Selective changes in μ, δ and ϰ opioid receptor binding in certain limbic regions of the brain in Alzheimer's disease patients

Hiller, Jacob M.; Itzhak, Yossef; Simon, Eric J.

doi:10.1016/0006-8993(87)90764-5

Cited by 81 publications

(22 citation statements)

References 25 publications

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“…However, enhanced DYN tone in the aged hippocampus may contribute to cognitive decline by decreasing hippocampal glutamatergic transmission via KOR activation or through DYN actions on non-opioid receptors. DYN/KOR system in Alzheimer's disease Changes in KOR have been observed in the striatum of Alzheimer's patients but the data are inconsistent, with decreased [433], increased [434,435], or no difference [436] in KOR binding relative to controls. Enhanced amygdala KOR binding is present in Alzheimer's patients [433] whereas several studies reported no differences in KOR binding in frontal and temporal cortex [433][434][435].…”

Section: Dyn and Age-related Cognitive Declinementioning

confidence: 98%

“…DYN/KOR system in Alzheimer's disease Changes in KOR have been observed in the striatum of Alzheimer's patients but the data are inconsistent, with decreased [433], increased [434,435], or no difference [436] in KOR binding relative to controls. Enhanced amygdala KOR binding is present in Alzheimer's patients [433] whereas several studies reported no differences in KOR binding in frontal and temporal cortex [433][434][435]. Interestingly, increased DYN A 1-8, but not DYN B, immunoreactivity is observed in frontal cortical tissue of patients with Down syndrome and Alzheimer's disease [437].…”

Section: Dyn and Age-related Cognitive Declinementioning

confidence: 98%

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The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

Tejeda

Shippenberg

Henriksson

2011

Cell. Mol. Life Sci.

144

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The dynorphin/κ-opioid receptor system has been implicated in the pathogenesis and pathophysiology of several psychiatric disorders. In the present review, we present evidence indicating a key role for this system in modulating neurotransmission in brain circuits that subserve mood, motivation, and cognitive function. We overview the pharmacology, signaling, post-translational, post-transcriptional, transcriptional, epigenetic and cis regulation of the dynorphin/κ-opioid receptor system, and critically review functional neuroanatomical, neurochemical, and pharmacological evidence, suggesting that alterations in this system may contribute to affective disorders, drug addiction, and schizophrenia. We also overview the dynorphin/κ-opioid receptor system in the genetics of psychiatric disorders and discuss implications of the reviewed material for therapeutics development.

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Section: Dyn and Age-related Cognitive Declinementioning

confidence: 98%

Section: Dyn and Age-related Cognitive Declinementioning

confidence: 98%

The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

Tejeda

Shippenberg

Henriksson

2011

Cell. Mol. Life Sci.

144

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“…Different types of Memory-enhancing effect of aspirin is mediated through opioid system modulation in an AlCl 3 opioid receptor (including µ, δ and κ) have unique patterns of distribution within the human brain, typically displaying a high density in gray matter, and are preferentially found in limbic and limbic-associated brain structures (19,20). The distribution of opioid receptors in these areas have a critical role in higher cognitive and emotional behaviors.…”

Section: Introductionmentioning

confidence: 99%

Memory-enhancing effect of aspirin is mediated through opioid system modulation in an AlCl3-induced neurotoxicity mouse model

