Opioid receptors in the ventral tegmental area contribute to stress-induced analgesia in the formalin test for tonic pain
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Cited by (34)
Blockade of the orexin receptors in the ventral tegmental area could attenuate the stress-induced analgesia: A behavioral and molecular study
2023, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :VTA stimulation has been shown to reduce nociceptive experience (Li et al., 2016), and VTA lesion exacerbates pain and enhances pain threshold in several pain models (Saadé et al., 1997; Sotres-Bayón et al., 2001; Takeda et al., 2005). Moreover, a body of evidence implied the role of acute stress in VTA neuron activity and thereby the induction of analgesia (Altier and Stewart, 1996; Altier and Stewart, 1999; Askari et al., 2021). An extracellular signal-regulated kinase (ERK) is a candidate signaling molecule mediating stress responses (Iniguez et al., 2010).
Enriched environment and social isolation differentially modulate addiction-related behaviors in male offspring of morphine-addicted dams: The possible role of μ-opioid receptors and ΔFosB in the brain reward pathway
2021, Brain Research BulletinCitation Excerpt :Opioid neurons and their receptors widely express throughout limbic structures. Activation of μ-opioid receptors in the midbrain modulate behavioral and autonomic responses to external stressors (Altier and Stewart, 1996; Cristina-Silva et al., 2017). Endogenous μ-opioid receptor agonist, β-endorphins regulates stress hormone and its negative feedback in HPA axis (Lovallo et al., 2015).
Stress-induced modulation of pain: Role of the endogenous opioid system
2018, Progress in Brain ResearchCitation Excerpt :Initial evidence suggesting a role of the opioids came from the work of Akil and coworkers who reported that both stimulation-produced analgesia and SIA were blocked by naloxone, a nonselective opioid receptor antagonist (Akil et al., 1976a,b). Since then, a large number of studies have been reported where systemic, intracerebral, or intrathecal administration of nonselective opioid receptor antagonists (mostly naloxone and naltrexone) reversed SIA in rodents exposed to a variety of stress paradigms including, but not limited to, restraint/immobilization (Amir and Amit, 1978; Kavaliers and Hirst, 1986; Konecka and Sroczynska, 1990; Porro and Carli, 1988), foot or tail shock (Altier and Stewart, 1996; Whitehouse et al., 1985), forced swim (Carmody and Cooper, 1987; Vaccarino et al., 1992), acoustic (Helmstetter and Bellgowan, 1994), social isolation (Han et al., 2016; Konecka and Sroczynska, 1990), social defeat (Miczek et al., 1985), conditioned fear (Butler et al., 2008; Foo and Helmstetter, 2000), and odors from stressed conspecifics (Fanselow, 1985), strongly suggesting the involvement of both supraspinal and spinal opioidergic signaling in mediating SIA (see Table 1 for the complete list). However, many studies have also demonstrated SIA in rodents that was not sensitive to opioid receptor antagonists and several different mechanisms have been proposed in the mediation of such nonopioid SIA (for review, see Butler and Finn, 2009; Yamada and Nabeshima, 1995).
Mechanisms of placebo analgesia: A dual-process model informed by insights from cross-species comparisons
2018, Progress in NeurobiologyModulation of pain, nociception, and analgesia by the brain reward center
2016, NeuroscienceCitation Excerpt :Furthermore, there is very little information on the actions of opiate analgesics in the brain reward circuit under chronic pain states, and most of the published studies concern behavioral findings. Initial evidence came from a study showing that blockade of dopamine receptors in the NAc prevented the analgesic effects of morphine in the formalin test in rats (Altier and Stewart, 1996). Furthermore, blockade of dopamine D2-type receptors in the NAc shell by raclopride prevented the effects of morphine and substance P-analogs, providing the first evidence of tonic pain inhibition by the mesolimbic dopamine system.
Uliginosin B presents antinociceptive effect mediated by dopaminergic and opioid systems in mice
2012, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :The interaction between opioid and dopaminergic pathways in pain modulation and nociception has been discussed by several authors: dopaminergic receptor antagonists attenuate nociception induced by morphine in ventral tegmental area (Altier and Stewart, 1998); systemic administration of morphine alters dopamine spinal levels (Weilfugazza and Godefroy, 1991) and this raise was not influenced by dopaminergic antagonists (Millan, 2002); depletion of the gene encoding D2 receptors or administration of an antisense probe directed against D2 receptors potentiated antinociception elicited by μ and κ-opioid agonists (King et al., 2001); D2 agonists enhance opioid antinociception (Kamei and Saitoh, 1996; Millan, 2002; Zarrindast et al., 1999). Furthermore, Altier and Stewart (1993, 1996) demonstrated that the ventral tegmental area is associated with opioid and dopaminergic nociception and Ambrose and co-workers suggested the co-existence between opioid and dopaminergic receptors in striatal neurons (Ambrose et al., 2004, 2006). Dorsolateral striatum D2 receptors, but not D1, are involved in the modulation of persistent nociception (Magnusson and Fisher, 2000).