Donald M. Kuhn

Mass mapping sites of nitration in tyrosine hydroxylase: random vs selective nitration of three tyrosine residues.

Peroxynitrite-induced nitration of tyrosine hydroxylase: identification of tyrosines 423, 428, and 432 as sites of modification by matrix-assisted laser desorption ionization time-of-flight mass spectrometry and tyrosine-scanning mutagenesis.

Reduced nicotinamide nucleotides prevent nitration of tyrosine hydroxylase by peroxynitrite.

Peroxynitrite inactivates the human dopamine transporter by modification of cysteine 342: potential mechanism of neurotoxicity in dopamine neurons.

Dopamine biosynthesis is regulated by S-glutathionylation. Potential mechanism of tyrosine hydroxylast inhibition during oxidative stress.

Dopamine prevents nitration of tyrosine hydroxylase by peroxynitrite and nitrogen dioxide: is nitrotyrosine formation an early step in dopamine neuronal damage?

Tetrahydrobiopterin prevents nitration of tyrosine hydroxylase by peroxynitrite and nitrogen dioxide.

Identification of differentially regulated transcripts in mouse striatum following methamphetamine treatment--an oligonucleotide microarray approach.

Gene expression profile of the nucleus accumbens of human cocaine abusers: evidence for dysregulation of myelin.

Nitrotyrosine as a marker for peroxynitrite-induced neurotoxicity: the beginning or the end of the end of dopamine neurons?

Methamphetamine neurotoxicity in dopamine nerve endings of the striatum is associated with microglial activation.

Microglial activation is a pharmacologically specific marker for the neurotoxic amphetamines.

Attenuated microglial activation mediates tolerance to the neurotoxic effects of methamphetamine.

Cyclooxygenase-2 is an obligatory factor in methamphetamine-induced neurotoxicity.

MK-801 and dextromethorphan block microglial activation and protect against methamphetamine-induced neurotoxicity.

S-thiolation of tyrosine hydroxylase by reactive nitrogen species in the presence of cysteine or glutathione.

Gene expression profile of activated microglia under conditions associated with dopamine neuronal damage.

Mouse tryptophan hydroxylase isoform 2 and the role of proline 447 in enzyme function.

Differential tissue distribution of tryptophan hydroxylase isoforms 1 and 2 as revealed with monospecific antibodies.

MDMA and fenfluramine reduce L-DOPA-induced dyskinesia via indirect 5-HT1A receptor stimulation.

Dopamine quinones activate microglia and induce a neurotoxic gene expression profile: relationship to methamphetamine-induced nerve ending damage.

Phosphorylation and activation of tryptophan hydroxylase 2: identification of serine-19 as the substrate site for calcium, calmodulin-dependent protein kinase II.

The newly synthesized pool of dopamine determines the severity of methamphetamine-induced neurotoxicity.

A serotonergic system in veins: serotonin transporter-independent uptake.

Methamphetamine-induced neurotoxicity and microglial activation are not mediated by fractalkine receptor signaling.

Dopamine disposition in the presynaptic process regulates the severity of methamphetamine-induced neurotoxicity.

Increases in cytoplasmic dopamine compromise the normal resistance of the nucleus accumbens to methamphetamine neurotoxicity.

Soman increases neuronal COX-2 levels: possible link between seizures and protracted neuronal damage.

Potential mechanisms underlying anxiety and depression in Parkinson's disease: consequences of l-DOPA treatment.

The role of endogenous serotonin in methamphetamine-induced neurotoxicity to dopamine nerve endings of the striatum.

MDMA administration decreases serotonin but not N-acetylaspartate in the rat brain.

Tryptophan hydroxylase 2 aggregates through disulfide cross-linking upon oxidation: possible link to serotonin deficits and non-motor symptoms in Parkinson's disease.

A mouse model of human repetitive mild traumatic brain injury.

Mephedrone, an abused psychoactive component of 'bath salts' and methamphetamine congener, does not cause neurotoxicity to dopamine nerve endings of the striatum.

Genetic depletion of brain 5HT reveals a common molecular pathway mediating compulsivity and impulsivity.

Altered gene expression in cultured microglia in response to simulated blast overpressure: possible role of pulse duration.

Evidence of 5-HT components in human sperm: implications for protein tyrosine phosphorylation and the physiology of motility.

Mice genetically depleted of brain serotonin display social impairments, communication deficits and repetitive behaviors: possible relevance to autism.

Mephedrone does not damage dopamine nerve endings of the striatum, but enhances the neurotoxicity of methamphetamine, amphetamine, and MDMA.

Nucleus accumbens invulnerability to methamphetamine neurotoxicity.

Effects of combined treatment with mephedrone and methamphetamine or 3,4-methylenedioxymethamphetamine on serotonin nerve endings of the hippocampus.

Ventilatory long-term facilitation is evident after initial and repeated exposure to intermittent hypoxia in mice genetically depleted of brain serotonin.