Neonatal hypothalamic c-fos expression in an excitotoxicity-induced model of precocious puberty

Smyth, Catherine; Natarajan, Meenakshi Sundari Subramaniyan; Wilkinson, Michael

doi:10.1016/s0165-3806(97)00150-8

Cited by 5 publications

(2 citation statements)

References 21 publications

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“…Vagotomy decreased high insulin secretion induced in MSG-obese rats [ 96 ]. Although still widely used in lesion-induced obesity models [ 97 , 98 , 99 , 100 , 101 , 102 ], MSG-induced damage is not limited to distinct hypothalamic nuclei as it also penetrates the brain on other sites of circumventricular organs, e.g., subfornical organ and area prostrema, as well as eyes and pituitary [ 91 , 92 , 103 , 104 , 105 , 106 ]. In addition, MSG-induced obesity is not associated with hyperphagia [ 88 ].…”

Section: Studying Hypothalamic Obesity In Ratsmentioning

confidence: 99%

Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention

Roth

2015

JCM

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Hypothalamic obesity (HO) occurs in patients with tumors and lesions in the medial hypothalamic region. Hypothalamic dysfunction can lead to hyperinsulinemia and leptin resistance. This review is focused on HO caused by craniopharyngiomas (CP), which are the most common childhood brain tumors of nonglial origin. Despite excellent overall survival rates, CP patients have substantially reduced quality of life because of significant long-term sequelae, notably severe obesity in about 50% of patients, leading to a high rate of cardiovascular mortality. Recent studies reported that both hyperphagia and decreased energy expenditure can contribute to severe obesity in HO patients. Recognized risk factors for severe obesity include large hypothalamic tumors or lesions affecting several medial and posterior hypothalamic nuclei that impact satiety signaling pathways. Structural damage in these nuclei often lead to hyperphagia, rapid weight gain, central insulin and leptin resistance, decreased sympathetic activity, low energy expenditure, and increased energy storage in adipose tissue. To date, most efforts to treat HO have shown disappointing long-term success rates. However, treatments based on the distinct pathophysiology of disturbed energy homeostasis related to CP may offer options for successful interventions in the future.

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Section: Studying Hypothalamic Obesity In Ratsmentioning

confidence: 99%

Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention

Roth

2015

JCM

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“…These BBB regional differences in response to damage (Kuriakose, Rama Rao, Younger, & Chandra, 2018;Mastorakos & McGavern, 2019) or hypertonicity (Rapoport et al, 1980;Stonestreet et al, 2006) have been widely studied. Similarly, it is well known that besides the Hyp (Smyth, Natarajan, & Wilkinson, 1997), also the cerebral cortex and Hp highly susceptible regions to neonatal MSG treatment (Chaparro-Huerta, Rivera-Cervantes, Flores-Soto, Gómez-Pinedo, & Beas-Zárate, 2005; Chaparro-Huerta, Rivera-Cervantes, Torres-Mendoza, & Beas-Zárate, 2002;Rivera-Cervantes et al, 2009;Ureña-Guerrero et al, 2009). The susceptibility to neonatal excitotoxicity of these cerebral regions is mainly due to low expression level of glutamate transporters (Rose, Ziemens, Untiet, & Fahlke, 2018) and high expression level of glutamate receptors (Shinohara & Hirase, 2009;Somogyi, Tamás, Lujan, & Buhl, 1998)…”

Section: Discussionmentioning

confidence: 99%

Neonatal excitotoxicity modifies blood‐brain barrier properties increasing its susceptibility to hypertonic shock in adulthood

Fajardo-Fregoso¹,

Castañeda‐Cabral²,

Beas‐Zárate³

et al. 2020

Intl J of Devlp Neuroscience

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Early responses to a neurological excitotoxic process include blood‐brain barrier (BBB) impairment and overexpression of vascular endothelial growth factor (VEGF), but the long‐term effects of excitotoxicity on the BBB properties remain unknown. To assess this, we induced an excitotoxic process on male rats by neonatal monosodium glutamate (MSG) treatment. At postnatal day (PD) 60, we measured the expression level of structural proteins of the BBB and the VEGF type‐2 receptor (VEGFR‐2) protein in the cerebral motor cortex (CMC), striatum (STR), hippocampus (Hp), entorhinal cortex (Ent), and hypothalamus (Hyp). We also measured BBB permeability in the same cerebral regions. Neonatal MSG treatment significantly reduced the protein expression level of claudin‐5 in the CMC, and of ZO‐1 in the CMC and Hp, and increased the expression level of plasmalemmal vesicle‐associated protein in the CMC, and of VEGFR‐2 in all regions except for the Hyp. BBB permeability was significantly higher in all studied regions of MSG‐treated animals after hypertonic shock (HS). The increased BBB permeability observed in the MSG‐treated animals after HS was reversed by VEGFR‐2 inhibition with SU5416. We conclude that neonatal excitotoxicity leads to lasting impairment on BBB properties in adulthood, increasing its susceptibility to HS that could be regulated by VEGFR‐2 activity inhibition.

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Non-NMDA glutamatergic receptors modulate acetylcholine release in the rat subfornical organ area

Shibata

Tanaka

Nomura

2006

Autonomic Neuroscience

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Neonatal hypothalamic c-fos expression in an excitotoxicity-induced model of precocious puberty

Cited by 5 publications

References 21 publications

Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention

Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention

Neonatal excitotoxicity modifies blood‐brain barrier properties increasing its susceptibility to hypertonic shock in adulthood

Non-NMDA glutamatergic receptors modulate acetylcholine release in the rat subfornical organ area

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