Dextromethorphan moderates reward deficiency associated with central serotonin transporter availability in 3,4-methylenedioxy-methamphetamine-treated animals.

Background: The neurotoxicity of 3,4-methylenedioxy-methamphetamine (MDMA) to the serotonergic system is well-documented. Dextromethorphan (DM), an antitussive drug, decreased morphine- or methamphetamine (MA)-induced reward in rats and may prevent MDMA-induced serotonergic deficiency in primates, as indicated by increased serotonin transporter (SERT) availability. We aimed to investigate the effects of DM on reward, behavioral sensitization, and neurotoxicity associated with loss of SERT induced by chronic MDMA administration in rats.

Amitriptyline Accelerates SERT Binding Recovery in a Rat 3,4-Methylenedioxymethamphetamine (MDMA) Model: In Vivo 4-[F]-ADAM PET Imaging.

Numerous studies have confirmed that 3,4-Methylenedioxymethamphetamine (MDMA) produces long-lasting changes to the density of the serotonin reuptake transporter (SERT). Amitriptyline (AMI) has been shown to exert neuroprotective properties in neuropathologic injury. Here, we used a SERT-specific radionuclide, 4-[F]-ADAM, to assess the longitudinal alterations in SERT binding and evaluate the synergistic neuroprotective effect of AMI in a rat MDMA model.

Preliminary Results on the Long-Term Effects of Dextromethorphan on MDMA-Mediated Serotonergic Deficiency and Volumetric Changes in Primates Based on 4-[F]-ADAM PET/MRI.

Alterations to the serotonergic system due to 3,4-methylenedioxymethamphetamine (MDMA) (ecstasy) consumption have been extensively documented. However, knowledge of the reversibility of these neurotoxic effects based on evaluations of serotonin transport (SERT) availability remains limited. This study aimed to evaluate the long-term neurotoxicity of MDMA after 66 months abstinence and explored whether Dextromethorphan, a non-competitive -methyl--aspartate (NMDA) receptor, could attenuate MDMA-induced neurotoxicity using 4-[F]-ADAM, an imaging ligand that selectively targets SERT, with positron emission tomography technology (PET).

99mTc-TRODAT-1 SPECT Revealed That Striatal Dopamine Transport Availability Significantly Decreases in Late Mid-Aged Healthy Taiwanese and Then Remains Stable.

Objectives: Neuroimaging studies in the past 20 years have documented an age-related decline in striatal dopamine transporters (DATs), which is a marker of dopaminergic neurodegeneration; however, concerns about ethnic variations in the decline in DAT with age have not been addressed. The purpose of this study was to assess the rate of striatal DAT loss in healthy Taiwanese adults using kit-based 99mTc-TRODAT-1, a radioligand for DAT SPECT.

Patients And Methods: Fifty healthy subjects (mean age ± SD, 63 ± 12 years; range, 30-80 years) were studied.

Automated Synthesis and Initial Evaluation of (4'-Amino-5',8'-difluoro-1'H-spiro[piperidine-4,2'-quinazolin]-1-yl)(4-[F]fluorophenyl)methanone for PET/MR Imaging of Inducible Nitric Oxide Synthase.

Background: Inducible nitric oxide synthase (iNOS) plays a crucial role in neuroinflammation, especially microglial activity, and may potentially represent a useful biomarker of neuroinflammation. In this study, we carefully defined a strategic plan to develop iNOS-targeted molecular PET imaging using (4'-amino-5',8'-difluoro-1'H-spiro[piperidine-4,2'-quinazolin]-1-yl)(4-fluorophenyl)methanone ([F]FBAT) as a tracer in a mouse model of lipopolysaccharide- (LPS-) induced brain inflammation.

Methods: An model, murine microglial BV2 cell line, was used to assess the uptake of [F]FBAT in response to iNOS induction at the cellular level.

GMP-compliant fully automated radiosynthesis of [F]FEPPA for PET/MRI imaging of regional brain TSPO expression.

Background: Expression of translocator protein (TSPO) on the outer mitochondrial membrane of activated microglia is strongly associated with neuroinflammation. The second-generation PET ligand [F]FEPPA specifically binds TSPO to enable in vivo visualization and quantification of neuroinflammation. We optimized a fully automated radiosynthesis method and evaluated the utility of [F]FEPPA, the second-generation PET ligand specifically binds TSPO, in a mouse model of systemic LPS challenge to detect TSPO-associated signals of central and peripheral inflammation.