A newly designed method for removal of the pineal body, and depression of convulsions and enhancement of exploratory movements by pinealectomy in mice.

Hata, Taeko; Kita, Tomitaro

doi:10.1507/endocrj1954.25.407

Cited by 9 publications

(3 citation statements)

References 13 publications

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“…After bilateral enucleation, El mice became transiently less sensitive to seizureinducing stimuli but returned to baseline within 15 days (Hata et al, 1975). Pinealectomy reduced the convulsion rate in El mice postoperatively relative to sham-operated animals (Hata and Kita, 1978).…”

Section: The El Mousementioning

confidence: 91%

El Mouse as a Model of Focal Epilepsy: A Review

King

LaMotte

1989

Epilepsia

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The El mouse is a model of hereditary sensory precipitated temporal lobe epilepsy. All adult El mice given rhythmic vestibular stimulation (e.g. tossing, rocking) during development will experience tonic-clonic convulsions when given similar stimulation as adults. The seizures have prodromal, convulsive, and postictal stages. EEG and 2-deoxyglucose studies have localized the seizures to the temporal lobe, with onset in the hippocampus. El mice have a decreased threshold for convulsion by electrical or pharmacologic stimulation. A variety of anticonvulsant medications eliminate El mouse seizures, including phenytoin (PHT), phenobarbital (PB), valproate (VPA), and ethosuximide (ESM). Anatomic studies have shown subtle differences in the thalamus and hippocampus of El mice. Immunohistochemistry of the El mouse hippocampus has revealed changes in peptidergic and gabaergic cell populations. Numerous biochemical differences have been found between El and nonconvulsive mice, including increased acetylcholine (ACh), dopamine (DA), GABA, serotonin (5-HT), and decreased norepinephrine (NE).

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Section: The El Mousementioning

confidence: 91%

El Mouse as a Model of Focal Epilepsy: A Review

King

LaMotte

1989

Epilepsia

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“…Pineal surgery. Between 7 -10 weeks of age, C3Sn mice were surgically pinealectomized (PinealX) or were sham operated leaving the pineal gland intact (Intact-control) [34]. To prevent selection and treatment bias, we evenly and randomly assigned animals in a litter to pinealX or sham surgery, then housed those animals together irrespective of their pineal status and masked experimenters to pineal status.…”

Section: Methodsmentioning

confidence: 99%

“…Pineal melatonin competent C3Sn mice were sham operated (Intact-control), or had the pineal gland tip surgically removed (PinealX) to generate a model of ~50% melatonin deficiency [12,[32][33][34]. First, an orthotopic 4t1 cell allograft was used to assess the effect of pineal melatonin on viability and formation of solid tumors [35].…”

Section: Introductionmentioning

confidence: 99%

Effects of physiological deficits in pineal melatonin on Triple Negative Breast Cancer

Dearing

Silva

Turner

et al. 2020

Preprint

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BackgroundTriple negative breast cancer (TNBC) is aggressive and treatment resistant. Evidence suggests that deficits in melatonin signaling increase TNBC risk: conditions that suppress melatonin increased incidence, low melatonin receptor expression correlates with worse prognosis, and high-dose melatonin can inhibit TNBC. Together this suggests that normalizing pineal melatonin could reduce TNBC incidence and/or mortality. The goal of this study was to determine whether small physiological deficits in melatonin alone, can increase risk for TNBC, and how ‘normal’ melatonin would be protective.MethodsThe effect of melatonin treatment on 4t1 cellsin vitrowas measured using the MTT cell viability assay, and gene expression of breast cancer and melatonin signaling markers. The effect of pineal gland status on 4t1 cell allografts was tested in C3Sn mice (Mus Musculus) with either an intact pineal (control) or surgical removal of the pineal causing a ~50% deficit in plasma melatonin. Orthotopic tumors were assessed by histopathology and metastasis by strain specific qPCR against 4t1 cell and host gDNA.ResultsMelatonin treatment induced significant changes in gene expression, with a significant reduction in derived PAM50 Risk of Recurrence score (ROR in Not treated = 65.5 ± 10.6 Mean SEM; Treated with 25pg/ml of melatonin 20.8 ± 8.3; P = 0.008), suggesting melatonin treatment would improve prognosis. A ~50% reduction in plasma melatonin increased orthotopic tumors, but this was non-significant, and had no effect on metastasis from tail vein allograft.ConclusionsPhysiological deficits in melatonin do alter the oncogenic status of 4t1 tumor cells but this has only a limited effect on growth and metastasisin vivo. Lack of significance in orthotopic tumor formation may be due to small sample size, and it is possible that any protective effect of melatonin occurs earlier in tumor development than we have tested.

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