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        <identifier>oai:figshare.com:article/33809638</identifier>
        <datestamp>2026-09-15T17:24:52Z</datestamp>
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        <oai_dc:dc xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"  xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
          <dc:title>&lt;p&gt;Open-field motor activity outcomes.&lt;/p&gt;</dc:title>
          <dc:creator>Kaitlyn M. Miller (18831310)</dc:creator>
          <dc:creator>Dakota R. McMeans (24680662)</dc:creator>
          <dc:creator>Martha J. Sonner (3697321)</dc:creator>
          <dc:creator>David R. Ladle (3697324)</dc:creator>
          <dc:creator>Shannon H. Romer (14297822)</dc:creator>
          <dc:subject>Biochemistry</dc:subject>
          <dc:subject>Cell Biology</dc:subject>
          <dc:subject>Molecular Biology</dc:subject>
          <dc:subject>Neuroscience</dc:subject>
          <dc:subject>Physiology</dc:subject>
          <dc:subject>Biotechnology</dc:subject>
          <dc:subject>Environmental Sciences not elsewhere classified</dc:subject>
          <dc:subject>Chemical Sciences not elsewhere classified</dc:subject>
          <dc:subject>Biological Sciences not elsewhere classified</dc:subject>
          <dc:subject>Science Policy</dc:subject>
          <dc:subject>Infectious Diseases</dc:subject>
          <dc:subject>would provide neuroprotection</dc:subject>
          <dc:subject>various pathological effects</dc:subject>
          <dc:subject>plasma cholinesterase activity</dc:subject>
          <dc:subject>field motor activity</dc:subject>
          <dc:subject>causes adverse effects</dc:subject>
          <dc:subject>functional deficits corresponded</dc:subject>
          <dc:subject>galantamine treatment protected</dc:subject>
          <dc:subject>hindlimb nmj innervation</dc:subject>
          <dc:subject>health effects associated</dc:subject>
          <dc:subject>like repeated exposure</dc:subject>
          <dc:subject>week recovery period</dc:subject>
          <dc:subject>kg ), galantamine</dc:subject>
          <dc:subject>like malathion exposure</dc:subject>
          <dc:subject>concentration malathion exposure</dc:subject>
          <dc:subject>reversible ache inhibitor</dc:subject>
          <dc:subject>kg ),</dc:subject>
          <dc:subject>reversible acetylcholinesterase</dc:subject>
          <dc:subject>locomotor deficits</dc:subject>
          <dc:subject>repeated low</dc:subject>
          <dc:subject>final exposure</dc:subject>
          <dc:subject>acute exposure</dc:subject>
          <dc:subject>synaptic remodeling</dc:subject>
          <dc:subject>suggesting remodeling</dc:subject>
          <dc:subject>spinal mns</dc:subject>
          <dc:subject>spinal astrogliosis</dc:subject>
          <dc:subject>performance changes</dc:subject>
          <dc:subject>nmjs consistent</dc:subject>
          <dc:subject>neuromuscular junction</dc:subject>
          <dc:subject>neuromuscular alterations</dc:subject>
          <dc:subject>less understood</dc:subject>
          <dc:subject>indicating involvement</dc:subject>
          <dc:subject>evaluated immediately</dc:subject>
          <dc:subject>anatomical alterations</dc:subject>
          <dc:subject>adult male</dc:subject>
          <dc:subject>50 mg</dc:subject>
          <dc:subject>0 mg</dc:subject>
          <dc:description>&lt;div&gt;&lt;p&gt;Organophosphate pesticides, such as malathion, have been linked to various pathological effects, including neurodegeneration. Acute exposure to malathion, a non-reversible acetylcholinesterase (AChE) inhibitor, causes adverse effects in mammals. However, the impact of subacute, occupational-like repeated exposure on motoneuron (MN) and neuromuscular junction (NMJ) anatomy is less understood. We hypothesized that repeated malathion exposure would produce motor performance deficits accompanied by anatomical alterations in spinal MNs and NMJs consistent with neurodegeneration. We also hypothesized that galantamine, a reversible AChE inhibitor, would provide neuroprotection. Adult male and female Sprague–Dawley rats received subcutaneous saline, malathion (50 mg/kg), galantamine (5.0 mg/kg), or both once daily, five days per week for four weeks. Animals were evaluated immediately after the final exposure and following a four-week recovery period. After exposure, no evidence of spinal astrogliosis and plasma cholinesterase activity was detected. Despite this, cholinergic (C-bouton) synaptic remodeling was observed on lumbar spinal MN somas in females and both sexes showed decreased open-field motor activity. Exposed males performed worse on the accelerod, while exposed females exhibited reduced grip strength. These functional deficits corresponded with a 25% decrease in hindlimb NMJ innervation in both sexes. After recovery, exposed rats showed increased NMJ fragmentation, suggesting remodeling during recovery. Galantamine treatment protected against health effects associated with repeated occupational-like malathion exposure, indicating involvement of cholinergic mechanisms despite minimal changes in plasma cholinesterase activity. Overall, repeated low-concentration malathion exposure is associated with locomotor deficits and peripheral neuropathy.&lt;/p&gt;&lt;/div&gt;</dc:description>
          <dc:date>2026-09-15T17:24:33Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.1371/journal.pone.0357900.t002</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/_p_Open-field_motor_activity_outcomes_p_/33809638</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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