Thyroid hormone treatment alleviates the impairments of neurogenesis, mitochondrial biogenesis and memory performance induced by methamphetamine
•Repeated MA exposure induced cognitive deficits.•MA induced impairments in neurogenesis and mitochondrial biogenesis.•MA induced neuroinflammation in the hippocampus of rats.•THs administration decreased cognitive deficits mediated by MA.•THs partially decreased alterations induced by MA in the mol...
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| Veröffentlicht in: | Neurotoxicology (Park Forest South) 2019-09, Vol.74, p.7-18 |
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| creator | Seyedhosseini Tamijani, Seyedeh Masoumeh Beirami, Elmira Ahmadiani, Abolhassan Dargahi, Leila |
| description | •Repeated MA exposure induced cognitive deficits.•MA induced impairments in neurogenesis and mitochondrial biogenesis.•MA induced neuroinflammation in the hippocampus of rats.•THs administration decreased cognitive deficits mediated by MA.•THs partially decreased alterations induced by MA in the molecular level.
Chronic use of methamphetamine (MA), a neurotoxic psychostimulant, leads to long-lasting cognitive dysfunctions in humans and animal models. Thyroid hormones (THs) have several physiological actions and are crucial for normal behavioral, intellectual and neurological development. Considering the importance of THs in the cognitive processes, the present study was designed to evaluate the therapeutic effects of THs on cognitive and neurological impairments induced by MA. Escalating doses of MA (1–10 mg/kg, IP) were injected twice daily for 10 consecutive days in rats and cognitive functions were evaluated using behavioral tests. The expression of factors involved in neurogenesis (NES and DCX), mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM), neuroinflammation (GFAP, Iba-1, and COX-2) as well as Reelin and NT-3 (synaptic plasticity and neurotrophic factor, respectively) was measured in the hippocampus of MA-treated animals. The effects of three different doses of T4 (20, 40 or 80 μg/kg; intraperitoneally) or T3 (20, 40 or 80 μg/rat; 2.5 μl/nostril; intranasal) treatment, once a day for one week after MA cessation, were assessed in MA-treated rats. After the last behavioral test, serum T4 and T3 levels were measured using radioimmunoassay. The results revealed that repeated escalating regimen of MA impaired cognitive functions concomitant with neurogenesis and synaptic plasticity impairments, mitochondrial dysfunction, and neuroinflammation. T4 or T3 treatment partially decreased the alterations induced by MA. These findings suggest that THs can be considered as potential candidates for the reduction of MA abuse related neurocognitive disturbances. |
| doi_str_mv | 10.1016/j.neuro.2019.05.003 |
| format | Article |
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Chronic use of methamphetamine (MA), a neurotoxic psychostimulant, leads to long-lasting cognitive dysfunctions in humans and animal models. Thyroid hormones (THs) have several physiological actions and are crucial for normal behavioral, intellectual and neurological development. Considering the importance of THs in the cognitive processes, the present study was designed to evaluate the therapeutic effects of THs on cognitive and neurological impairments induced by MA. Escalating doses of MA (1–10 mg/kg, IP) were injected twice daily for 10 consecutive days in rats and cognitive functions were evaluated using behavioral tests. The expression of factors involved in neurogenesis (NES and DCX), mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM), neuroinflammation (GFAP, Iba-1, and COX-2) as well as Reelin and NT-3 (synaptic plasticity and neurotrophic factor, respectively) was measured in the hippocampus of MA-treated animals. The effects of three different doses of T4 (20, 40 or 80 μg/kg; intraperitoneally) or T3 (20, 40 or 80 μg/rat; 2.5 μl/nostril; intranasal) treatment, once a day for one week after MA cessation, were assessed in MA-treated rats. After the last behavioral test, serum T4 and T3 levels were measured using radioimmunoassay. The results revealed that repeated escalating regimen of MA impaired cognitive functions concomitant with neurogenesis and synaptic plasticity impairments, mitochondrial dysfunction, and neuroinflammation. T4 or T3 treatment partially decreased the alterations induced by MA. These findings suggest that THs can be considered as potential candidates for the reduction of MA abuse related neurocognitive disturbances.