The effect of forced swim stress on morphine sensitization: Involvement of D1/D2-like dopamine receptors within the nucleus accumbens

Charmchi, Elham; Zendehdel, Morteza; Haghparast, Abbas

doi:10.1016/j.pnpbp.2016.05.006

Cited by 13 publications

(4 citation statements)

References 46 publications

(69 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present study indicates that subcutaneous injection of morphine (5 mg/kg) for three consecutive days followed by five days of free-morphine administration induced sensitization to the antinociceptive response of morphine (1 mg/kg but not morphine 0.1 or 0.5 mg/kg). In this respect, certain similar studies indicated that repeated administration of morphine (5 mg/kg; SC) for three consecutive days followed by five days of washout increased antinociceptive responses of morphine (1 mg/kg) in sensitized animals ( Charmchi et al, 2016 ; Molaei, Sanati, Zaringhalam, & Haghparast, 2014 ; Reisi et al, 2014 ). On the other hand, it has been reported that repeated morphine administration (20 mg/kg; IP) for seven days ( Roeckel et al, 2017 ) or a regimen of three days of morphine (20 mg/kg; IP) followed by a five days washout led to opioid-induced hyperalgesia in mice ( Ahmadi, Golbaghi, Azizbeigi, & Esmailzadeh, 2014 ).…”

Section: Discussionmentioning

confidence: 92%

“…Development of behavioral sensitization, defined as an enhanced systemic reaction to the same dose of morphine or any other addictive substance, occurs in response to continuous and intermittent administration of these drugs in rodents ( Lv et al, 2019 ; Reisi, Bani-Ardalan, Zarepour, & Haghparast, 2014 ; Vezina & Leyton, 2009 ). Several neurotransmitters and neuromodulators are involved in opioid-induced behavioral sensitization, including dopamine ( Charmchi, Zendehdel, & Haghparast, 2016 ), glutamate ( Sepehrizadeh, Sahebgharani, Ahmadi, Shapourabadi, Bozchlou, & Zarrindast, 2008 ), serotonin ( Pang et al, 2016 ), and orexin ( Łupina et al, 2018 ; Razavi, Karimi, Bani-Ardalan, & Haghparast, 2014 ). The Ventral Tegmental Area (VTA) and Nucleus Accumbens (NAc) play a predominant role in developing morphine sensitization via dopamine receptor activation ( Reisi et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Role of the Orexinergic System Within the Ventral Tegmental Area in the Development of Sensitization to Morphine Induced by Lateral Hypothalamus Stimulation

Haghparast¹,

Rashvand²

2022

BCN

View full text Add to dashboard Cite

The lateral hypothalamus (LH) has long been known to implicate in the addictive behaviors of drugs of abuse. The ventral tegmental area (VTA) is a major area of the mesolimbic system that is strongly involved in the development of morphine sensitization. The current study aimed to examine the role of intra-VTA orexin receptors in the LH stimulation-induced sensitization to the antinociceptive response of morphine. One hundred fourteen adult male Wistar rats underwent unilateral implantation of two separate cannulae into the LH and VTA using the stereotaxic apparatus. Intra-VTA administration of the orexin-1 (OX1) and orexin-2 (OX2) receptor antagonists, SB334867 and TCS OX2 29 (1, 3, and 10nM/0.3μl DMSO), respectively, was performed five minutes before concurrent microinjection of carbachol (250nM/0.5μl saline) into the LH and an ineffective dose of morphine (0.5 mg/kg; sc) during 3-day sensitization period. After a 5-day free drug period, on the 9th day, for assessing the morphine sensitization, the nociceptive response was measured before and after morphine injection (1 mg/kg; sc) using the tail-flick test. The results revealed that the concurrent administration of carbachol (250 nM) and an ineffective dose of morphine significantly induced morphine sensitization. Besides, the blockade of OX1 and OX2 receptors within the VTA before intra-LH carbachol injection attenuated morphine sensitization. These findings suggest that LH stimulation potentiates the sensitization to morphine antinociceptive responses via affecting orexin receptors located in the VTA. However, the contribution of OX1Rs in the VTA was more predominant than that of OX2Rs to morphine sensitization in the rat.

show abstract

Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Role of the Orexinergic System Within the Ventral Tegmental Area in the Development of Sensitization to Morphine Induced by Lateral Hypothalamus Stimulation

