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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Published in:Brain research Vol. 1698; pp. 151 - 160
Main Authors: Shahidi, Siamak, Komaki, Alireza, Sadeghian, Reihaneh, Soleimani Asl, Sara
Format: Journal Article
Language:English
Published: Elsevier B.V 01.11.2018
Subjects:
Long-term potentiation
Methamphetamine
Reinstatement
Reward
Serotonin receptor
PP
CPP
DG
PS
Long-term potentiation
Methamphetamine
EPSP
METH
LTP
fEPSP
HFS
Serotonin receptor
Reinstatement
Reward
ISSN:0006-8993, 1872-6240, 1872-6240
Online Access:Get full text
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Summary:•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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ISSN:0006-8993
1872-6240
1872-6240
DOI:10.1016/j.brainres.2018.07.030