Publications by authors named "T Perlmann"

Article Synopsis
  • The Claustrum/dorsal endopiriform cortex complex (CLA) is a complex brain region that heavily influences other cortical areas and expresses the transcription factor Nurr1, whose specific role in CLA was not clearly defined.
  • Research using genetically modified mice demonstrated that Nurr1 is essential for maintaining the unique gene expression pattern of CLA neurons, although these neurons remain physically intact without it.
  • The study also found that Nurr1 deletion in CLA disrupts hallucinogen receptor expression and alters the functional connectivity effects of hallucinogens on brain regions that interact with CLA, suggesting that targeting Nurr1 could enhance our understanding of CLA’s functions.
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Article Synopsis
  • * Conditional knockout studies in PARKIN-deficient mice reveal that loss of PARKIN does not impact mitochondrial functions such as oxidative phosphorylation or worsen brain defects, challenging previous assumptions about its importance.
  • * A case study of a patient with PARKIN deficiency shows no impairment in mitochondrial function, suggesting that PARKIN is not necessary for maintaining OXPHOS activity in adult tissues.
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Midbrain dopamine (mDA) neurons comprise diverse cells with unique innervation targets and functions. This is illustrated by the selective sensitivity of mDA neurons of the substantia nigra compacta (SNc) in patients with Parkinson's disease, while those in the ventral tegmental area (VTA) are relatively spared. Here, we used single nuclei RNA sequencing (snRNA-seq) of approximately 70,000 mouse midbrain cells to build a high-resolution atlas of mouse mDA neuron diversity at the molecular level.

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Article Synopsis
  • In Parkinson's disease, axons of dopaminergic neurons deteriorate before their cell bodies, and calcium influx may play a role in this neuronal loss.
  • In a study using two mouse models of Parkinson's, differing impacts on voltage-gated calcium channels (VGCCs) were observed: L-type VGCCs were linked to pacemaker firing in G2019S mice, while T-type VGCCs showed decreased contribution in cNurr1 mice.
  • The research highlights how oxidative stress influences the function of these VGCCs in the somatic region of dopaminergic neurons, but not at the axon terminals.
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How neurons can maintain cellular identity over an entire life span remains largely unknown. Here, we show that maintenance of identity in differentiated dopaminergic and serotonergic neurons is critically reliant on the Polycomb repressive complex 2 (PRC2). Deletion of the obligate PRC2 component, , in these neurons resulted in global loss of H3K27me3, followed by a gradual activation of genes harboring both H3K27me3 and H3K9me3 modifications.

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