</description><identifier>ISSN: 0161-813X</identifier><identifier>EISSN: 1872-9711</identifier><identifier>DOI: 10.1016/j.neuro.2019.05.003</identifier><identifier>PMID: 31075280</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animal cognition ; Animal models ; Animals ; Behavior, Animal - drug effects ; Behavioral plasticity ; Biosynthesis ; Central Nervous System Stimulants - toxicity ; Cognition ; Cognition - drug effects ; Cognition Disorders - chemically induced ; Cognition Disorders - prevention & control ; Cognition Disorders - psychology ; Cognitive ability ; Cognitive deficits ; Cyclooxygenase-2 ; Doublecortin protein ; Drug abuse ; Glial fibrillary acidic protein ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hormones ; Inflammation ; Inflammation - chemically induced ; Inflammation - prevention & control ; Male ; Memory Disorders - chemically induced ; Memory Disorders - prevention & control ; Memory Disorders - psychology ; Menopause ; Methamphetamine ; Methamphetamine - toxicity ; Mitochondria ; Mitochondrial biogenesis ; Neurogenesis ; Neurogenesis - drug effects ; Neurotoxicity ; Neurotrophic factors ; Neurotrophin 3 ; Organelle Biogenesis ; Plasticity ; Psychomotor Performance - drug effects ; Radioimmunoassay ; Rats ; Rats, Wistar ; Reelin protein ; Synapses - drug effects ; Synaptic plasticity ; Thyroid ; Thyroid gland ; Thyroid hormones ; Thyroid Hormones - blood ; Thyroid Hormones - therapeutic use ; Thyroxine ; Thyroxine - therapeutic use ; Triiodothyronine ; Triiodothyronine - therapeutic use</subject><ispartof>Neurotoxicology (Park Forest South), 2019-09, Vol.74, p.7-18</ispartof><rights>2019 Elsevier B.V.</rights><rights>Copyright © 2019 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier BV Sep 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-5b6c241a5ca65eebdb9e042dec32b6e6bffdddc78aad9ff6c23ecde0e5809f2a3</citedby><cites>FETCH-LOGICAL-c387t-5b6c241a5ca65eebdb9e042dec32b6e6bffdddc78aad9ff6c23ecde0e5809f2a3</cites><orcidid>0000-0001-7777-5435</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuro.2019.05.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31075280$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Seyedhosseini Tamijani, Seyedeh Masoumeh</creatorcontrib><creatorcontrib>Beirami, Elmira</creatorcontrib><creatorcontrib>Ahmadiani, Abolhassan</creatorcontrib><creatorcontrib>Dargahi, Leila</creatorcontrib><title>Thyroid hormone treatment alleviates the impairments of neurogenesis, mitochondrial biogenesis and memory performance induced by methamphetamine</title><title>Neurotoxicology (Park Forest South)</title><addtitle>Neurotoxicology</addtitle><description>•Repeated MA exposure induced cognitive deficits.•MA induced impairments in neurogenesis and mitochondrial biogenesis.•MA induced neuroinflammation in the hippocampus of rats.•THs administration decreased cognitive deficits mediated by MA.•THs partially decreased alterations induced by MA in the molecular level.
Chronic use of methamphetamine (MA), a neurotoxic psychostimulant, leads to long-lasting cognitive dysfunctions in humans and animal models. Thyroid hormones (THs) have several physiological actions and are crucial for normal behavioral, intellectual and neurological development. Considering the importance of THs in the cognitive processes, the present study was designed to evaluate the therapeutic effects of THs on cognitive and neurological impairments induced by MA. Escalating doses of MA (1–10 mg/kg, IP) were injected twice daily for 10 consecutive days in rats and cognitive functions were evaluated using behavioral tests. The expression of factors involved in neurogenesis (NES and DCX), mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM), neuroinflammation (GFAP, Iba-1, and COX-2) as well as Reelin and NT-3 (synaptic plasticity and neurotrophic factor, respectively) was measured in the hippocampus of MA-treated animals. The effects of three different doses of T4 (20, 40 or 80 μg/kg; intraperitoneally) or T3 (20, 40 or 80 μg/rat; 2.5 μl/nostril; intranasal) treatment, once a day for one week after MA cessation, were assessed in MA-treated rats. After the last behavioral test, serum T4 and T3 levels were measured using radioimmunoassay. The results revealed that repeated escalating regimen of MA impaired cognitive functions concomitant with neurogenesis and synaptic plasticity impairments, mitochondrial dysfunction, and neuroinflammation. T4 or T3 treatment partially decreased the alterations induced by MA. These findings suggest that THs can be considered as potential candidates for the reduction of MA abuse related neurocognitive disturbances.