The chronic treatment in vivo of salicylate or morphine alters excitatory effects of subsequent salicylate or morphine tests in vitro in hippocampus area CA1

Sadegh, Mehdi; Fathollahi, Yaghoub; Semnanian, Saeed

doi:10.1016/j.ejphar.2013.09.048

Cited by 8 publications

(3 citation statements)

References 32 publications

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“…Herein, basal synaptic transmission at Sch‐CA1 synapses in the VH was affected by RME in such a way that basal synaptic transmission at Sch‐CA1 synapses was almost the same against the same stimulus intensity for the DH and VH slices obtained from animals that have been repeatedly exposed to morphine. It seems likely that RME entailed lasting changes in different regions along the hippocampal long axis in particular on Sch‐CA1 synapses as we have previously reported (Sadegh, Fathollahi, & Semnanian, 2013; Salmanzadeh et al, 2003). In this line, prior studies indicated that extracellular glutamate concentration in area CA1 was decreased in the mouse hippocampus after chronic morphine treatment, which suggests an adaptation of the glutamatergic neuronal transmission in the hippocampus (Guo et al, 2005).…”

Section: Discussionsupporting

confidence: 62%

A distinct impact of repeated morphine exposure on synaptic plasticity at Schaffer collateral‐CA1, temporoammonic‐CA1, and perforant pathway‐dentate gyrus synapses along the longitudinal axis of the hippocampus

et al. 2022

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We aimed to study how morphine affects synaptic transmission in the dentate gyrus and CA1 regions along the hippocampal long axis. For this, recording and measuring of field excitatory postsynaptic potentials (fEPSPs) were utilized to test the effects of repeated morphine exposure on paired-pulse evoked responses and long-term potentiation (LTP) at Schaffer collateral-CA1 (Sch-CA1), temporoammonic-CA1 (TA-CA1) and perforant pathway-dentate gyrus (PP-DG) synapses in transverse slices from the dorsal (DH), intermediate (IH), and ventral (VH) hippocampus in adult male rats. After repeated morphine exposure, the expression of opioid receptors and the α1 and α5 GABA A subunits were also examined. We found that repeated morphine exposure blunt the difference between the DH and the VH in their basal levels of synaptic transmission at Sch-CA1 synapses that were seen in the control groups. Significant paired-pulse facilitation of excitatory synaptic transmission was observed at Sch-CA1 synapses in slices taken from all three hippocampal segments as well as at PP-DG synapses in slices taken from the VH segment in the morphine-treated groups as compared to the control groups. Interestingly, significant paired-pulse inhibition of excitatory synaptic transmission was observed at TA-CA1 synapses in the DH slices from the morphine-treated group as compared to the control group. While primedburst stimulation (a protocol reflecting normal neuronal firing) induced a robust LTP in hippocampal subfields in all control groups, resulting in a decaying LTP at TA-CA1 synapses in the VH slices and at PP-DG synapses in both the IH and VH slices taken from the morphine-treated rats. In the DH of morphine-treated rats, we found increased levels of the mRNAs encoding the α1 and α5 GABA A subunits as compared to the control group. Taken together, these findings suggest the potential mechanisms through which repeated morphine exposure causes differential changes in circuit excitability and synaptic plasticity in the dentate gyrus and CA1 regions along the hippocampal long axis.

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Section: Discussionsupporting

confidence: 62%

A distinct impact of repeated morphine exposure on synaptic plasticity at Schaffer collateral‐CA1, temporoammonic‐CA1, and perforant pathway‐dentate gyrus synapses along the longitudinal axis of the hippocampus

et al. 2022

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“…Because chronic morphine consumption has shown epigenetic effects and causes durable abnormal activities in the hippocampus (9,16,31,32), epigenetic modifications are inheritable from parents to their offspring (12), and TNF-α and S100B are present in the hippocampus and involved in anomalous hippocampal functions (18,23). In the current research study, we investigate the consequences of chronic consumption of morphine by both male and female parents before mating and gestation on the hippocampus TNF-α and S100B levels of the parents themselves and their offspring.…”

Section: Introductionmentioning

confidence: 99%

Transgenerational modification of hippocampus TNF-α and S100B levels in the offspring of rats chronically exposed to morphine during adolescence

Amri

Sadegh

Moulaei

et al. 2017

The American Journal of Drug and Alcohol Abuse

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“…Salicylate treatment was reported to increase spontaneous neuronal activity and decrease the efficacy of inhibitory neurotransmission in the inferior colliculus and auditory cortex (7,8). However, the effect of salicylate on neural plasticity in the hippocampus, a key structure for numerous complex brain functions, including exploration, cognition, and memory, remains to be elucidated (9). …”

Section: Introductionmentioning

confidence: 99%

Salicylate-induced changes in immediate-early genes in the hippocampal CA1 area

Yin

et al. 2015

Molecular Medicine Reports

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Studies have suggested that salicylate affects neuronal function via interactions with specific membrane channels/receptors. However, the effect of salicylate on activity and synaptic morphology of the hippocampal Cornu Ammonis (CA) 1 area remains to be elucidated. The activation of immediate-early genes (IEGs) was reported to correlate with neuronal activity, in particular activity-regulated cytoskeleton-associated protein and early growth response gene 1. The aim of the present study was to evaluate the expression of these IEGs, as well that of N-methyl D-aspartate (NMDA) receptor subunit 2B in rats following acute and chronic salicylate treatment. Protein and messenger RNA levels of all three genes were increased in rats following chronic administration of salicylate (300 mg/kg for 10 days), returning to baseline levels 14 days post-cessation of treatment. The transient upregulation of gene expression following treatment was accompanied by ultrastructural alterations in hippocampal CA1 area synapses. An increase in synaptic interface curvature was observed as well as an increased number of presynaptic vesicles; in addition, postsynaptic densities thickened and lengthened. In conclusion, the results of the present study indicated that chronic exposure to salicylate may lead to structural alteration of hippocampal CA1 neurons, and it was suggested that this process occurs through induced expression of IEGs via NMDA receptor activation.

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The chronic treatment in vivo of salicylate or morphine alters excitatory effects of subsequent salicylate or morphine tests in vitro in hippocampus area CA1

Cited by 8 publications

References 32 publications

A distinct impact of repeated morphine exposure on synaptic plasticity at Schaffer collateral‐CA1, temporoammonic‐CA1, and perforant pathway‐dentate gyrus synapses along the longitudinal axis of the hippocampus

A distinct impact of repeated morphine exposure on synaptic plasticity at Schaffer collateral‐CA1, temporoammonic‐CA1, and perforant pathway‐dentate gyrus synapses along the longitudinal axis of the hippocampus

Transgenerational modification of hippocampus TNF-α and S100B levels in the offspring of rats chronically exposed to morphine during adolescence

Salicylate-induced changes in immediate-early genes in the hippocampal CA1 area

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