Case Report: Suspected Solitary Osseous Plasmacytoma in a Cat: Use of Magnetic Resonance Imaging to Diagnose and Confirm Resolution of Disease Following Chemotherapy.

A 9-year-old female spayed Domestic Shorthair cat presented for pain, reluctance to jump, and hyporexia of 14 days duration. Neurologic examination was consistent with C6-T2 myelopathy. Magnetic resonance imaging (MRI) revealed a solitary, contrast-enhancing lesion within the T2 vertebral body. Solitary osseous plasmacytoma was diagnosed based on neurologic examination, advanced imaging, and clinicopathologic findings. Melphalan and prednisolone therapy were initiated. Complete resolution of clinical signs and the vertebral lesion were documented at a 2-year follow up examination with neurologic examination and repeat spinal MRI, respectively. Solitary osseous plasmacytoma are rare neoplasms in humans and domestic animals. As such, there is a paucity of published information regarding diagnostic criteria, MRI findings, treatment modalities, progression, and remission of disease in the feline patient. Most data are extrapolated from human medicine. The purpose of this report is to document neurologic exam and MR findings at the time of diagnosis and complete resolution of a solitary osseous vertebral plasmacytoma following melphalan and prednisolone therapy.

Alterations in amphetamine-stimulated dopamine overflow due to the Nurr1-null heterozygous genotype and postweaning isolation.

The nuclear receptor Nurr1 functions to regulate dopamine neurotransmission, as Nurr1-null heterozygous (+/-) mice have alterations in dopamine function and, when raised in isolation immediately after weaning, have disruptions in sensorimotor gaiting, a behavior altered in schizophrenia and modulated by dopamine neurotransmission. The goal of this study was to determine nigrostriatal and mesoaccumbens dopamine neurotransmission using microdialysis in +/- and wild-type (+/+) mice raised in groups or isolation. In the striatum, isolation significantly reduced amphetamine-stimulated dopamine overflow and levels of the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC). The +/- genotype alone caused a small, nonsignificant reduction in basal dopamine levels but a significant reduction in basal DOPAC levels. In the nucleus accumbens shell, the +/- genotype elevated basal dopamine levels. Isolation had genotype specific effects, causing an elevation in amphetamine-stimulated dopamine overflow in +/- mice but a reduction in +/+ mice, resulting in a large difference in stimulated dopamine overflow when comparing the +/+ and +/- isolated mice. These data indicate that a deletion of a single allele of Nurr1, which produces only subtle changes alone, when coupled with a developmental stressor, can dramatically alter mesoaccumbens dopamine neurotransmission. These observations demonstrate how the combination of genetic predisposition and an environmental insult during development can cause dysfunction of dopamine neurotransmission and could contribute to diseases such as schizophrenia or attention deficit hyperactivity disorder.