</description><subject>Animal cognition</subject><subject>Animal models</subject><subject>Animals</subject><subject>Behavior, Animal - drug effects</subject><subject>Behavioral plasticity</subject><subject>Biosynthesis</subject><subject>Central Nervous System Stimulants - toxicity</subject><subject>Cognition</subject><subject>Cognition - drug effects</subject><subject>Cognition Disorders - chemically induced</subject><subject>Cognition Disorders - prevention & control</subject><subject>Cognition Disorders - psychology</subject><subject>Cognitive ability</subject><subject>Cognitive deficits</subject><subject>Cyclooxygenase-2</subject><subject>Doublecortin protein</subject><subject>Drug abuse</subject><subject>Glial fibrillary acidic protein</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hormones</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - prevention & control</subject><subject>Male</subject><subject>Memory Disorders - chemically induced</subject><subject>Memory Disorders - prevention & control</subject><subject>Memory Disorders - psychology</subject><subject>Menopause</subject><subject>Methamphetamine</subject><subject>Methamphetamine - toxicity</subject><subject>Mitochondria</subject><subject>Mitochondrial biogenesis</subject><subject>Neurogenesis</subject><subject>Neurogenesis - drug effects</subject><subject>Neurotoxicity</subject><subject>Neurotrophic factors</subject><subject>Neurotrophin 3</subject><subject>Organelle Biogenesis</subject><subject>Plasticity</subject><subject>Psychomotor Performance - drug effects</subject><subject>Radioimmunoassay</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reelin protein</subject><subject>Synapses - drug effects</subject><subject>Synaptic plasticity</subject><subject>Thyroid</subject><subject>Thyroid gland</subject><subject>Thyroid hormones</subject><subject>Thyroid Hormones - blood</subject><subject>Thyroid Hormones - therapeutic use</subject><subject>Thyroxine</subject><subject>Thyroxine - therapeutic use</subject><subject>Triiodothyronine</subject><subject>Triiodothyronine - therapeutic use</subject><issn>0161-813X</issn><issn>1872-9711</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1KJDEUhYM4aNvjEwgScGvVJBXrb-FCxD8QZtMDswup5MZK00nKJCX0W8wjT9pWl66yON89h5yD0BklJSW0-bUuHczBlxWhfUnqkhB2gBa0a6uibyk9RItM0aKj7O8xOolxTQit26Y_QseMkrauOrJA_1bjNnij8OiD9Q5wCiCSBZew2GzgzYgEEacRsLGTMGGnROw1fs9-AQfRxEtsTfJy9E4FIzZ4MJ8KFk5hC9aHLZ4g6BwinMxmTs0SFB62WU2jsNMISVjj4Cf6ocUmwunHu0R_7u9Wt4_F8--Hp9ub50Kyrk1FPTSyuqKilqKpAQY19ECuKgWSVUMDzaC1Ukq2nRCq1zrDDKQCAnVHel0JtkQXe98p-NcZYuJrPweXI3nFcqOkzyVniu0pGXyMATSfgrEibDklfLcCX_P3JvhuBU5qnlfIV-cf3vNgQX3dfNaeges9APmHbwYCj9JALkaZADJx5c23Af8BXRqgUQ</recordid><startdate>201909</startdate><enddate>201909</enddate><creator>Seyedhosseini Tamijani, Seyedeh Masoumeh</creator><creator>Beirami, Elmira</creator><creator>Ahmadiani, Abolhassan</creator><creator>Dargahi, Leila</creator><general>Elsevier B.V</general><general>Elsevier BV</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><orcidid>https://orcid.org/0000-0001-7777-5435</orcidid></search><sort><creationdate>201909</creationdate><title>Thyroid hormone treatment alleviates the impairments of neurogenesis, mitochondrial biogenesis and memory performance induced by methamphetamine</title><author>Seyedhosseini Tamijani, Seyedeh Masoumeh ; Beirami, Elmira ; Ahmadiani, Abolhassan ; Dargahi, Leila</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-5b6c241a5ca65eebdb9e042dec32b6e6bffdddc78aad9ff6c23ecde0e5809f2a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animal cognition</topic><topic>Animal models</topic><topic>Animals</topic><topic>Behavior, Animal - drug effects</topic><topic>Behavioral plasticity</topic><topic>Biosynthesis</topic><topic>Central Nervous System Stimulants - toxicity</topic><topic>Cognition</topic><topic>Cognition - drug effects</topic><topic>Cognition Disorders - chemically induced</topic><topic>Cognition Disorders - prevention & control</topic><topic>Cognition Disorders - psychology</topic><topic>Cognitive ability</topic><topic>Cognitive deficits</topic><topic>Cyclooxygenase-2</topic><topic>Doublecortin protein</topic><topic>Drug abuse</topic><topic>Glial fibrillary acidic protein</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hormones</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - prevention & control</topic><topic>Male</topic><topic>Memory Disorders - chemically induced</topic><topic>Memory Disorders - prevention & control</topic><topic>Memory Disorders - psychology</topic><topic>Menopause</topic><topic>Methamphetamine</topic><topic>Methamphetamine - toxicity</topic><topic>Mitochondria</topic><topic>Mitochondrial biogenesis</topic><topic>Neurogenesis</topic><topic>Neurogenesis - drug effects</topic><topic>Neurotoxicity</topic><topic>Neurotrophic factors</topic><topic>Neurotrophin 3</topic><topic>Organelle Biogenesis</topic><topic>Plasticity</topic><topic>Psychomotor Performance - drug effects</topic><topic>Radioimmunoassay</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reelin protein</topic><topic>Synapses - drug effects</topic><topic>Synaptic plasticity</topic><topic>Thyroid</topic><topic>Thyroid gland</topic><topic>Thyroid hormones</topic><topic>Thyroid Hormones - blood</topic><topic>Thyroid Hormones - therapeutic use</topic><topic>Thyroxine</topic><topic>Thyroxine - therapeutic use</topic><topic>Triiodothyronine</topic><topic>Triiodothyronine - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Seyedhosseini Tamijani, Seyedeh Masoumeh</creatorcontrib><creatorcontrib>Beirami, Elmira</creatorcontrib><creatorcontrib>Ahmadiani, Abolhassan</creatorcontrib><creatorcontrib>Dargahi, Leila</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Neurotoxicology (Park Forest South)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Seyedhosseini Tamijani, Seyedeh Masoumeh</au><au>Beirami, Elmira</au><au>Ahmadiani, Abolhassan</au><au>Dargahi, Leila</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thyroid hormone treatment alleviates the impairments of neurogenesis, mitochondrial biogenesis and memory performance induced by methamphetamine</atitle><jtitle>Neurotoxicology (Park Forest South)</jtitle><addtitle>Neurotoxicology</addtitle><date>2019-09</date><risdate>2019</risdate><volume>74</volume><spage>7</spage><epage>18</epage><pages>7-18</pages><issn>0161-813X</issn><eissn>1872-9711</eissn><abstract>•Repeated MA exposure induced cognitive deficits.•MA induced impairments in neurogenesis and mitochondrial biogenesis.•MA induced neuroinflammation in the hippocampus of rats.•THs administration decreased cognitive deficits mediated by MA.•THs partially decreased alterations induced by MA in the molecular level.
Chronic use of methamphetamine (MA), a neurotoxic psychostimulant, leads to long-lasting cognitive dysfunctions in humans and animal models. Thyroid hormones (THs) have several physiological actions and are crucial for normal behavioral, intellectual and neurological development. Considering the importance of THs in the cognitive processes, the present study was designed to evaluate the therapeutic effects of THs on cognitive and neurological impairments induced by MA. Escalating doses of MA (1–10 mg/kg, IP) were injected twice daily for 10 consecutive days in rats and cognitive functions were evaluated using behavioral tests. The expression of factors involved in neurogenesis (NES and DCX), mitochondrial biogenesis (PGC-1α, NRF-1, and TFAM), neuroinflammation (GFAP, Iba-1, and COX-2) as well as Reelin and NT-3 (synaptic plasticity and neurotrophic factor, respectively) was measured in the hippocampus of MA-treated animals. The effects of three different doses of T4 (20, 40 or 80 μg/kg; intraperitoneally) or T3 (20, 40 or 80 μg/rat; 2.5 μl/nostril; intranasal) treatment, once a day for one week after MA cessation, were assessed in MA-treated rats. After the last behavioral test, serum T4 and T3 levels were measured using radioimmunoassay. The results revealed that repeated escalating regimen of MA impaired cognitive functions concomitant with neurogenesis and synaptic plasticity impairments, mitochondrial dysfunction, and neuroinflammation. T4 or T3 treatment partially decreased the alterations induced by MA. These findings suggest that THs can be considered as potential candidates for the reduction of MA abuse related neurocognitive disturbances.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>31075280</pmid><doi>10.1016/j.neuro.2019.05.003</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-7777-5435</orcidid></addata></record> |
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| subjects | Animal cognition Animal models Animals Behavior, Animal - drug effects Behavioral plasticity Biosynthesis Central Nervous System Stimulants - toxicity Cognition Cognition - drug effects Cognition Disorders - chemically induced Cognition Disorders - prevention & control Cognition Disorders - psychology Cognitive ability Cognitive deficits Cyclooxygenase-2 Doublecortin protein Drug abuse Glial fibrillary acidic protein Hippocampus - drug effects Hippocampus - metabolism Hormones Inflammation Inflammation - chemically induced Inflammation - prevention & control Male Memory Disorders - chemically induced Memory Disorders - prevention & control Memory Disorders - psychology Menopause Methamphetamine Methamphetamine - toxicity Mitochondria Mitochondrial biogenesis Neurogenesis Neurogenesis - drug effects Neurotoxicity Neurotrophic factors Neurotrophin 3 Organelle Biogenesis Plasticity Psychomotor Performance - drug effects Radioimmunoassay Rats Rats, Wistar Reelin protein Synapses - drug effects Synaptic plasticity Thyroid Thyroid gland Thyroid hormones Thyroid Hormones - blood Thyroid Hormones - therapeutic use Thyroxine Thyroxine - therapeutic use Triiodothyronine Triiodothyronine - therapeutic use |
| title | Thyroid hormone treatment alleviates the impairments of neurogenesis, mitochondrial biogenesis and memory performance induced by methamphetamine |
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