Motion-compensated diffusion encoding in multi-shot human brain acquisitions: Insights using high-performance gradients.

Purpose: To evaluate the utility of up to second-order motion-compensated diffusion encoding in multi-shot human brain acquisitions.

Methods: Experiments were performed with high-performance gradients using three forms of diffusion encoding motion-compensated through different orders: conventional zeroth-order-compensated pulsed gradients (PG), first-order-compensated gradients (MC1), and second-order-compensated gradients (MC2). Single-shot acquisitions were conducted to correlate the order of motion compensation with resultant phase variability.

Evaluating diffusion dispersion across an extended range of b-values and frequencies: Exploiting gap-filled OGSE shapes, strong gradients, and spiral readouts.

Purpose: To address the long echo times and relatively weak diffusion sensitization that typically limit oscillating gradient spin-echo (OGSE) experiments, an OGSE implementation combining spiral readouts, gap-filled oscillating gradient shapes providing stronger diffusion encoding, and a high-performance gradient system is developed here and utilized to investigate the tradeoff between b-value and maximum OGSE frequency in measurements of diffusion dispersion (i.e., the frequency dependence of diffusivity) in the in vivo human brain.

Improved gradient waveforms for oscillating gradient spin-echo (OGSE) diffusion tensor imaging.

The dependence of the diffusion tensor on frequency is of great interest in studies of tissue microstructure because it reveals restrictions to the Brownian motion of water molecules caused by cell membranes. Oscillating gradient spin-echo (OGSE) sequences can sample this dependence with gradient shapes for which the power spectrum of the zeroth moment is focused at a target frequency. In order to maintain the total spectral power (ie the b-value), oscillating gradient amplitudes must grow with the frequency squared.

TPA-023 attenuates subchronic phencyclidine-induced declarative and reversal learning deficits via GABA receptor agonist mechanism: possible therapeutic target for cognitive deficit in schizophrenia.

GABAergic drugs are of interest for the treatment of anxiety, depression, bipolar disorder, pain, cognitive impairment associated with schizophrenia (CIAS), and other neuropsychiatric disorders. Some evidence suggests that TPA-023, (7-(1,1-dimethylethyl)-6-(2-ethyl-2H-1,2,4-triazol-3-ylmethoxy)-3-(2-fluorophenyl)-1,2,4-triazolo[4,3-b] pyridazine), a GABA α2,3 subtype-selective GABA partial agonist and α antagonist, and the neurosteroid, pregnenolone sulfate, a GABA antagonist, may improve CIAS in pilot clinical trials. The goal of this study was to investigate the effect of TPA-023 in mice after acute or subchronic (sc) treatment with the N-methyl-D-aspartate receptor (NMDAR) antagonist, phencyclidine (PCP), on novel object recognition (NOR), reversal learning (RL), and locomotor activity (LMA) in rodents.

RP5063, an atypical antipsychotic drug with a unique pharmacologic profile, improves declarative memory and psychosis in mouse models of schizophrenia.

Various types of atypical antipsychotic drugs (AAPDs) modestly improve the cognitive impairment associated with schizophrenia (CIAS). RP5063 is an AAPD with a diverse and unique pharmacology, including partial agonism at dopamine (DA) D, D, D, serotonin (5-HT), and 5-HT receptors (Rs), full agonism at αβ nicotinic acetylcholine (ACh)R (nAChR), and antagonism at 5-HT, 5-HT, and 5-HTRs. Most atypical APDs are 5-HT inverse agonists.

Skin conductance at baseline and postheel lance reflects sympathetic activation in neonatal opiate withdrawal.

Aim: Skin conductance (SC) provides an objective measure of autonomic system regulation through sympathetic-mediated filling of sweat glands. This study aimed to test the utility of SC to detect sympathetic activation in neonatal abstinence syndrome (NAS).

Methods: Fourteen term (mean, SE: 38.

Serotonin (5-HT)1A receptor agonism and 5-HT7 receptor antagonism ameliorate the subchronic phencyclidine-induced deficit in executive functioning in mice.

Rationale: Reversal learning (RL), a type of executive function, dependent on prefrontal cortical function, is impaired in rodents by subchronic (sc) treatment with the N-methyl-D-aspartate receptor antagonist, phencyclidine (PCP), a widely studied model of cognitive impairment in schizophrenia (CIS).

Objective: The principal objective of this study was to determine the ability of serotonin (5-HT)1A partial agonism and 5-HT7 receptor antagonism to improve RL in scPCP-treated mice.

Methods: Male C57BL/6J mice were trained on an operant RL (ORL) task, then received PCP, 10 mg/kg, or saline, bid, for 7 days, followed by a 7-day washout period.