Rizwan

Idrees

Ashraf

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Neurodegenerative disorders such as Alzheimer's disease (AD) are multifaceted and there are currently a limited number of therapeutic strategies available to treat them. Aspirin is known to act on multiple therapeutic targets and is a successful anti-inflammatory agent in various tissues. The present study aimed to ascertain the performance of aspirin when employed as a therapeutic agent to treat neurodegeneration on novel targets, including opioid system genes, in an AlCl 3 -induced neurotoxicity mouse model. The effects of two doses of aspirin (5 and 20 mg/kg aspirin for 12 days) were investigated in an AlCl 3 -induced neurotoxicity mouse model (150 mg/kg AlCl 3 for 12 days). Neurological improvements were assessed through different behavioral tests and the effects of aspirin on opioid system gene expression levels were assessed by reverse transcription-polymerase chain reaction. Both doses resulted in improvements in cognitive behavior. A 5 mg/kg dose of aspirin was revealed to be effective for spatial memory improvement (7.14±0.84 sec), whilst a 20 mg/kg dose was superior for improving extinction learning (7.63±4.04%). Aspirin (5 mg/kg) also significantly improved contextual memory (48.05±10.6%) when compared with the AlCl 3 -treated group (1.49±0.62%; P<0.001). Aspirin was also observed to significantly decrease δ-opioid receptor expression in the cortex (1.09±0.08 and 1.27±0.08, respectively) at both doses (5 and 20 mg/kg) when compared with the AlCl 3 -treated group (3.69±1.43; P<0.05). Furthermore, aspirin at 5 mg/kg significantly reduced expression of prodynorphin in the cortex (0.57±0.20) when compared with the AlCl 3 -treated group (1.95±0.84; P<0.05). Notably, the effect of aspirin was significant in the cortex but not in the hippocampus. In summary, aspirin was effective in ameliorating the AD-like symptoms via the modulation of opioid systems. However, additional studies are required to determine the long term effects of aspirin on such conditions.

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“…Reports of increased K-opioid receptor density in the brain of Alzheimer's patients (Hiller et al, 1987) and dynorphin A (1-8)-like immunoreactivity in the hippocampus of aged rats (Jiang et al, 1989) suggest that disruption of opioidergic neurotransmission may play a role in the cognitive deficits associated with Alzheimer's disease and aging. Of particular interest was the observation that an endogenous K-opioid agonist, dynorphin A (1-13), improves scopolamine-induced impairment of spontaneous alternation performance in mice (Itoh et al, 1993) and carbon monoxide-induced delayed amnesia in mice (Kameyama et al, 1994a;Hiramatsu et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Improvement by dynorphin A (1–13) of galanin‐induced impairment of memory accompanied by blockade of reductions in acetylcholine release in rats

Hiramatsu

Mori

Murasawa

et al. 1996

British J Pharmacology

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1 Human galanin (0.32 nmol per rat, i.c.v.), an endogenous neuropeptide, administered 30 min before acquisition or retention trials, significantly impaired the acquisition of learning and recall of memory in a step-through type passive avoidance performance. 2 The role of dynorphin A (1 -13) in learning and memory is controversial. Dynorphin A (1-13) (0.5 nmol per rat, i.c.v.) administered 5 min before galanin injection, completely antagonized these impairments. 3 Galanin significantly decreased acetylcholine release in the hippocampus 40 to 120 min after injection as determined by in vivo brain microdialysis. This peptide also decreased acetylcholine release, albeit to a lesser extent, from the frontal cortex. 4 Dynorphin A (1-13) (0.5 nmol per rat, i.c.v.) 5 min before galanin injection, completely blocked the decrease in extracellular acetylcholine concentration induced by galanin. 5 These antagonistic effects of dynorphin A (1-13) were abolished by treatment with norbinaltorphimine (5.44 nmol per rat, i.c.v.), a selective K-opioid receptor antagonist, 5 min before dynorphin A (1-13). 6 Dynorphin A (1-13) (0.5 nmol) itself had no effect on learning and memory and on the acetylcholine concentration in the hippocampus or the frontal cortex in normal rats. 7 These results suggest that the neuropeptide dynorphin A (1-13) ameliorates the galanin-induced impairment of learning and memory accompanied by abolition of reductions in acetylcholine release via K-opioid receptors.

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Selective changes in μ, δ and ϰ opioid receptor binding in certain limbic regions of the brain in Alzheimer's disease patients

Cited by 81 publications

References 25 publications

The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

The dynorphin/κ-opioid receptor system and its role in psychiatric disorders

Memory-enhancing effect of aspirin is mediated through opioid system modulation in an AlCl3-induced neurotoxicity mouse model

Improvement by dynorphin A (1–13) of galanin‐induced impairment of memory accompanied by blockade of reductions in acetylcholine release in rats

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