Medial septal injection of naloxone elevates acetylcholine release in the hippocampus and induces behavioral seizures in rats

Mizuno, Tooru M.; Kimura, Fukuko

doi:10.1016/0006-8993(95)01287-7

Cited by 31 publications

(10 citation statements)

References 45 publications

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“…The major neurotransmitter imbalances currently thought to underlie this process are acetylcholine deficiency and dopamine excess . Data from animal experiments suggest that naloxone may regulate the release of acetylcholine and inhibit dopamine in humans . The findings of the current study indicate that the opioid system may also be involved in the pathophysiology of delirium.…”

Section: Resultsmentioning

confidence: 60%

Naloxone Treatment for Poststroke Agitated Delirium in Hospitalized Older Adults: A Pilot Study

Duan¹,

Li²,

Qiu³

et al. 2016

J American Geriatrics Society

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Section: Resultsmentioning

confidence: 60%

Naloxone Treatment for Poststroke Agitated Delirium in Hospitalized Older Adults: A Pilot Study

Duan¹,

Li²,

Qiu³

et al. 2016

J American Geriatrics Society

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“…NAL elevates the Acetylcholine release in the hippocampus of rat. [21] Aluminum decreases the Choline acetyltransferase content and Acetylcholine activity of mice, which may be one of the important mechanisms of its neurotoxity. [22] There was no significant difference in the Al and Zn content between the non-treated model rats and the NAL-treated rats, which suggests that the beneficial effects of NAL on cognitive function may not be through decreasing the level of Al or Zn in rats.…”

Section: Discussionmentioning

confidence: 99%

Effect of naloxone on aluminum-induced learning and memory impairment in rats

Sun

Ma²,

Bachelor

et al. 2005

Neurol India

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“…Notably, we found that cholinergic terminals expressing ER␣ were prominent in regions overlapping hippocampal pathways containing proepileptic opioids (Hong et al, 1993). Moreover, elevation of hippocampal acetylcholine release can induce behavioral seizures (Mizuno and Kimura, 1996).…”

Section: Functional Considerationsmentioning

confidence: 98%

Subcellular relationships between cholinergic terminals and estrogen receptor‐α in the dorsal hippocampus

Towart

Alves

Znamensky

et al. 2003

J of Comparative Neurology

105

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Cholinergic septohippocampal neurons are affected by circulating estrogens. Previously, we found that extranuclear estrogen receptor-alpha (ERalpha) immunoreactivity in presynaptic profiles had an overlapping distribution with cholinergic afferents in the rat hippocampal formation. To determine the subcellular relationships between cholinergic presynaptic profiles and ERalpha, hippocampal sections were dually immunolabeled for vesicular acetylcholine transporter (VAChT) and ERalpha and examined by electron microscopy. Within the hippocampal formation, immunoreactivities for VAChT and ERalpha both were presynaptic, although their subcellular targeting was distinct. VAChT immunoreactivity was found exclusively within presynaptic profiles and was associated with small synaptic vesicles, which usually filled axon terminals. VAChT-labeled presynaptic profiles were most concentrated in stratum oriens of the hippocampal CA1 region and dentate inner molecular layer and hilus. In contrast, ERalpha immunoreactivity was found in clusters affiliated either with select vesicles or with the plasmalemma within preterminal axons and axon terminals. ERalpha-immunoreactive (IR) presynaptic profiles were more evenly distributed between hippocampal lamina than VAChT-IR profiles. Quantitative ultrastructural analysis revealed that VAChT-IR presynaptic profiles contained ERalpha immunoreactivity (ranging from 3% to 17%, depending on the lamina). Additionally, VAChT-IR presynaptic profiles apposed ERalpha-IR dendritic spines, presynaptic profiles, and glial profiles; many of the latter two types of profiles abutted unlabeled dendritic spines that received asymmetric (excitatory-type) synapses from unlabeled terminals. The presence of ERalpha immunoreactivity in cholinergic terminals suggests that estrogen could rapidly and directly affect the local release and/or uptake of acetylcholine. The affiliation of cholinergic terminals with excitatory terminals near ERalpha-labeled dendritic spines or glial profiles suggests that alterations in acetylcholine release could indirectly affect estrogen-modulated structural plasticity.

show abstract

Medial septal injection of naloxone elevates acetylcholine release in the hippocampus and induces behavioral seizures in rats

Cited by 31 publications

References 45 publications

Naloxone Treatment for Poststroke Agitated Delirium in Hospitalized Older Adults: A Pilot Study

Naloxone Treatment for Poststroke Agitated Delirium in Hospitalized Older Adults: A Pilot Study

Effect of naloxone on aluminum-induced learning and memory impairment in rats

Subcellular relationships between cholinergic terminals and estrogen receptor‐α in the dorsal hippocampus

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