D1‐ and D2‐like dopamine receptors within the nucleus accumbens contribute to stress‐induced analgesia in formalin‐related pain behaviours in rats

Faramarzi, Golnaz; Zendehdel, Morteza; Haghparast, Abbas

doi:10.1002/ejp.865

Cited by 39 publications

(21 citation statements)

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“…Electrophysiological and neuroanatomical evidence has also shown that distinct populations of NAc neurons differentially encode information about goal-directed behaviors for natural (food/water) and cocaine reinforcement (Carelli et al, 2000; Carelli and Wondolowski, 2003; Carelli and Wondolowski, 2006; Castro et al, 2015), while selected neuronal subpopulations of the NAc in the monkey are differently activated by cocaine and juice rewards (Bowman et al, 1996; Hutsell et al, 2016). All these data suggest that there are different and parallel microcircuits mediating the natural and drug-rewarding effects in the NAc (Alizamini et al, 2017; Faramarzi et al, 2016), although the relevant neurotransmitters have not been identified. Our results are consistent with the view that there are distinct neuronal populations within the NAc that mediate seeking behaviors for natural and drug rewards.…”

Section: Discussionmentioning

confidence: 99%

Melanin-concentrating hormone in rat nucleus accumbens or lateral hypothalamus differentially impacts morphine and food seeking behaviors

et al. 2020

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Background: Identifying neural substrates that are differentially affected by drugs of abuse and natural rewards is key to finding a target for an efficacious treatment for substance abuse. Melanin-concentrating hormone is a polypeptide with an inhibitory effect on the mesolimbic dopamine system. Here we test the hypothesis that melanin-concentrating hormone in the lateral hypothalamus and nucleus accumbens shell is differentially involved in the regulation of morphine and food-rewarded behaviors. Methods: Male Sprague–Dawley rats were trained with morphine (5.0 mg/kg, subcutaneously) or food pellets (standard chow, 10–14 g) to induce a conditioned place preference, immediately followed by extinction training. Melanin-concentrating hormone (1.0 µg/side) or saline was infused into the nucleus accumbens shell or lateral hypothalamus before the reinstatement primed by morphine or food, and locomotor activity was simultaneously monitored. As the comparison, melanin-concentrating hormone was also microinjected into the nucleus accumbens shell or lateral hypothalamus before the expression of food or morphine-induced conditioned place preference. Results: Microinfusion of melanin-concentrating hormone into the nucleus accumbens shell (but not into the lateral hypothalamus) prevented the reinstatement of morphine conditioned place preference but had no effect on the reinstatement of food conditioned place preference. In contrast, microinfusion of melanin-concentrating hormone into the lateral hypothalamus (but not in the nucleus accumbens shell) inhibited the reinstatement of food conditioned place preference but had no effect on the reinstatement of morphine conditioned place preference. Conclusions: These results suggest a clear double dissociation of melanin-concentrating hormone in morphine/food rewarding behaviors and melanin-concentrating hormone in the nucleus accumbens shell. Melanin-concentrating hormone could be a potential target for therapeutic intervention for morphine abuse without affecting natural rewards.

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Section: Discussionmentioning

confidence: 99%

Melanin-concentrating hormone in rat nucleus accumbens or lateral hypothalamus differentially impacts morphine and food seeking behaviors

et al. 2020

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“…Moreover, it has been reported that the pain relief produced by an intrathecal injection of pregabalin in a model of spinal nerve ligation is accompanied by increase in the levels of NAc dopamine, and effect detected during the early but not during the late phase of the experimentally induced neuropathic pain ( Kato et al, 2016 ). Conversely, intra-accumbal infusions of D1- (SCH-23390) and D2-like (Sulpiride) dopamine receptors antagonists reduces stress-induced analgesia in a dose-dependent manner, in the early and late phases of an experimental model of persistent inflammatory pain, though with more pronounced effects found throughout the late phase ( Faramarzi et al, 2016 ).…”

