Effect of a neuraminidase inhibitor (oseltamivir) on mouse jump-down behavior via stimulation of dopamine receptors

Suzuki, Minoru; Masuda, Yutaka

doi:10.2220/biomedres.29.233

Cited by 16 publications

(16 citation statements)

References 20 publications

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“…This mechanism has been implicated in an animal study linking oseltamivir with abnormal behavior. 12 Oseltamivir may assert a similar influence on the human nervous systems and cause prominent psychiatric symptoms. Further investigations by human experimental studies are indicated.…”

Section: Discussionmentioning

confidence: 99%

Acute exacerbation of psychiatric symptoms during influenza treatment with oseltamivir in chronic schizophrenia

Lan

Liu

Chen

2015

Journal of the Chinese Medical Association

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Influenza treatment and prophylaxis with oseltamivir are critically important in reducing the morbidity and mortality of patients in chronic psychiatric facilities. Abnormal behavior, delusions, perceptual disturbances, mania, and depression have all been reported as oseltamivir-related psychiatric side effects. We hereby report two chronic schizophrenia patients in Taiwan manifesting psychiatric instability who were being treated with oseltamivir for suspected influenza infection, and further discuss other potential contributing factors. The possibility that oseltamivir can cause psychotic or affective symptoms suggests that additional caution is necessary for its use in patients with an established psychiatric diagnosis.

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Section: Discussionmentioning

confidence: 99%

Acute exacerbation of psychiatric symptoms during influenza treatment with oseltamivir in chronic schizophrenia

Lan

Liu

Chen

2015

Journal of the Chinese Medical Association

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“…Suzuki et al [64] reported that oseltamivir sialylates a serum glycolipid and that this modified glycolipid induced jump-down behaviour via stimulation of dopamine D2 receptors; they suggest that this mechanism may be involved in the abnormal behaviour seen in some children taking oseltamivir.…”

Section: Toxicity and Toxicokinetics Studies In Juvenile Rats: An mentioning

confidence: 99%

The mechanisms of sudden-onset type adverse reactions to oseltamivir

Hama¹,

Bennett

2016

Acta Neurol Scand

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Oseltamivir is contraindicated for people aged 10 to 19 in principle in Japan, due to concern about abnormal behaviours. Sudden death is another concern. This review examines growing evidence of their association and discusses underlying mechanisms of these sudden-onset type reactions to oseltamivir. First the importance of animal models and the concept of human equivalent dose (HED) is summarised. Second, the specific condition for oseltamivir use: influenza infection, is reviewed. Third, findings from toxicity studies conducted prior to and after the marketing of oseltamivir are reported on to provide context on the observation of a possible causal association. Fourth, similarity and consistency of toxicity in humans with that in other animals is described. Finally, coherence of toxicokinetic and molecular-level of evidence (channels, receptors, and enzymes), including differences from the toxicity of other neuraminidase inhibitors, is reviewed. It is concluded that unchanged oseltamivir has various effects on the central nervous system (CNS) that may be related to clinical findings including hypothermia, abnormal behaviours including with fatal outcome, and sudden death. Among receptors and enzymes related to CNS action, it is known that oseltamivir inhibits nicotinic acetylcholine receptors, which are closely related to hypothermia, as well as human monoamine oxidase-A (MAO-A), which is closely related to abnormal or excitatory behaviours. Receptors such as GABAA, GABAB, and NMDA and their related receptors/channels including Na+ and Ca2+ channels are thought to be other candidates for investigation related to respiratory suppression followed by sudden death and psychotic reactions (both acute and chronic) respectively.

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“…The modules are followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAclipid (3-O-Sulfo-Beta-D-Galactosyl-(1->4)-N-Acetyl-Beta-D-Glucosamine-lipid: sG1-4GN) promotes the serotonergic module regulating the emotional behaviors for not-wasting the physical strength [3,4], GalNAcalpha1-3GalNAc-lipid (GalNAcalpha1->3GalNAc-lipid: GN1-3GN) promotes the adrenergic module inducing the stress-coping behaviors [5,6], sulfated Fucalpha1-2Glc-lipid (Fucalpha1-2[6OSO3]Galbeta1-4Glcbeta-lipid: sF1-2G) protects the cholinergic module keeping the valid stresscoping memories from the ischemia-stress, as an adaptogen does [4,7,8], and Sialalpha2-3Gal-lipid (NeuAcalpha2-3Gal-lipid: S2-3G) promotes the dopaminergic module integrating the emotion and recognition-behaviors [9,10,11]. Now, major depression patients have the functional abnormalities in their amygdala, caudate nucleus and hippocampus [12], manic patients have the functional abnormalities in their amygdala, ventral striatum and hippocampus [13], and schizophrenia patients have the functional abnormalities in their frontal and temporal lobes [14].…”

Section: Introductionmentioning

confidence: 99%

Recognition-behavioral stress-coping humoral glycolipids produced by medicated major psychoses patients

Masuda¹

2019

Preprint

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Background Mammalians have the recognition-behavioral stress-coping system regulated via the neuronal modules followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAc-lipid promotes the serotonergic module. GalNAcalpha1-3GalNAc-lipid promotes the adrenergic module. A Fucalpha1-2Glc-lipid protects the cholinergic module. Sialalpha2-3Gal-lipid promotes the dopaminergic module.Methods Major psychoses patients show the emotional and recognition-behavioral symptoms, and long-time medication does not completely delete the symptoms. I examined the recognitionbehavioral stress-coping humoral glycolipids produced by medicated major psychoses patients. ResultsThe major depression patients produced the sulfated Galbeta1-4GlcNAc-lipid and the sulfated Fucalpha1-2Glc-lipid, but deduced the GalNAcalpha1-3GalNAc-lipid. The mania patients produced the sulfated Galbeta1-4GlcNAc-lipid. The schizophrenia patients produced the sulfated Galbeta1-4GlcNAclipid, and remarkably produced the Sialalpha2-3Gal-lipid. Ruled out the medication-effects, the major depression patients decreased the serotonergic module function and the adrenergic module function, but increased the cholinergic module function. The mania patients increased the serotonergic module function and the adrenergic module function. The schizophrenia patients increased the serotonergic module function, and particularly increased the dopaminergic module function.Conclusion These suggest the stress-coping humoral glycolipids produced by the patients corresponded to the symptoms. Furthermore, I understood the humoral Sialalpha2-3Gal-lipid would be considered as another biomarker identifying schizophrenia.

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Effect of a neuraminidase inhibitor (oseltamivir) on mouse jump-down behavior via stimulation of dopamine receptors

Cited by 16 publications

References 20 publications

Acute exacerbation of psychiatric symptoms during influenza treatment with oseltamivir in chronic schizophrenia

Acute exacerbation of psychiatric symptoms during influenza treatment with oseltamivir in chronic schizophrenia

The mechanisms of sudden-onset type adverse reactions to oseltamivir

Recognition-behavioral stress-coping humoral glycolipids produced by medicated major psychoses patients

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