Enhanced GABA action on the substantia gelatinosa neurons of the medullary dorsal horn in the offspring of streptozotocin-injected mice

Nguyen, Hoang Thi Thanh; Bhattarai, Janardhan P.; Park, Soo Joung; Lee, Jeong Chae; Cho, Dong Hyu; Han, Seong Kyu

doi:10.1016/j.jdiacomp.2015.03.007

Cited by 11 publications

(8 citation statements)

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“…All experiments were approved by the Institutional Animal Research Committee and Ethics Committee of Zhejiang University (ZJU20170337). The typical diabetic model was established according to the method of Nguyen et al [17]. In brief, pregnant mice (control model) were administered an intraperitoneal injection of streptozocin (STZ, 40 mg/kg) at 3 days, for 5 consecutive days.…”

Section: Methodsmentioning

confidence: 99%

Chemerin-induced macrophages pyroptosis in fetal brain tissue leads to cognitive disorder in offspring of diabetic dams

Liang

Han

Sun

et al. 2019

J Neuroinflammation

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BackgroundChemerin is highly expressed in the serum, placenta tissue, and umbilical cord blood of diabetic mother; however, the impact of chemerin on cognitive disorders of offspring from mothers with diabetes in pregnancy remains unclear.MethodsA diabetic phenotype in pregnant mice dams was induced by streptozocin (STZ) injection or intraperitoneal injection of chemerin. Behavioral changes in offspring of diabetic dams and nondiabetic controls were assessed, and changes in chemerin, two receptors of chemerin [chemerin receptor 23 (ChemR23) and chemokine (C-C motif) receptor-like 2 (CCRL2)], macrophages, and neurons in the brain tissue were studied to reveal the underlying mechanism of the behavioral changes.ResultsChemerin treatment mimicked the STZ-induced symptom of maternal diabetes in mice along with the altered behavior of offspring in the open field test (OFT) assay. In the exploring process for potential mechanism, the brain tissues of offspring from chemerin-treated dams were observed with an increase level of macrophage infiltration and a decrease number of neuron cells. Moreover, an increased level of NOD-like receptor family pyrin domain containing 3 (NLRP3) and apoptosis-associated speck-like (Asc) protein as well as pyroptosis [characterized by increased active caspase-1 content and secretion of cytokines such as interleukin (IL) 1 beta (IL-1β) and IL-18] more activated in macrophages is also observed in the brain of these diabetic dam’s offspring, in the presence of ChemR23. In vitro, it was found that pyroptosis activation was increased in macrophages separated from the abdominal cavity of normal mice, after chemerin treatment. However, depletion of CCRL2 decreased the level of chemerin in the brain tissues of diabetic dams’ offspring; depletion of ChemR23 decreased macrophage pyroptosis, and depletion of either receptor reversed chemerin-mediated neurodevelopmental deficits and cognitive impairment of offspring of diabetic pregnant dams.ConclusionsChemerin induced diabetic pregnant disease and CCRL2 were required to enrich chemerin in the brain of offspring. Aggregation of chemerin could lead to macrophage recruitment, activation of pyroptosis, the release of inflammatory cytokines, a decrease in the number of neurons, and cognitive impairment in offspring in a ChemR23-dependent manner. Targeting CCRL2 and/or ChemR23 could be useful for treating neuropsychological deficits in offspring of dams with diabetes in pregnancy.Electronic supplementary materialThe online version of this article (10.1186/s12974-019-1573-6) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Chemerin-induced macrophages pyroptosis in fetal brain tissue leads to cognitive disorder in offspring of diabetic dams

Liang

Han

Sun

et al. 2019

J Neuroinflammation

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“…Immature male ICR mice (7–20 postnatal day) (Damul Science, Suwon, Korea) used in the present study were housed under 12-h light/dark cycles (lights on at 06:00 h) with access to water and food ad libitum . The procedure to prepare brain slices was similar to our previous study [24]. After ICR mice were decapitated, their brains were taken out quickly and coronal slices (180–200 µm thick) including the MDH were cut using a vibratome (VT1200S; Leica biosystems, Wetzlar, Germany) in ice-cold artificial cerebrospinal fluid (ACSF).…”

Section: Methodsmentioning

confidence: 99%

Potentiation of the glycine response by serotonin on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice

