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Reward System Activation Improves Recovery from Acute Myocardial Infarction".

ABSTRACT: The recovery from acute myocardial infarction (AMI) is influenced by physiological and psychological factors. While the physiological effects have been extensively studied, the contribution of psychological factors and whether they can be modulated is not completely clear. Here we show that the activity of the reward system, a brain network involved in motivation and positive expectation, affects outcomes in mice following AMI. We found that chemogenetic activation of dopaminergic neurons in the ventral tegmental area (VTA) significantly attenuated the remodeling process following AMI, resulting in improved left-ventricular performance compared to controls. VTA activation was associated with modulation of the immune response following AMI and increased blood vessel formation in the damaged area, mediated, at least in part, by changes in liver-secreted proteins. Together, our findings reveal a potential mechanism by which specific brain activity can affect the multifactorial systemic and local tissue response to AMI, introducing a novel target for therapeutic interventions

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Heart

SUBMITTER: Tamar Ziv

LAB HEAD: Asya Rolls

PROVIDER: PXD043448 | Pride | 2024-05-03

REPOSITORIES: Pride

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Project description:Implications for neuroprotection in Parkinson's disease Parkinson’s disease and its characteristic symptoms are thought to arise from the progressive degeneration of specific midbrain dopamine (DA) neurons. In humans, DA neurons of the substantia nigra (SN) and their projections to the striatum show selective vulnerability, while neighboring DA neurons of the ventral tegmental area (VTA) are relatively spared from degeneration. This pattern of cell loss is mimicked in humans, primates, and certain rodents by the neurotoxin MPTP. In this study, we aimed to test the hypothesis that there are factors in the VTA that are potentially neuroprotective against MPTP and that these factors change over time. We have found a differential transcriptional response within the cells of the SN and VTA to sustained exposure to a low dose of MPTP. Specifically, the VTA has increased expression of 148 genes as an early response to MPTP and 113 genes as a late response to MPTP toxicity. This response encompasses many areas of cellular function, including protein regulation (Phf6) and ion/metal regulation (PANK2, Car4). Notably, these responses were largely absent from the cells of the SN. Our data show a clear dynamic response in maintaining the homeostasis and viability of the neurons in the VTA that is lacking in the SN after neurotoxin challenge. We used microarrays to analyze the differential response of the substantia nigra (SN) and ventral tegmental area (VTA) to a chronic low dose of the neurotoxin MPTP. Transgenic hTH-GFP mice were treated with MPTP (4mg/kg) for either 2 or 10 days. Control mice were given an equal volume of saline for 10 days. Dopamine neurons from the substantia nigra and ventral tegmental areas of control and MPTP treated animals were laser captured. The RNA was isolated and processed for microarray hybridization. Each group had three biological replicates, for a total of 18 samples. Three each in the following: Control SN, Control VTA, 2 day MPTP SN, 2 day MPTP VTA, 10 day MPTP SN, 10 day MPTP VTA. Samples were log2 transformed and RMA normalized using Agilent Genespring 10.0 GX.

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Reward System Activation Improves Recovery from Acute Myocardial Infarction".

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