions.

Methods: We assessed the effects of dopamine and glutamate receptor blockade in the core and shell on intravenous cocaine self-administration in rats.

Endocrine and gene expression changes following forced swim stress exposure during cocaine abstinence in mice.

Rationale: Stress can reinstate previous cocaine-seeking long after drug is no longer present. However, little is known regarding the effect of chronic drug exposure and subsequent drug abstinence on responsivity to stress.

Objective: To determine the effect of acute (24-h) and prolonged (14-day) drug-free periods in cocaine-experienced mice on behavioral, endocrine, and molecular outputs following stress exposure.

Surfactant removal and silica condensation during the photochemical calcination of thin film silica mesophases.

The evolution of photochemical surfactant removal and silica condensation from organically templated thin film silica nanocomposites with mesoscopic ordering has been probed using a combined application of Fourier transform infrared (FT-IR) spectroscopy and single wavelength ellipsometry. Thin films of silica nanocomposites were prepared by a previously reported evaporation-induced self-assembly process. Specifically, oxidized silicon and gold substrates were withdrawn at 25 mm/min from a subcritical micelle concentration solution containing an ethylene oxide surfactant as a structure-directing agent and tetraethyl orthosilicate as a silica precursor.