Blockers of adenosine A1, but not muscarinic acetylcholine, receptors improve excessive extracellular glutamate-induced synaptic depression

Narimatsu, Eichi; Niiya, Tomohisa; Takada, Y.; Takahashi, K; Yamauchi, M.; Yamakage, Michiaki

doi:10.1016/j.neures.2012.11.002

Cited by 5 publications

(4 citation statements)

References 36 publications

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“…The protocol (Table 1) was derived according to a previous study by the coauthors 21,28 . Briefly, rACSF was perfused at a high flow rate of 10-20 mL/min using drip infusion sets and a suction pump.…”

Section: Protocolmentioning

confidence: 99%

Mechanism of central hypopnoea induced by organic phosphorus poisoning

Nomura

Narimatsu

Inoue

et al. 2020

Sci Rep

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Whether central apnoea or hypopnoea can be induced by organophosphorus poisoning remains unknown to date. By using the acute brainstem slice method and multi-electrode array system, we established a paraoxon (a typical acetylcholinesterase inhibitor) poisoning model to investigate the time-dependent changes in respiratory burst amplitudes of the pre-Bötzinger complex (respiratory rhythm generator). We then determined whether pralidoxime or atropine, which are antidotes of paraoxon, could counteract the effects of paraoxon. Herein, we showed that paraoxon significantly decreased the respiratory burst amplitude of the pre-Bötzinger complex (p < 0.05). Moreover, pralidoxime and atropine could suppress the decrease in amplitude by paraoxon (p < 0.05). Paraoxon directly impaired the pre-Bötzinger complex, and the findings implied that this impairment caused central apnoea or hypopnoea. Pralidoxime and atropine could therapeutically attenuate the impairment. This study is the first to prove the usefulness of the multi-electrode array method for electrophysiological and toxicological studies in the mammalian brainstem.

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Section: Protocolmentioning

confidence: 99%

Mechanism of central hypopnoea induced by organic phosphorus poisoning

Nomura

Narimatsu

Inoue

et al. 2020

Sci Rep

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“…These results indicate that late sepsis facilitates LTP of action potentials generated on soma. In our previous study, it was reported that the regression of the PS-fEPSP relationship, simultaneously recorded using the MEA system, is linear in the normal rat hippocampus (Narimatsu et al, 2013); therefore, the divergences between PSs and fEPSPs suggest an increase in somatic excitability. It has been reported in our previous study using the neuromuscular junction that CLP-late sepsis decreased critical depolarization on the postsynaptic membrane (Niiya et al, 2006).…”

Section: Discussionmentioning

confidence: 90%

Sepsis-induced modulation of long-term potentiation induced by theta burst stimulation in the rat hippocampus

Kakizaki,

Narimatsu,

Kasai

et al. 2023

Front. Neurosci.

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We investigated the influences of sepsis on central synaptic plasticity in vitro. Cecal ligation and puncture (CLP) was performed by creating rat sepsis models, which were divided into early and late sepsis groups (8 and 16 h after CLP, respectively). In the CA1 of the rat hippocampal slices, orthodromically elicited population spikes (PSs) and field excitatory postsynaptic potentials (fEPSPs) were simultaneously recorded, and their long-term potentiation (LTP) was induced by theta burst stimulation (TBS). TBS induced LTPs of PSs and fEPSPs in all groups. In the sham and early sepsis groups, there was no significant difference in LTPs between PSs and fEPSPs. However, in the late sepsis group, the LTP of PSs was greater than that of fEPSPs (p < 0.05) and was greater than the LTPs of PSs in the sham and early sepsis groups (p < 0.05). Superoxide dismutase, administered immediately before CLP, inhibited the enhancement of LTP in PS, as observed in the late sepsis group. The initial rapid potentiation component of LTP in fEPSPs was suppressed or reduced in all groups that underwent CLP. The results indicate that CLP-induced sepsis modulates hippocampal synaptic plasticity, depressing excitatory synaptic transmissions and facilitating somatic excitability, which is induced by septic oxygen superoxide.

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“…26 A1R is expressed in both neurons and astrocytes in the central nervous system 27,28 and functionally associated with glutamate clearance; impaired glutamate clearance contributes to pain development. [29][30][31] Thus, facilitation of the activation of spinal dorsal horn neurons contributes to the pain process. 32 Even a single exposure to OXA can cause severe neuropathic pain.…”

Section: Discussionmentioning

confidence: 99%

“…A recent study revealed that the A1R signaling cascade was involved in mediated analgesia 26 . A1R is expressed in both neurons and astrocytes in the central nervous system 27,28 and functionally associated with glutamate clearance; impaired glutamate clearance contributes to pain development 29–31 . Thus, facilitation of the activation of spinal dorsal horn neurons contributes to the pain process 32 .…”

Section: Discussionmentioning

confidence: 99%

Loss of astrocytic A1 adenosine receptor is involved in a chemotherapeutic agent–induced rodent model of neuropathic pain

2023

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Introduction/Aims Oxaliplatin is a commonly used platinum chemotherapy drug, whereas peripheral neurotoxicity is a widely observed adverse reaction lacking a satisfactory therapeutic strategy. Different adenosine receptors underlying the common neuropathic phenotype play different roles through varied pathophysiological mechanisms. In this study, we investigated the role of adenosine receptor A1 (A1R) in oxaliplatin‐induced neuropathic pain and its potential use in an effective therapeutic strategy. Methods We established an oxaliplatin‐induced neuropathic pain model simulating the mode of chemotherapy administration and observed the related neuropathic behavioral phenotype and implicated mechanisms. Results Five weekly injections of oxaliplatin for 2 weeks induced a severe and persistent neuropathic pain phenotype in mice. A1R expression in the spinal dorsal horn decreased during this process. Pharmacological intervention against A1R verified its importance in this process. Mechanistically, the loss of A1R expression was mainly attributed to its decreased expression in astrocytes. Consistent with the pharmacological results, the oxaliplatin‐induced neuropathic pain phenotype was blocked by specific therapeutic interventions of A1R in astrocytes via lentiviral vectors, and the expression of glutamate metabolism–related proteins was upregulated. Neuropathic pain can be alleviated by pharmacological or astrocytic interventions via this pathway. Discussion These data reveal a specific adenosine receptor signaling pathway involved in oxaliplatin‐induced peripheral neuropathic pain, which is related to the suppression of the astrocyte A1R signaling pathway. This may provide new opportunities for the treatment and management of neuropathic pain observed during oxaliplatin chemotherapy.

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Blockers of adenosine A1, but not muscarinic acetylcholine, receptors improve excessive extracellular glutamate-induced synaptic depression

Cited by 5 publications

References 36 publications

Mechanism of central hypopnoea induced by organic phosphorus poisoning

Mechanism of central hypopnoea induced by organic phosphorus poisoning

Sepsis-induced modulation of long-term potentiation induced by theta burst stimulation in the rat hippocampus

Loss of astrocytic A1 adenosine receptor is involved in a chemotherapeutic agent–induced rodent model of neuropathic pain

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