Endogenous opiates and behavior: 2012

Bodnar, Richard J.

doi:10.1016/j.peptides.2013.10.001

Cited by 88 publications

(59 citation statements)

References 950 publications

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“…Moreover, inhibitory networks in the amygdala were found to control the specificity of fear learning, thus preventing fear generalization (Lange et al, 2014), and are crucial for fear extinction (Paré et al, 2003;Likhtik et al, 2008;Ehrlich et al, 2009;Amano et al, 2010). Among the diverse inhibitory neurons of the amygdala, the subpopulation of intercalated neurons (ITCs) has attracted much attention.…”

Section: Introductionmentioning

confidence: 99%

μ-Opioid Receptor-Mediated Inhibition of Intercalated Neurons and Effect on Synaptic Transmission to the Central Amygdala

et al. 2015

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Section: Introductionmentioning

confidence: 99%

μ-Opioid Receptor-Mediated Inhibition of Intercalated Neurons and Effect on Synaptic Transmission to the Central Amygdala

et al. 2015

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“…The opioid system plays a central role in nociception and analgesia, and also regulates numerous physiological functions as respiration, gastrointestinal transit and response to stress, as well as endocrine and immune functions (BODNAR 2013). Since 1992 when the first opioid receptor gene was identified by expression cloning several homologous genes were discovered.…”

mentioning

confidence: 99%

“…The opioid receptor gene family consists of three members encoding mu (MOR, Oprm1), delta (DOR, Oprd1), kappa (KOR, Oprk1) receptors and recently the nonopioid orphaninFQ/nociceptin (NOR, Oprl1) receptor was included. These receptors are membrane receptors with a seven-transmembrane topology and belong to the large G protein-coupled receptor superfamily (BODNAR 2013).…”

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confidence: 99%

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The Effect of CRH, Dexamethasone and Naltrexone on the Mu, Delta and Kappa Opioid Receptor Agonist Binding in Lamb Hypothalamic-Pituitary-Adrenal Axis

Pierzchała-Koziec¹,

Dziedzicka-Wasylewska²,

Oeltgen³

et al. 2015

folia biol (krakow)

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PIERZCHA£A-KOZIEC K., DZIEDZICKA-WASYLEWSKA M.,OELTGEN P., ZUBEL-£OJEK J., LATACZ A., OC£OÑ E. 2015. The effect of CRH, dexamethasone and naltrexone on the mu, delta and kappa opioid receptors agonist binding in lamb hypothalamic-pituitary-adrenal axis. Folia Biologica (Kraków) 63: [187][188][189][190][191][192][193].The aim of the study was to evaluate changes in the opioid receptor binding (mu, delta and kappa) in the hypothalamus, anterior pituitary and adrenal cortex (HPA) of lambs treated in vivo with corticotrophin releasing hormone (CRH), naltrexone, an opioid receptor antagonist (NAL), and dexamethasone, a potent cortisol analog (DEX). Experiment was carried out on 3 months old female lambs of polish mountain strain. Lambs received a single i.v. injection of NaCl (control), CRH (alone or in combination with naltrexone), naltrexone or dexamethasone. One hour later animals were decapitated under anaesthesia, tissues were dissected out and receptor binding assays were performed with radioligands for each type of opioid receptors -! H-DAGO, ! H-DPDPE and ! H-EKC for mu, delta and kappa receptor, respectively. Coexistence of specific binding sites for each type of opioid receptor was demonstrated in all levels of HPA axis of control lambs, however their distribution was uneven. Acute treatment with CRH, DEX and NAL caused downregulation or upregulation of mu, delta, kappa receptor binding in each level of HPA axis. CRH effects on mu, delta and kappa opioid receptor binding varied within the HPA axis and were modulated by naltrexone. Treatment with naltrexone increased in vitro mu, delta and kappa receptor binding in most tested structures except delta receptor binding in adrenal (decrease by 52%) and kappa receptor binding in pituitary (decrease by 41%). Dexamethasone significantly decreased the mu, delta and kappa opioid receptor binding in adrenal cortex but differentially affected opioid receptor binding in hypothalamus and pituitary. It seems probable that endogenous opioid peptides acting through mu, delta and kappa receptors interact with the hormones released from the hypothalamic-pituitary-adrenal axis in physiological and pathophysiological situations.

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“…[22][23][24] Nitric oxide acts as an intracellular signaling molecule -neurotransmitter itself and/or as a neuromodulator and influences the plastic properties of the neurons. [25][26] It is also involved in NO-molecular ways, which affect through auto-regulation different signaling molecules-like opioids, endocannabinoids and others. [27] In addition, it is well known that immobilization stress activates neuronal NOS in the HPA axis.…”

Section: Page 28mentioning

confidence: 99%

Effects of Immobilization Stress on Nitric Oxide Active Neurons in Rat’s dlPAG; Histochemical Study

Георгиев¹

2016

AANAT

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Background: Exposure to stress-factors caused an array of biochemical, physiological and behavioral changes. According to literature data, specific stressors may elicit specific responses, and different stressors may activate different brain systems by using specific pathways within the central nervous system. Several brain structures, including the periaqueductal gray (PAG), have been implicated in the functional neuroanatomy of stress response. The dorsolateral column of the periaqueductal gray (dlPAG) integrates aversive emotional experiences and represents an important site responding to life threatening situations. It was reported that nitric oxide (NO) affects the neuronal activity of the PAG. The goal of the present study was to investigate the changes of NO activity in the dlPAG of immobilized rats using a histochemical examination of the distribution of NADPH-d reactivity neurons. Our results showed that NO activity in rat's dlPAG was significantly increased by acute immobilization stress. This suggests a pivotal role of this part of the brain and NO-ergic system in stress response which main role is to attenuate the effect of stress and to restore the homeostasis. Methods: The experiments were carried out on male Wistar rats (180-200g), divided into two groups. The first group represented intact controls. The second group was subjected to acute immobilization stress. Results: The acute stressor -1 hour immobilization, showed statistically significant increase in the number of the NADPH-d positive neurons compared to the control group (p < 0.01). Conclusion: NO activity in rat's dlPAG was significantly increased by acute immobilization stress.

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Endogenous opiates and behavior: 2012

Cited by 88 publications

References 950 publications

μ-Opioid Receptor-Mediated Inhibition of Intercalated Neurons and Effect on Synaptic Transmission to the Central Amygdala

μ-Opioid Receptor-Mediated Inhibition of Intercalated Neurons and Effect on Synaptic Transmission to the Central Amygdala

The Effect of CRH, Dexamethasone and Naltrexone on the Mu, Delta and Kappa Opioid Receptor Agonist Binding in Lamb Hypothalamic-Pituitary-Adrenal Axis

Effects of Immobilization Stress on Nitric Oxide Active Neurons in Rat’s dlPAG; Histochemical Study

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