glutaminase and nisoxetine

glutaminase has been researched along with nisoxetine* in 1 studies

Other Studies

1 other study(ies) available for glutaminase and nisoxetine

Article	Year
Cortico-subcortical neuromodulation involved in the amelioration of prepulse inhibition deficits in dopamine transporter knockout mice. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012, Volume: 37, Issue:11 Prepulse inhibition (PPI) deficits are among the most reproducible phenotypic markers found in schizophrenic patients. We recently reported that nisoxetine, a selective norepinephrine transporter (NET) inhibitor, reversed the PPI deficits that have been identified in dopamine transporter (DAT) knockout (KO) mice. However, the mechanisms underlying nisoxetine-induced PPI recovery in DAT KO mice were unclear in previous experiments. To clarify these mechanisms, PPI was tested after microinjections of nisoxetine into the medial prefrontal cortex (mPFc) or nucleus accumbens (NAc) in wildtype (WT) and DAT KO mice. c-Fos immunohistochemistry provided an indicator of neural activation. Multiple-fluorescent-labeling procedures and the retrograde tracer fluorogold were employed to identify nisoxetine-activated neurons and circuits. Systemic nisoxetine activated the mPFc, the NAc shell, the basolateral amygdala, and the subiculum. Infusions of nisoxetine into the mPFc reversed PPI deficits in DAT KO mice, but produced no changes in WT mice, while infusion of nisoxetine into the NAc had no effect on PPI in both WT and DAT KO mice. Experiments using multiple-fluorescent labeling/fluorogold revealed that nisoxetine activates presumed glutamatergic pyramidal cells that project from the mPFc to the NAc. Activated glutamatergic projections from the mPFc to the NAc appear to have substantial roles in the ability of a NET inhibitor to normalize PPI deficits in DAT KO. Thus, this data suggest that selective NET inhibitors such as nisoxetine might improve information processing deficits in schizophrenia via regulation of cortico-subcortical neuromodulation. Topics: Acoustic Stimulation; Analysis of Variance; Animals; Brain; Dopamine Plasma Membrane Transport Proteins; Drug Administration Routes; Fluoxetine; Gene Expression Regulation; Glutamate Decarboxylase; Glutaminase; Inhibition, Psychological; Mice; Mice, Inbred C57BL; Mice, Knockout; Nerve Tissue Proteins; Neurotransmitter Agents; Neurotransmitter Uptake Inhibitors; Proto-Oncogene Proteins c-fos; Reflex, Startle; Sex Factors; Stilbamidines	2012

Article

Year

Cortico-subcortical neuromodulation involved in the amelioration of prepulse inhibition deficits in dopamine transporter knockout mice.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012, Volume: 37, Issue:11

Prepulse inhibition (PPI) deficits are among the most reproducible phenotypic markers found in schizophrenic patients. We recently reported that nisoxetine, a selective norepinephrine transporter (NET) inhibitor, reversed the PPI deficits that have been identified in dopamine transporter (DAT) knockout (KO) mice. However, the mechanisms underlying nisoxetine-induced PPI recovery in DAT KO mice were unclear in previous experiments. To clarify these mechanisms, PPI was tested after microinjections of nisoxetine into the medial prefrontal cortex (mPFc) or nucleus accumbens (NAc) in wildtype (WT) and DAT KO mice. c-Fos immunohistochemistry provided an indicator of neural activation. Multiple-fluorescent-labeling procedures and the retrograde tracer fluorogold were employed to identify nisoxetine-activated neurons and circuits. Systemic nisoxetine activated the mPFc, the NAc shell, the basolateral amygdala, and the subiculum. Infusions of nisoxetine into the mPFc reversed PPI deficits in DAT KO mice, but produced no changes in WT mice, while infusion of nisoxetine into the NAc had no effect on PPI in both WT and DAT KO mice. Experiments using multiple-fluorescent labeling/fluorogold revealed that nisoxetine activates presumed glutamatergic pyramidal cells that project from the mPFc to the NAc. Activated glutamatergic projections from the mPFc to the NAc appear to have substantial roles in the ability of a NET inhibitor to normalize PPI deficits in DAT KO. Thus, this data suggest that selective NET inhibitors such as nisoxetine might improve information processing deficits in schizophrenia via regulation of cortico-subcortical neuromodulation.

Topics: Acoustic Stimulation; Analysis of Variance; Animals; Brain; Dopamine Plasma Membrane Transport Proteins; Drug Administration Routes; Fluoxetine; Gene Expression Regulation; Glutamate Decarboxylase; Glutaminase; Inhibition, Psychological; Mice; Mice, Inbred C57BL; Mice, Knockout; Nerve Tissue Proteins; Neurotransmitter Agents; Neurotransmitter Uptake Inhibitors; Proto-Oncogene Proteins c-fos; Reflex, Startle; Sex Factors; Stilbamidines

2012