The Administration of Cadmium for 2, 3 and 4 Months Causes a Loss of Recognition Memory, Promotes Neuronal Hypotrophy and Apoptosis in the Hippocampus of Rats
Cadmium (Cd) is a toxic metal and classified as a carcinogen whose exposure could affect the function of the central nervous system. There are studies that suggest that Cd promotes neurodegeneration in different regions of the brain, particularly in the hippocampus. It is proposed that its mechanism...
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| Veröffentlicht in: | Neurochemical research 2019-02, Vol.44 (2), p.485-497 |
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| creator | Pulido, Guadalupe Treviño, Samuel Brambila, Eduardo Vazquez-Roque, Ruben Moreno-Rodriguez, Albino Peña Rosas, Ulises Moran-Perales, Jose Luis Handal Silva, Anhabella Guevara, Jorge Flores, Gonzalo Diaz, Alfonso |
| description | Cadmium (Cd) is a toxic metal and classified as a carcinogen whose exposure could affect the function of the central nervous system. There are studies that suggest that Cd promotes neurodegeneration in different regions of the brain, particularly in the hippocampus. It is proposed that its mechanism of toxicity maybe by an oxidative stress pathway, which modifies neuronal morphology and causes the death of neurons and consequently affecting cognitive tasks. However, this mechanism is not yet clear. The aim of the present work was to study the effect of Cd administration on recognition memory for 2, 3 and 4 months, neuronal morphology and immunoreactivity for caspase-3 and 9 in rat hippocampi. The results show that the administration of Cd decreased recognition memory. Likewise, it caused the dendritic morphology of the CA1, CA3 and dentate gyrus regions of the hippocampus to decrease with respect to the time of administration of this heavy metal. In addition, we observed a reduction in the density of dendritic spines as well as an increase in the immunoreactivity of caspase-3 and 9 in the same hippocampal regions of the animals treated with Cd. These results suggest that Cd affects the structure and function of the neurons of the hippocampus, which contribute to the deterioration of recognition memory. Our results suggest that the exposure to Cd represents a critical health problem, which if not addressed quickly, could cause much more serious problems in the quality of life of the human population, as well as in the environment in which they develop. |
| doi_str_mv | 10.1007/s11064-018-02703-2 |
| format | Article |
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There are studies that suggest that Cd promotes neurodegeneration in different regions of the brain, particularly in the hippocampus. It is proposed that its mechanism of toxicity maybe by an oxidative stress pathway, which modifies neuronal morphology and causes the death of neurons and consequently affecting cognitive tasks. However, this mechanism is not yet clear. The aim of the present work was to study the effect of Cd administration on recognition memory for 2, 3 and 4 months, neuronal morphology and immunoreactivity for caspase-3 and 9 in rat hippocampi. The results show that the administration of Cd decreased recognition memory. Likewise, it caused the dendritic morphology of the CA1, CA3 and dentate gyrus regions of the hippocampus to decrease with respect to the time of administration of this heavy metal. In addition, we observed a reduction in the density of dendritic spines as well as an increase in the immunoreactivity of caspase-3 and 9 in the same hippocampal regions of the animals treated with Cd. These results suggest that Cd affects the structure and function of the neurons of the hippocampus, which contribute to the deterioration of recognition memory. Our results suggest that the exposure to Cd represents a critical health problem, which if not addressed quickly, could cause much more serious problems in the quality of life of the human population, as well as in the environment in which they develop.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-018-02703-2</identifier><identifier>PMID: 30673958</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Cadmium ; Carcinogens ; Caspase ; Caspase-3 ; Cell Biology ; Cell death ; Central nervous system ; Cognitive ability ; Cognitive tasks ; Dendritic spines ; Dentate gyrus ; Exposure ; Heavy metals ; Hippocampus ; Human populations ; Immunoreactivity ; Memory ; Morphology ; Neurochemistry ; Neurodegeneration ; Neurology ; Neurons ; Neurosciences ; Occupational health ; Original Paper ; Oxidative stress ; Quality of life ; Recognition ; Structure-function relationships ; Toxicity</subject><ispartof>Neurochemical research, 2019-02, Vol.44 (2), p.485-497</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Neurochemical Research is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-d70d4ed45d8269222b9a0edb55a3ffb48e1a3002fef356e8f070c241b4a157b23</citedby><cites>FETCH-LOGICAL-c375t-d70d4ed45d8269222b9a0edb55a3ffb48e1a3002fef356e8f070c241b4a157b23</cites><orcidid>0000-0003-4092-6636</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-018-02703-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-018-02703-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30673958$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pulido, Guadalupe</creatorcontrib><creatorcontrib>Treviño, Samuel</creatorcontrib><creatorcontrib>Brambila, Eduardo</creatorcontrib><creatorcontrib>Vazquez-Roque, Ruben</creatorcontrib><creatorcontrib>Moreno-Rodriguez, Albino</creatorcontrib><creatorcontrib>Peña Rosas, Ulises</creatorcontrib><creatorcontrib>Moran-Perales, Jose Luis</creatorcontrib><creatorcontrib>Handal Silva, Anhabella</creatorcontrib><creatorcontrib>Guevara, Jorge</creatorcontrib><creatorcontrib>Flores, Gonzalo</creatorcontrib><creatorcontrib>Diaz, Alfonso</creatorcontrib><title>The