Role of thyroid hormones in the maturation and organisation of rat barrel cortex

Berbel, Pere; Ausó, Eva; García-Velasco, José Victor; Molina, Manuel; Camacho, Miguel Asai

doi:10.1016/s0306-4522(01)00368-2

Cited by 77 publications

(42 citation statements)

References 42 publications

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“…Interestingly, in CB1KO mice, the density of pyramidal neurons in superficial layers decreased whereas it increased in deep cortical layers as a result of abnormal radial migration (Mulder et al, 2008). Abnormal radial migration also causes blurred layering in the neocortex (Berbel et al, 2001). In agreement, our results show that in CB1KO mice the borders between layers are blurred and the radial distribution of PV-ir neurons is altered.…”

Section: Cb1 Receptors and Sensorimotor Gating Regulationsupporting

confidence: 85%

“…In total, 10 sections per experimental group were analyzed (2 sections per mouse). Immunolabeled cells were counted in 10 probes (200 μm-wide; 1 probe/section), covering the central area of M2 and spanned from layer I to the subcortical white matter, as previously detailed ( Figure 4; Berbel et al, 2001). The borders between layers and strata were placed at the same relative depth, as measured from adjacent neuronal nuclei (NeuN)-ir sections (Supplementary Figure S1).…”

Section: Immunohistochemical Analysesmentioning

confidence: 99%

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Differential Pharmacological Regulation of Sensorimotor Gating Deficit in CB1 Knockout Mice and Associated Neurochemical and Histological Alterations

Ortega-Álvaro

Navarrete

Aracil-Fernández

et al. 2015

Neuropsychopharmacol

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The endocannabinoid system has been widely involved in the pathophysiology of sensorimotor gating deficits. This study aimed to evaluate the pharmacological modulation of the sensorimotor gating impairment induced by cannabinoid CB1 receptor (CB1r) deletion. For this purpose, the prepulse inhibition (PPI) paradigm was used to evaluate the effect of two antipsychotics drugs (risperidone and haloperidol) and a psychostimulant (methylphenidate) on the preattentional deficit presented by CB1KO mice. Furthermore, the effects of the CB1r antagonist AM251 on PPI were evaluated in WT mice. Real-time PCR and immunohistochemical studies were carried out to analyze dopamine transporter (DAT) and α-2C adrenergic receptor (ADRA2C) gene expressions and the distribution of parvalbumin (PV) and cholecystokinin-8 (CCK) immunoreactive (ir) cortical neurons, respectively. Neither risperidone nor haloperidol significantly modified the PPI of WT and CB1KO mice, whereas methylphenidate improved the preattentional deficit of CB1KO mice. In addition, treatment with AM251 (3 mg/kg; i.p.) significantly decreased the PPI of WT animals. The administration of methylphenidate increased DAT and ADRA2C gene expressions in CB1KO mice without producing any effect in WT animals. Immunohistochemical studies revealed that there were no significant changes in CCK immunolabeling between WT and CB1KO mice, whereas the radial distribution of PV-ir neurons was abnormal in CB1KO mice. These data further support the important role of CB1r in sensorimotor gating regulation and the therapeutic usefulness of methylphenidate for the treatment of psychiatric disorders with associated preattentional deficits.

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Section: Cb1 Receptors and Sensorimotor Gating Regulationsupporting

confidence: 85%

Section: Immunohistochemical Analysesmentioning

confidence: 99%

Differential Pharmacological Regulation of Sensorimotor Gating Deficit in CB1 Knockout Mice and Associated Neurochemical and Histological Alterations

Ortega-Álvaro

Navarrete

Aracil-Fernández

et al. 2015

Neuropsychopharmacol

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“…However, the systematic finding of labeled cells in aberrant locations is not explained by such a delay alone. Moreover, when goitrogen-treated dams were given single pulses of BrdU at various times between E14 and P0, no differences were found between the pups from the normal and hypothyroid dams in the proportion of labeled cells in S1, whatever the timing of the BrdU injections (28). After labeling at E19, the number of labeled cells was equally very low in both groups of pups.…”

Section: Discussionmentioning

confidence: 85%

Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny

Ausó²,

et al. 2003

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“…Heterotopias (i.e. cellular malformations with clusters of neurons in untypical places, a result of defective migration) in the white matter of the corpus callosum and subcortical band heterotopias can be detected in offspring of dams with moderate forms of thyroid disruption (Berbel et al, 2001, Goodman and Gilbert, 2007, Gilbert et al, 2014), and they remain present in adult animals even after returning to an euthyroid state (Powell, 2012). Developmental hypothyroidism has been shown to produce a decrease of neurons in cortical layers I-III and an increase in layers V-VI, thereby resulting in a reduction of radial glial density and loss of neuronal bipolarity, which is crucial for neurons to migrate in radial direction to form the cortical plate (Pathak et al, 2011).…”

Section: Influence Of Ths On Brain and Cognitive Developmentmentioning

confidence: 99%

Influence of maternal thyroid hormones during gestation on fetal brain development

et al. 2017

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Thyroid hormones (TH) play an obligatory role in many fundamental processes underlying brain development and maturation. The developing embryo/fetus is dependent on maternal supply of TH. The fetal thyroid gland does not commence THs synthesis until mid gestation, and the adverse consequences of severe maternal TH deficiency on offspring neurodevelopment are well established. Recent evidence suggests that even more moderate forms of maternal thyroid dysfunction, particularly during early gestation, may have a long-lasting influence on child cognitive development and risk of neurodevelopmental disorders. Moreover, these observed alterations appear to be largely irreversible after birth. It is, therefore, important to gain a better understanding of the role of maternal thyroid dysfunction on offspring neurodevelopment in terms of the nature, magnitude, time-specificity, and context-specificity of its effects. With respect to the issue of context specificity, it is possible that maternal stress and stress-related biological processes during pregnancy may modulate maternal thyroid function. The possibility of an interaction between the thyroid and stress systems in the context of fetal brain development has, however, not been addressed to date. We begin this review with a brief overview of TH biology during pregnancy and a summary of the literature on its effect on the developing brain. Next, we consider and discuss whether and how processes related to maternal stress and stress biology may interact with and modify the effects of maternal thyroid function on offspring brain development. We synthesize several research areas and identify important knowledge gaps that may warrant further study. The scientific and public health relevance of this review relates to achieving a better understanding of the timing, mechanisms and contexts of thyroid programming of brain development, with implications for early identification of risk, primary prevention and intervention.

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Role of thyroid hormones in the maturation and organisation of rat barrel cortex

Cited by 77 publications

References 42 publications

Differential Pharmacological Regulation of Sensorimotor Gating Deficit in CB1 Knockout Mice and Associated Neurochemical and Histological Alterations

Differential Pharmacological Regulation of Sensorimotor Gating Deficit in CB1 Knockout Mice and Associated Neurochemical and Histological Alterations

Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny

Influence of maternal thyroid hormones during gestation on fetal brain development

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