Nguyen

Cho

Jang

et al. 2019

Korean J Physiol Pharmacol

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The lamina II, also called the substantia gelatinosa (SG), of the trigeminal subnucleus caudalis (Vc), is thought to play an essential role in the control of orofacial nociception. Glycine and serotonin (5-hydroxytryptamine, 5-HT) are the important neurotransmitters that have the individual parts on the modulation of nociceptive transmission. However, the electrophysiological effects of 5-HT on the glycine receptors on SG neurons of the Vc have not been well studied yet. For this reason, we applied the whole-cell patch clamp technique to explore the interaction of intracellular signal transduction between 5-HT and the glycine receptors on SG neurons of the Vc in mice. In nine of 13 neurons tested (69.2%), pretreatment with 5-HT potentiated glycine-induced current (I Gly ). Firstly, we examined with a 5-HT 1 receptor agonist (8-OH-DPAT, 5-HT 1/7 agonist, co-applied with SB-269970, 5-HT 7 antagonist) and antagonist (WAY-100635), but 5-HT 1 receptor agonist did not increase I Gly and in the presence of 5-HT 1 antagonist, the potentiation of 5-HT on I Gly still happened. However, an agonist (α-methyl-5-HT) and antagonist (ketanserin) of the 5-HT 2 receptor mimicked and inhibited the enhancing effect of 5-HT on I Gly in the SG neurons, respectively. We also verified the role of the 5-HT 7 receptor by using a 5-HT 7 antagonist (SB-269970) but it also did not block the enhancement of 5-HT on I Gly . Our study demonstrated that 5-HT facilitated I Gly in the SG neurons of the Vc through the 5-HT 2 receptor. The interaction between 5-HT and glycine appears to have a significant role in modulating the transmission of the nociceptive pathway.

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“…We used the same method to prepare brain slices as in our previous study (Nguyen et al 2015). Firstly, ICR mice were beheaded; the brains were removed quickly and placed in ice-cold bicarbonate-buffered artificial cerebrospinal fluid (ACSF) containing (in mM): 126 NaCl, 2.5 KCl, 2.4 CaCl 2 , 1.2 MgCl 2 , 11 D-glucose, 1.4 NaH 2 PO 4 , 25 NaHCO 3 and 0.5 sodium ascorbate (pH 7.3~7.4, bubbled with 95% O 2 and 5% CO 2 ).…”

Section: Animal and Brain Slice Preparationmentioning

confidence: 99%

Modulation of inhibitory and excitatory neurotransmissions by Zn2+ on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice

Nguyen

Jang

Park

et al. 2019

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The substantia gelatinosa of the trigeminal subnucleus caudalis has been considered to be an essential location for the transference of orofacial sensory signals. The co-localization of inhibitory and excitatory neurotransmitters in the same substantia gelatinosa (SG) neurons has demonstrated their essential part in the modification of nociceptive transmission. Zn 2+ is particularly numerous in the mammalian central nervous system. There are proofs demonstrating the role of Zn 2+ in the modulation of voltage-and ligand-gated ion channels. However, little is known about what roles Zn 2+ may play in the modulation of signal transmission in the SG neurons of the trigeminal subnucleus caudalis (Vc). Therefore, in this study, we used the whole-cell patch clamp technique to find out the effect of Zn 2+ on the responses of three main neurotransmitters (glycine, GABA, and glutamate) on SG neurons of the Vc in mice. We have proved that Zn 2+ induces a big potentiation of glycine receptor-mediated response but attenuates GABA-and glutamate-induced responses at micromolar concentrations, however, enhances glutamate-induced response at nanomolar concentration. Taken together, these data demonstrated that Zn 2+ can modulate glycine, GABA and glutamate-mediated actions on the SG neurons of the Vc and support an important mechanism in spinal sensory information signaling.

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Enhanced GABA action on the substantia gelatinosa neurons of the medullary dorsal horn in the offspring of streptozotocin-injected mice

Cited by 11 publications

References 54 publications

Chemerin-induced macrophages pyroptosis in fetal brain tissue leads to cognitive disorder in offspring of diabetic dams

Chemerin-induced macrophages pyroptosis in fetal brain tissue leads to cognitive disorder in offspring of diabetic dams

Potentiation of the glycine response by serotonin on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice

Modulation of inhibitory and excitatory neurotransmissions by Zn2+ on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis in mice

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