Serotonin‐Mediated Increases in the Extracellular Levels of β‐Endorphin in the Arcuate Nucleus and Nucleus Accumbens : A Microdialysis Study

Zangen, Abraham; Nakash, R.; Yadid, Gal

doi:10.1046/j.1471-4159.1999.0732569.x

Cited by 42 publications

(36 citation statements)

References 31 publications

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“…In the case of nicotine-induced increases in BP, this 'deactivation' of neurotransmission would require that considerable endogenous opioid tone would be present in the denicotinized smoking condition. Although this was not directly investigated in the present report, substantial baseline endogenous opioid tone has been described in the rodent basal ganglia (Zangen et al, 1999) and amygdala (Kraus et al, 1996;Gestreau and Besson, 2000). Consistent with the presence of this tone in human subjects, the opioid receptor antagonist naloxone increased the activity of a number of cortical (eg anterior cingulate, prefrontal and insular, entorhinal and parahippocampal cortices) and subcortical (eg basal ganglia, hippocampus) regions in a recent fMRI study (Borras et al, 2004).…”

Section: Discussionsupporting

confidence: 63%

Smoking Modulation of μ-Opioid and Dopamine D2 Receptor-Mediated Neurotransmission in Humans

Scott

Domino

Heitzeg

et al. 2006

Neuropsychopharmacol

112

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This is a pilot examination of the hypothesis that some of the effects of smoking cigarettes in humans are mediated through nicotine activation of opioid and dopamine (DA) neurotransmission. Neuroimaging was performed using positron emission tomography and the radiotracers [11 C]carfentanil and [ 11 C]raclopride, labeling m-opioid and DA D2 receptors, respectively. Six healthy male smokers were abstinent overnight. After radiotracer administration, subjects smoked two denicotinized cigarettes, followed 45 min later by two average nicotine cigarettes. Dynamic data were acquired over 90 min, and transformed into parametric maps of receptor availability in vivo (binding potential, BP), corresponding to low and high nicotine smoking periods and analyzed on a voxel-by-voxel basis using SPM'99 and correction for multiple comparisons. Significant activation of m-opioid receptor-mediated neurotransmission from denicotinized to average nicotine conditions was observed in the right anterior cingulate cortex. DA D2 neurotransmission was activated in the ventral basal ganglia, correlating with Fagerströ m scale nicotine dependence scores. Lower m-opioid receptor BP was also detected during the denicotinized smoking condition in the smoker group, compared to baseline scans in non-smokers, in the cingulate cortex, thalamus, ventral basal ganglia, and amygdala. These reductions were reversed during the average nicotine condition in the thalamus, ventral basal ganglia and amygdala. These data point to both the feasibility of simultaneously examining opioid and DA neurotransmission responses to smoking in humans, as well as to the need to examine non-nicotine aspects of smoking to more fully understand the behavioral effects of this drug.

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Section: Discussionsupporting

confidence: 63%

Smoking Modulation of μ-Opioid and Dopamine D2 Receptor-Mediated Neurotransmission in Humans

Scott

Domino

Heitzeg

et al. 2006

Neuropsychopharmacol

112

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“…It was also shown that 5-HT, either endogenous or exogenously delivered, facilitate the release of b-endorphin in the arcuate nucleus and nucleus accumbens (32). According to the findings of Gemma et al (33), activation of the hypothalamic serotonergic system was produced by central injection of IL-1b.…”

Section: Discussionmentioning

confidence: 97%

Pyrogens Enhance β-Endorphin Release in Hypothalamus and Trigger Fever That Can Be Attenuated by Buprenorphine

Tsai¹,

Lin

Wang

et al. 2003

J Pharmacol Sci

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Abstract. At first, we investigated whether both b-endorphin release level in the hypothalamus and body temperature can be altered after intracerebroventricular (i.c.v.) injection of either lipopolysaccharide (LPS), interleukin-1b (IL-1b), or prostaglandin E 2 (PGE 2 ) in rats. It was found that in the rat, i.c.v. administration of either LPS (0.5 m g in 10 m l), IL-1b (10 ng in 10 ml), or PGE 2 (200 ng in 10 ml), in addition to producing fever, upregulated the immunoreactivity of b-endorphin in the preoptic anterior hypothalamus of rat brain. Secondarily, we assessed whether the fever induced by either LPS, IL-1b, or PGE 2 can be altered by pretreatment with buprenorphine (an opioid receptor antagonist). The results revealed that i.c.v. administration of buprenorphine (1 -10 m g in 10 ml) alone had an insignificant effect on the body temperature. However, the fever induced by i.c.v. injection of either LPS, IL-1b, or PGE 2 was significantly attenuated by pretreatment with i.c.v. injection of buprenorphine 1 h before the pyrogen injection in rats. The results suggest that pyrogens enhance b-endorphin release in the hypothalamus and trigger fever which can be attenuated by buprenorphine, an opioid receptor antagonist.

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“…In this regard, considerable basal ␤-endorphin tone has been directly described in microdialysis studies in some of these regions (arcuate nucleus, nucleus accumbens) (Zangen et al, 1999). Indirectly, through the assessment of increases in glucose metabolism or c-fos expression after low dose naloxone administration, tonic endogenous opioid activity has been described in the brainstem regions and the amygdala of rodents (Kraus et al, 1996;Gestreau and Besson, 2000).…”

Section: Discussionmentioning

confidence: 99%

Pronociceptive and Antinociceptive Effects of Estradiol through Endogenous Opioid Neurotransmission in Women

Smith¹,

Stohler²,

Nichols³

et al. 2006

J. Neurosci.

304

188

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Prominent interindividual and sex-dependent differences have been described in responses to sustained pain and other stressful stimuli. Variations in -opioid receptor-mediated endogenous opioid neurotransmission may underlie some of these processes. We examined both baseline -opioid receptor levels and the activation of this neurotransmitter system during sustained pain using positron emission tomography in a sample of young healthy men and women. Women were studied twice, during low and high estrogen states. The high-estrogen state was associated with regional increases in baseline -opioid receptor availability in vivo and a greater activation of endogenous opioid neurotransmission during the pain stressor. The latter did not differ from that obtained in males. During the low estrogen condition, however, significant reductions in endogenous opioid tone were observed at the level of thalamus, nucleus accumbens, and amygdala, which were associated with hyperalgesic responses. Estrogen-associated variations in the activity of -opioid neurotransmission correlated with individual ratings of the sensory and affective perceptions of the pain and the subsequent recall of that experience. These data demonstrate a significant role of estrogen in modulating endogenous opioid neurotransmission and associated psychophysical responses to a pain stressor in humans.

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Serotonin‐Mediated Increases in the Extracellular Levels of β‐Endorphin in the Arcuate Nucleus and Nucleus Accumbens : A Microdialysis Study

Cited by 42 publications

References 31 publications

Smoking Modulation of μ-Opioid and Dopamine D2 Receptor-Mediated Neurotransmission in Humans

Smoking Modulation of μ-Opioid and Dopamine D2 Receptor-Mediated Neurotransmission in Humans

Pyrogens Enhance β-Endorphin Release in Hypothalamus and Trigger Fever That Can Be Attenuated by Buprenorphine

Pronociceptive and Antinociceptive Effects of Estradiol through Endogenous Opioid Neurotransmission in Women

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