Effect of a 5-HT1D receptor agonist on the reinstatement phase of the conditioned place preference test and hippocampal long-term potentiation in methamphetamine-treated rats
•The 5-HT1D receptor agonist, PNU142633, attenuates METH-seeking behavior.•Preference for the METH-associated environment decreased in PNU + METH-primed rats.•PNU decreased LTP components in METH-primed rats.•PNU may decrease synaptic transmission and prevent METH reinstatement. Methamphetamine (MET...
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| Vydáno v: | Brain research Ročník 1698; s. 151 - 160 |
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| Médium: | Journal Article |
| Jazyk: | angličtina |
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Elsevier B.V
01.11.2018
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| ISSN: | 0006-8993, 1872-6240, 1872-6240 |
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| Abstract | •The 5-HT1D receptor agonist, PNU142633, attenuates METH-seeking behavior.•Preference for the METH-associated environment decreased in PNU + METH-primed rats.•PNU decreased LTP components in METH-primed rats.•PNU may decrease synaptic transmission and prevent METH reinstatement.
Methamphetamine (METH)-seeking relapse is associated with memory and synaptic plasticity changes. Serotonin is a key neuromodulator in this process. While there is a known distribution of 5-HT1D receptors in reward and memory areas, such as the hippocampus, its physiological function is currently unknown. Here, we evaluated effect of a 5-HT1D receptor agonist, PNU142633, on the reinstatement of METH-seeking behavior and long-term potentiation. Rats were implanted with a cannula into lateral ventricle, then treated with saline or METH (5 mg/kg) during the acquisition phase of the conditioned place preference (CPP) test. On day 13 of the extinction phase, METH groups were divided into four groups: METH (0: saline, 1, or 2.5 (priming METH) mg/kg; i.p.) + vehicle (5 µl/rat) or a priming dose of METH (2.5 mg/kg; i.p.) + PNU (2 µg/5 µl; i.c.v.) and their preference scores were calculated on reinstatement day (day 14). Immediately following this, electrophysiology was performed to assay the field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude between groups. The results showed that CPP induction by METH gradually declined to extinction on days 12 and 13. A priming METH treatment significantly increased preference for the METH-paired chamber when compared with other groups, but pre-treatment with PNU significantly attenuated this effect. PS amplitude and fEPSP slopes in vehicle + priming METH rats were greater when compared with other groups. Furthermore, PNU attenuated the priming METH-induced increase in PS amplitude. These findings suggest that PNU can decrease synaptic transmission and prevent METH reinstatement in rats. |
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| AbstractList | Methamphetamine (METH)-seeking relapse is associated with memory and synaptic plasticity changes. Serotonin is a key neuromodulator in this process. While there is a known distribution of 5-HT1D receptors in reward and memory areas, such as the hippocampus, its physiological function is currently unknown. Here, we evaluated effect of a 5-HT1D receptor agonist, PNU142633, on the reinstatement of METH-seeking behavior and long-term potentiation. Rats were implanted with a cannula into lateral ventricle, then treated with saline or METH (5 mg/kg) during the acquisition phase of the conditioned place preference (CPP) test. On day 13 of the extinction phase, METH groups were divided into four groups: METH (0: saline, 1, or 2.5 (priming METH) mg/kg; i.p.) + vehicle (5 µl/rat) or a priming dose of METH (2.5 mg/kg; i.p.) + PNU (2 µg/5 µl; i.c.v.) and their preference scores were calculated on reinstatement day (day 14). Immediately following this, electrophysiology was performed to assay the field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude between groups. The results showed that CPP induction by METH gradually declined to extinction on days 12 and 13. A priming METH treatment significantly increased preference for the METH-paired chamber when compared with other groups, but pre-treatment with PNU significantly attenuated this effect. PS amplitude and fEPSP slopes in vehicle + priming METH rats were greater when compared with other groups. Furthermore, PNU attenuated the priming METH-induced increase in PS amplitude. These findings suggest that PNU can decrease synaptic transmission and prevent METH reinstatement in rats.Methamphetamine (METH)-seeking relapse is associated with memory and synaptic plasticity changes. Serotonin is a key neuromodulator in this process. While there is a known distribution of 5-HT1D receptors in