Administration of Cadmium for 2, 3 and 4 Months Causes a Loss of Recognition Memory, Promotes Neuronal Hypotrophy and Apoptosis in the Hippocampus of Rats</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>Cadmium (Cd) is a toxic metal and classified as a carcinogen whose exposure could affect the function of the central nervous system. There are studies that suggest that Cd promotes neurodegeneration in different regions of the brain, particularly in the hippocampus. It is proposed that its mechanism of toxicity maybe by an oxidative stress pathway, which modifies neuronal morphology and causes the death of neurons and consequently affecting cognitive tasks. However, this mechanism is not yet clear. The aim of the present work was to study the effect of Cd administration on recognition memory for 2, 3 and 4 months, neuronal morphology and immunoreactivity for caspase-3 and 9 in rat hippocampi. The results show that the administration of Cd decreased recognition memory. Likewise, it caused the dendritic morphology of the CA1, CA3 and dentate gyrus regions of the hippocampus to decrease with respect to the time of administration of this heavy metal. In addition, we observed a reduction in the density of dendritic spines as well as an increase in the immunoreactivity of caspase-3 and 9 in the same hippocampal regions of the animals treated with Cd. These results suggest that Cd affects the structure and function of the neurons of the hippocampus, which contribute to the deterioration of recognition memory. Our results suggest that the exposure to Cd represents a critical health problem, which if not addressed quickly, could cause much more serious problems in the quality of life of the human population, as well as in the environment in which they develop.</description><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Cadmium</subject><subject>Carcinogens</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell Biology</subject><subject>Cell death</subject><subject>Central nervous system</subject><subject>Cognitive ability</subject><subject>Cognitive tasks</subject><subject>Dendritic spines</subject><subject>Dentate gyrus</subject><subject>Exposure</subject><subject>Heavy metals</subject><subject>Hippocampus</subject><subject>Human populations</subject><subject>Immunoreactivity</subject><subject>Memory</subject><subject>Morphology</subject><subject>Neurochemistry</subject><subject>Neurodegeneration</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Occupational health</subject><subject>Original Paper</subject><subject>Oxidative stress</subject><subject>Quality of life</subject><subject>Recognition</subject><subject>Structure-function 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Anhabella</au><au>Guevara, Jorge</au><au>Flores, Gonzalo</au><au>Diaz, Alfonso</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Administration of Cadmium for 2, 3 and 4 Months Causes a Loss of Recognition Memory, Promotes Neuronal Hypotrophy and Apoptosis in the Hippocampus of Rats</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>44</volume><issue>2</issue><spage>485</spage><epage>497</epage><pages>485-497</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Cadmium (Cd) is a toxic metal and classified as a carcinogen whose exposure could affect the function of the central nervous system. There are studies that suggest that Cd promotes neurodegeneration in different regions of the brain, particularly in the hippocampus. It is proposed that its mechanism of toxicity maybe by an oxidative stress pathway, which modifies neuronal morphology and causes the death of neurons and consequently affecting cognitive tasks. However, this mechanism is not yet clear. The aim of the present work was to study the effect of Cd administration on recognition memory for 2, 3 and 4 months, neuronal morphology and immunoreactivity for caspase-3 and 9 in rat hippocampi. The results show that the administration of Cd decreased recognition memory. Likewise, it caused the dendritic morphology of the CA1, CA3 and dentate gyrus regions of the hippocampus to decrease with respect to the time of administration of this heavy metal. In addition, we observed a reduction in the density of dendritic spines as well as an increase in the immunoreactivity of caspase-3 and 9 in the same hippocampal regions of the animals treated with Cd. These results suggest that Cd affects the structure and function of the neurons of the hippocampus, which contribute to the deterioration of recognition memory. Our results suggest that the exposure to Cd represents a critical health problem, which if not addressed quickly, could cause much more serious problems in the quality of life of the human population, as well as in the environment in which they develop.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30673958</pmid><doi>10.1007/s11064-018-02703-2</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-4092-6636</orcidid></addata></record> |
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| subjects | Apoptosis Biochemistry Biomedical and Life Sciences Biomedicine Brain Cadmium Carcinogens Caspase Caspase-3 Cell Biology Cell death Central nervous system Cognitive ability Cognitive tasks Dendritic spines Dentate gyrus Exposure Heavy metals Hippocampus Human populations Immunoreactivity Memory Morphology Neurochemistry Neurodegeneration Neurology Neurons Neurosciences Occupational health Original Paper Oxidative stress Quality of life Recognition Structure-function relationships Toxicity |
| title | The Administration of Cadmium for 2, 3 and 4 Months Causes a Loss of Recognition Memory, Promotes Neuronal Hypotrophy and Apoptosis in the Hippocampus of Rats |
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