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Prefrontal Inhibitory Signaling in the Control of Social Behaviors
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Similar to findings from mouse models of ASD, both structural and functional impairments in mPFC inhibition were also observed in schizophrenia and depression animal models. In methylazoxymethanol acetate (MAM)-treated rats, a verified animal model of schizophrenia, the density of PV INs is decreased throughout the mPFC (Lodge et al. 2009). Functionally, the synaptic inhibition onto mPFC layer 2/3 excitatory pyramidal cells is reduced in disrupted-in-schizophrenia-1 (Disc1) locus impairment mice (Delevich et al. 2020). In mice expressing truncated Disc1, a genetic mouse model of depression, prelimibic PV INs are reduced in number and they receive fewer presynaptic excitatory inputs and form fewer release sites on postsynaptic targets (Sauer et al. 2015). Apart from the genetic mouse model of depression, mouse models of chronic stress also show defects in GABAergic transmission of layer V mPFC pyramidal neurons, concomitant with depressive-like behaviors (Ghosal et al. 2020).
In Vitro Effect of Bile Acids
Published in Herman Autrup, Gary M. Williams, Experimental Colon Carcinogenesis, 2019
In related studies on the effects of bile acids on DNA repair in cultures of human fetal intestinal cells treated with methylazoxymethanol acetate, lithocholic acid enhanced repair replication of the damaged DNA and also increased unscheduled DNA synthesis.46 Such enhancement of repair processes and unscheduled DNA synthesis by lithocholic acid may be relevant to the modifying effect of this bile acid in colon carcinogenesis.
Rationale and Possible Mechanisms by Which Selenium Inhibits Mammary Cancer
Published in Maryce M. Jacobs, Vitamins and Minerals in the Prevention and Treatment of Cancer, 2018
A variety of studies have established that dietary selenium supplementation can significantly inhibit the incidence of chemically induced tumors in animals (Table 1).29-48 Chemically induced tumors in skin, liver, colon, pancreas and mammary tissue have been shown to be inhibited by dietary selenium supplementation. A reduction in the incidence and/or total tumor number in animals treated with diverse carcinogens including: 3’-methyl-4-dimethylaminoazobenzene, 7,12-dimethylbenz(a)anthracene (DMBA), benzo(a)pyrene, 2-acetylaminofluorene, 1,2-dimethylhydrazine (DMH), methylazoxymethanol acetate (MAM), aflatoxin B1, methylbenzylnitrosamine and methylnitrosourea (MNU) have been shown to be inhibited by selenium supplementation. The ability of selenium to inhibit tumor formation resulting from such a wide variety of carcinogens and occurring in such a variety of tissues indicates a general mechanism rather than a tissue specific reaction.
Laterality in functional and metabolic state of the bulbectomised rat brain detected by ASL and 1H MRS: A pilot study
Published in The World Journal of Biological Psychiatry, 2023
Iveta Pavlova, Eva Drazanova, Lucie Kratka, Petra Amchova, Ondrej Macicek, Jana Starcukova, Zenon Starcuk, Jana Ruda-Kucerova
Regarding the lack of CBF differences between the OBX model and the control animals, our findings are supported by an earlier OBX model study (Gigliucci et al. 2014). However, this result contradicts the clinical data (Wang et al. 2014; Vasic et al. 2015; Li et al. 2018; Sheng et al. 2018; Cooper et al. 2020) as well as the results from the Wistar Kyoto rat model of depression (Gormley et al. 2016), reporting regional differences of the CBF between depression and control group. The clinical results are ambiguous, assessing various ununified brain regions. Lower CBF in the cortical regions was shown in MDD (Sheng et al. 2018) and the Wistar Kyoto depression model (Gormley et al. 2016) compared to the controls, which was not confirmed by our data. Hence, the OBX model may not be adequate to mimic clinically proven CBF alterations. The negative result seems convincing, given that we previously observed significant differences in regional CBF in a neurodevelopmental model of schizophrenia induced by prenatal exposure to methylazoxymethanol acetate with n = 6–8 rats per group (Drazanova et al. 2019). Furthermore, we reported both acute and chronic effects of olanzapine on regional CBF with n = 7 rats per group (Drazanova et al. 2019).
Aberrant plasticity in the hippocampus after neonatal seizures
Published in International Journal of Neuroscience, 2018
Xiaoqian Zhang, Huiling Qu, Ying Wang, Shanshan Zhao, Ting Xiao, Chuansheng Zhao, Weiyu Teng
However, few studies have reported ectopic migration after neonatal seizures. Recently, it has been reported that neonatal rats subjected to hypoxia treatment on P10 when examined one month after the insults had more ectopic migration of newborn neurons in hilus in comparison with the controls [47]. Germano et al. induced experimental neuronal migration disorders by exposing pregnant rats to methylazoxymethanol acetate and found that rats with neuronal migration disorders required less stimulation to develop seizures than controls, indicating that hippocampal kindling could be facilitated by the presence of severe neuronal migration disorders in the immature brain [50]. McCabe et al. showed that the overwhelming majority of neural precursor cells differentiated into DGCs within the dentate gyrus even after recurrent flurothyl-induced seizures between P0 and P4 in rats, indicating that neonatal seizures might not impair the migration of newly formed neurons compared with adult seizures [41]. The explanation may be that the neonatal seizures cause little neuronal damage, and the lack of neuronal damage in the neonatal models results in a lack of ectopic migration of neurons. Mossy fiber sprouting.