reward and memory areas, such as the hippocampus, its physiological function is currently unknown. Here, we evaluated effect of a 5-HT1D receptor agonist, PNU142633, on the reinstatement of METH-seeking behavior and long-term potentiation. Rats were implanted with a cannula into lateral ventricle, then treated with saline or METH (5 mg/kg) during the acquisition phase of the conditioned place preference (CPP) test. On day 13 of the extinction phase, METH groups were divided into four groups: METH (0: saline, 1, or 2.5 (priming METH) mg/kg; i.p.) + vehicle (5 µl/rat) or a priming dose of METH (2.5 mg/kg; i.p.) + PNU (2 µg/5 µl; i.c.v.) and their preference scores were calculated on reinstatement day (day 14). Immediately following this, electrophysiology was performed to assay the field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude between groups. The results showed that CPP induction by METH gradually declined to extinction on days 12 and 13. A priming METH treatment significantly increased preference for the METH-paired chamber when compared with other groups, but pre-treatment with PNU significantly attenuated this effect. PS amplitude and fEPSP slopes in vehicle + priming METH rats were greater when compared with other groups. Furthermore, PNU attenuated the priming METH-induced increase in PS amplitude. These findings suggest that PNU can decrease synaptic transmission and prevent METH reinstatement in rats. •The 5-HT1D receptor agonist, PNU142633, attenuates METH-seeking behavior.•Preference for the METH-associated environment decreased in PNU + METH-primed rats.•PNU decreased LTP components in METH-primed rats.•PNU may decrease synaptic transmission and prevent METH reinstatement. Methamphetamine (METH)-seeking relapse is associated with memory and synaptic plasticity changes. Serotonin is a key neuromodulator in this process. While there is a known distribution of 5-HT1D receptors in reward and memory areas, such as the hippocampus, its physiological function is currently unknown. Here, we evaluated effect of a 5-HT1D receptor agonist, PNU142633, on the reinstatement of METH-seeking behavior and long-term potentiation. Rats were implanted with a cannula into lateral ventricle, then treated with saline or METH (5 mg/kg) during the acquisition phase of the conditioned place preference (CPP) test. On day 13 of the extinction phase, METH groups were divided into four groups: METH (0: saline, 1, or 2.5 (priming METH) mg/kg; i.p.) + vehicle (5 µl/rat) or a priming dose of METH (2.5 mg/kg; i.p.) + PNU (2 µg/5 µl; i.c.v.) and their preference scores were calculated on reinstatement day (day 14). Immediately following this, electrophysiology was performed to assay the field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude between groups. The results showed that CPP induction by METH gradually declined to extinction on days 12 and 13. A priming METH treatment significantly increased preference for the METH-paired chamber when compared with other groups, but pre-treatment with PNU significantly attenuated this effect. PS amplitude and fEPSP slopes in vehicle + priming METH rats were greater when compared with other groups. Furthermore, PNU attenuated the priming METH-induced increase in PS amplitude. These findings suggest that PNU can decrease synaptic transmission and prevent METH reinstatement in rats. |
| Author | Sadeghian, Reihaneh Shahidi, Siamak Komaki, Alireza Soleimani Asl, Sara |
| Author_xml | – sequence: 1 givenname: Siamak orcidid: 0000-0001-8196-5223 surname: Shahidi fullname: Shahidi, Siamak organization: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran – sequence: 2 givenname: Alireza surname: Komaki fullname: Komaki, Alireza organization: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran – sequence: 3 givenname: Reihaneh surname: Sadeghian fullname: Sadeghian, Reihaneh email: re.sadeghian1414@gmail.com organization: Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran – sequence: 4 givenname: Sara surname: Soleimani Asl fullname: Soleimani Asl, Sara organization: Anatomy Departments, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran |
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| CitedBy_id | crossref_primary_10_1007_s12576_019_00660_1 crossref_primary_10_1016_j_jchemneu_2019_01_008 crossref_primary_10_1007_s00210_023_02411_x crossref_primary_10_1038_s41398_020_00956_6 crossref_primary_10_1016_j_brainresbull_2019_03_008 crossref_primary_10_1016_j_heliyon_2022_e11432 |
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| Title | Effect of a 5-HT1D receptor agonist on the reinstatement phase of the conditioned place preference test and hippocampal long-term potentiation in methamphetamine-treated rats |
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