Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats
Loss of function mutations in PARK6, the gene that encodes the protein PTEN-induced kinase 1 (PINK1), cause autosomal recessive familial Parkinson’s disease (PD). While PD is clinically diagnosed by its motor symptoms, recent studies point to the impact of non-motor symptoms, including cognitive dys...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2021-08-01
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| Series: | Frontiers in Neuroscience |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fnins.2021.655901/full |
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| author | Adeel A. Memon Adeel A. Memon Adeel A. Memon Adeel A. Memon Micah E. Bagley Rose B. Creed Rose B. Creed Rose B. Creed Amy W. Amara Amy W. Amara Amy W. Amara Matthew S. Goldberg Matthew S. Goldberg Matthew S. Goldberg Lori L. McMahon Lori L. McMahon Lori L. McMahon Lori L. McMahon |
| author_facet | Adeel A. Memon Adeel A. Memon Adeel A. Memon Adeel A. Memon Micah E. Bagley Rose B. Creed Rose B. Creed Rose B. Creed Amy W. Amara Amy W. Amara Amy W. Amara Matthew S. Goldberg Matthew S. Goldberg Matthew S. Goldberg Lori L. McMahon Lori L. McMahon Lori L. McMahon Lori L. McMahon |
| author_sort | Adeel A. Memon |
| collection | DOAJ |
| description | Loss of function mutations in PARK6, the gene that encodes the protein PTEN-induced kinase 1 (PINK1), cause autosomal recessive familial Parkinson’s disease (PD). While PD is clinically diagnosed by its motor symptoms, recent studies point to the impact of non-motor symptoms, including cognitive dysfunction in the early pre-motor stages of the disease (Aarsland et al., 2004; Chaudhuri and Schapira, 2009). As the hippocampus is a key structure for learning and memory, this study aimed to determine whether synaptic transmission is affected at CA3-CA1 excitatory synapses in PINK1 knockout rats at an age when we recently reported a gain of function at excitatory synapses onto spiny projection neurons in the dorsal striatum (Creed et al., 2020) and when motor symptoms are beginning to appear (Dave et al., 2014). Using extracellular dendritic field excitatory postsynaptic potential recordings at CA3-CA1 synapses in dorsal hippocampus 4-to 5- month old PINK1 KO rats and wild-type littermate controls, we observed no detectable differences in the strength of basal synaptic transmission, paired-pulse facilitation, or long-term potentiation. Our results suggest that loss of PINK1 protein does not cause a general dysfunction of excitatory transmission throughout the brain at this young adult age when excitatory transmission is abnormal in the striatum. |
| first_indexed | 2024-12-22T10:34:56Z |
| format | Article |
| id | doaj.art-449ffa7e71cd4f848c7743fdcb5a8336 |
| institution | Directory Open Access Journal |
| issn | 1662-453X |
| language | English |
| last_indexed | 2024-12-22T10:34:56Z |
| publishDate | 2021-08-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neuroscience |
| spelling | doaj.art-449ffa7e71cd4f848c7743fdcb5a83362022-12-21T18:29:13ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2021-08-011510.3389/fnins.2021.655901655901Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient RatsAdeel A. Memon0Adeel A. Memon1Adeel A. Memon2Adeel A. Memon3Micah E. Bagley4Rose B. Creed5Rose B. Creed6Rose B. Creed7Amy W. Amara8Amy W. Amara9Amy W. Amara10Matthew S. Goldberg11Matthew S. Goldberg12Matthew S. Goldberg13Lori L. McMahon14Lori L. McMahon15Lori L. McMahon16Lori L. McMahon17Department of Neurology, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neuroengineering, School of Engineering, The University of Alabama at Birmingham, Birmingham, AL, United StatesCenter for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Cell, Developmental, and Integrative Biology, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Cell, Developmental, and Integrative Biology, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neurology, The University of Alabama at Birmingham, Birmingham, AL, United StatesCenter for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Cell, Developmental, and Integrative Biology, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neurology, The University of Alabama at Birmingham, Birmingham, AL, United StatesCenter for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neurobiology, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neurology, The University of Alabama at Birmingham, Birmingham, AL, United StatesCenter for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neurobiology, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neurology, The University of Alabama at Birmingham, Birmingham, AL, United StatesCenter for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Cell, Developmental, and Integrative Biology, The University of Alabama at Birmingham, Birmingham, AL, United StatesDepartment of Neurobiology, The University of Alabama at Birmingham, Birmingham, AL, United StatesLoss of function mutations in PARK6, the gene that encodes the protein PTEN-induced kinase 1 (PINK1), cause autosomal recessive familial Parkinson’s disease (PD). While PD is clinically diagnosed by its motor symptoms, recent studies point to the impact of non-motor symptoms, including cognitive dysfunction in the early pre-motor stages of the disease (Aarsland et al., 2004; Chaudhuri and Schapira, 2009). As the hippocampus is a key structure for learning and memory, this study aimed to determine whether synaptic transmission is affected at CA3-CA1 excitatory synapses in PINK1 knockout rats at an age when we recently reported a gain of function at excitatory synapses onto spiny projection neurons in the dorsal striatum (Creed et al., 2020) and when motor symptoms are beginning to appear (Dave et al., 2014). Using extracellular dendritic field excitatory postsynaptic potential recordings at CA3-CA1 synapses in dorsal hippocampus 4-to 5- month old PINK1 KO rats and wild-type littermate controls, we observed no detectable differences in the strength of basal synaptic transmission, paired-pulse facilitation, or long-term potentiation. Our results suggest that loss of PINK1 protein does not cause a general dysfunction of excitatory transmission throughout the brain at this young adult age when excitatory transmission is abnormal in the striatum.https://www.frontiersin.org/articles/10.3389/fnins.2021.655901/fullParkinson’s diseasePINK1hippocampusCA3-CA1 synapseslong term plasticitybasal synaptic transmission |
| spellingShingle | Adeel A. Memon Adeel A. Memon Adeel A. Memon Adeel A. Memon Micah E. Bagley Rose B. Creed Rose B. Creed Rose B. Creed Amy W. Amara Amy W. Amara Amy W. Amara Matthew S. Goldberg Matthew S. Goldberg Matthew S. Goldberg Lori L. McMahon Lori L. McMahon Lori L. McMahon Lori L. McMahon Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats Frontiers in Neuroscience Parkinson’s disease PINK1 hippocampus CA3-CA1 synapses long term plasticity basal synaptic transmission |
| title | Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats |
| title_full | Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats |
| title_fullStr | Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats |
| title_full_unstemmed | Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats |
| title_short | Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats |
| title_sort | basal synaptic transmission and long term plasticity at ca3 ca1 synapses are unaffected in young adult pink1 deficient rats |
| topic | Parkinson’s disease PINK1 hippocampus CA3-CA1 synapses long term plasticity basal synaptic transmission |
| url | https://www.frontiersin.org/articles/10.3389/fnins.2021.655901/full |
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