Haghparast¹,

Rashvand²

2022

BCN

View full text Add to dashboard Cite

show abstract

“…Transgenic mice null to the expression of D1 dopamine receptors (D1DRs) do not develop locomotor sensitization to morphine (Becker et al, 2001). Both D1DRs and D2 dopamine receptors (D2DRs) were also demonstrated to mediate the rewarding properties of morphine (Wang et al, 2008; Assar et al, 2016; Charmchi et al, 2016; Maldonado et al, 1997; Shippenberg and Herz, 1988; Shippenberg et al, 1993; Wang et al, 2015), as well as drug- and stress-priming reinstatement of morphine CPP (Farahimanesh et al, 2018; Farzinpour et al, 2018; Assar et al, 2016). D1DRs were demonstrated to be involved in the induction of extracellular-signal-regulated kinase (ERK) and cAMP response element-binding protein (CREB) phosphorylation (Kirschmann et al, 2014; Shi and McGinty, 2011; Zhang and Xu, 2006; Jenab et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Pre-exposure of adolescent mice to morphine results in stronger sensitization and reinstatement of conditioned place preference than pre-exposure to hydrocodone

2020

View full text Add to dashboard Cite

Background: Opioids are commonly prescribed to treat moderate-to-severe pain. However, their use can trigger the development of opioid use disorder. A major problem in treating opioid use disorder remains the high rate of relapse. Aim: The purpose of this study was to determine whether there are differences among opioids in their ability to trigger relapse after pre-exposure during adolescence. Methods: On postnatal day 33, mice were examined for the acute locomotor response to saline, morphine, or hydrocodone (5 mg/kg). They were administered with the corresponding opioid or saline during postnatal days 34–38 (20 mg/kg) and 40–44 (40 mg/kg). On postnatal day 45, they were recorded for the development of locomotor sensitization (5 mg/kg). Starting on postnatal day 55, mice were examined for the acquisition (1, 5, 10, 20, and 40 mg/kg), extinction, and drug-induced reinstatement (1, 2.5, and 5 mg/kg) of conditioned place preference. Results: There were no significant differences in the acute locomotor response to morphine and hydrocodone. Morphine induced significantly stronger locomotor sensitization as compared to hydrocodone. Pre-exposure to morphine, but not hydrocodone, sensitized the acquisition of conditioned place preference. There were no significant differences in extinction rates. Mice pre-exposed to morphine reinstate conditioned place preference after priming with a 1 mg/kg dose. In contrast, higher priming doses were required for reinstatement in all other experimental groups. Conclusions: Adolescent mice administered with morphine develop greater sensitization to its effects and subsequently reinstate conditioned place preference more readily than mice administered with hydrocodone. This suggests higher risk for relapse after pre-exposure to morphine during adolescence as compared to hydrocodone.

show abstract

“…These neurotransmitters necessitate the abundant release of dopamine (100 times resting state) and subsequently temporary hypodopaminergic functioning. Repeated, or prolonged stress can induce a chronic hypodopaminergic state (40). Cue-triggered craving involves the basolateral nucleus of the amygdala, the hippocampus, and through glutaminergic activation causes an enhanced release of dopamine that if chronic ultimately leads to a hypodopaminergic state.…”

Section: The Epigenetics Of Prolonged Exposure and Stressmentioning

confidence: 99%

Substance use disorder a bio-directional subset of reward deficiency syndrome

et al. 2017

View full text Add to dashboard Cite

This commentary is to inform clinicians challenged with an increase in people seeking treatment for Substance Use Disorder (SUD), that the ninety percent revolving door, is, in part, due to post-withdrawal, untreated neurotoxicity. This impairment attenuates neurotransmitter signaling and compromises resting state functional connectivity, leading to unwanted sequelae including depression, sleep disturbances, sensation seeking, lack of satisfaction and impulsivity. Neuroimaging studies indicate that neurobiological recovery can take years. Like a "double edge sword" SUD has a biological bi -directional (bio-directional) effect on the brain reward circuitry. The acute intake of psychoactive drugs results in heightened dopaminergic activity, while, the opposite, hypodopaminergia occurs following chronic abuse. Individuals with SUD can have a genetic predisposition, compounded by stress and neurotoxically induced, epigenetic insults that impact recovery from protracted abstinence. Follow-up post -short-term recovery usually includes supportive therapies and programs like 12 -steps and other fellowships. However, relapse will usually occur if post -short-term recovery hypodopaminergia is not treated with attempts at epigenetic manipulation of compromised brain neurochemistry using some manner of pro-dopamine regulation.

show abstract

The effect of forced swim stress on morphine sensitization: Involvement of D1/D2-like dopamine receptors within the nucleus accumbens

Cited by 13 publications

References 46 publications

Role of the Orexinergic System Within the Ventral Tegmental Area in the Development of Sensitization to Morphine Induced by Lateral Hypothalamus Stimulation

Role of the Orexinergic System Within the Ventral Tegmental Area in the Development of Sensitization to Morphine Induced by Lateral Hypothalamus Stimulation

Pre-exposure of adolescent mice to morphine results in stronger sensitization and reinstatement of conditioned place preference than pre-exposure to hydrocodone

Substance use disorder a bio-directional subset of reward deficiency syndrome

Contact Info

Product

Resources

About