Section: Molecular Targets At the Reward Circuitry For Pain Reliefmentioning

confidence: 99%

Reward Circuitry Plasticity in Pain Perception and Modulation

2017

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Although pain is a widely known phenomenon and an important clinical symptom that occurs in numerous diseases, its mechanisms are still barely understood. Owing to the scarce information concerning its pathophysiology, particularly what is involved in the transition from an acute state to a chronic condition, pain treatment is frequently unsatisfactory, therefore contributing to the amplification of the chronic pain burden. In fact, pain is an extremely complex experience that demands the recruitment of an intricate set of central nervous system components. This includes cortical and subcortical areas involved in interpretation of the general characteristics of noxious stimuli. It also comprises neural circuits that process the motivational-affective dimension of pain. Hence, the reward circuitry represents a vital element for pain experience and modulation. This review article focuses on the interpretation of the extensive data available connecting the major components of the reward circuitry to pain suffering, including the nucleus accumbens, ventral tegmental area, and the medial prefrontal cortex; with especial attention dedicated to the evaluation of neuroplastic changes affecting these structures found in chronic pain syndromes, such as migraine, trigeminal neuropathic pain, chronic back pain, and fibromyalgia.

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“…17 , 19 In modulation of pain and hyperalgesia, dopamine plays a major role in different areas of the brain including basal ganglia, 38 and it is one of the main sensitive pathways implicated in pain management. 39 Dopamine D1 receptor antagonist SCH-23,390 attenuate prostaglandin E2 (PGE 2 ) induced hyperalgesia and neuropathic allodynia. 40 Computationally, 4-FBS is a D1 receptor antagonist (support file 1) and it may be suggested that its anti-nociceptive, anti-allodynic activity is due to its antagonistic activity on the D1 receptor.…”

Section: Discussionmentioning

confidence: 99%

<p>Analgesic and Antiallodynic Effects of 4-Fluoro-N-(4-Sulfamoylbenzyl) Benzene Sulfonamide in a Murine Model of Pain</p>

Rehman¹,

al‐Rashida²,

Tokhi³

et al. 2020

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Introduction Physical, chemical, thermal injuries along with infectious diseases lead to acute pain with associated inflammation, being the primary cause of hospital visits. Moreover, neuropathic pain associated with diabetes is a serious chronic disease leading to high morbidity and poor quality of life. Objective Earlier multiple sulphonamides have been reported to have an antinociceptive and antiallodynic profile. 4-Fluoro-N-(4-sulfamoylbenzyl) Benzene Sulfonamide (4-FBS), a synthetic sulfonamide with reported carbonic anhydrase inhibitory activity, was investigated for its potential effects in mice model of acute and diabetic neuropathic pain. Methods and Results 4-FBS was given orally (p.o.) one hour before the test and then mice were screened for antinociceptive activity by using the tail immersion test, which showed significant antinociceptive effect at both 20 and 40 mg/kg doses. To explore the possible mechanisms, thermal analgesia of 4-FBS was reversed by the 5HT 3 antagonist ondansetron 1mg/kg intraperitoneally (i.p.) and by the µ receptor antagonist naloxone (1 mg/kg i.p.), implying possible involvement of serotonergic and opioidergic pathways in the analgesic effect of 4-FBS. Diabetes was induced in mice by a single dose of streptozotocin (STZ) 200 mg/kg i.p. After two weeks, animals first became hyperalgesic and progressively allodynic in the fourth week, which was evaluated through behavioral parameters like thermal and mechanical tests. 4-FBS at 20 and 40 mg/kg p.o. significantly reversed diabetes-induced hyperalgesia and allodynia at 30, 60, 90, and 120 minutes. Conclusion These findings are significant and promising while further studies are warranted to explore the exact molecular mechanism and the potential of 4-FBS in diabetic neuropathic pain.

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D1‐ and D2‐like dopamine receptors within the nucleus accumbens contribute to stress‐induced analgesia in formalin‐related pain behaviours in rats

Cited by 39 publications

References 30 publications

Melanin-concentrating hormone in rat nucleus accumbens or lateral hypothalamus differentially impacts morphine and food seeking behaviors

Melanin-concentrating hormone in rat nucleus accumbens or lateral hypothalamus differentially impacts morphine and food seeking behaviors

Reward Circuitry Plasticity in Pain Perception and Modulation

<p>Analgesic and Antiallodynic Effects of 4-Fluoro-N-(4-Sulfamoylbenzyl) Benzene Sulfonamide in a Murine Model of Pain</p>

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