Glutamate-Glutamine Transfer and Chronic Stress-Induced Sex Differences in Cocaine Responses

Shimamoto, Akiko; Rappeneau, Virginie; Munjal, Havisha; Farris, Tonie; Davis, Christopher R.; Wilson, Alicia M.; Edwards, Malcolm; Moore, Charles F.; Reynolds, Collin; Meshul, Charles K.

doi:10.1016/j.neuroscience.2018.09.009

Cited by 7 publications

(2 citation statements)

References 70 publications

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“…Semi-quantitative Westerns were performed on striatal tissue using WES™ Protein Simple instrument, as previously described [ 32 , 33 ]. All of the samples were diluted to 0.5mg/mL (5 μL) with 0.1X sample buffer and 5X fluorescent Master Mix from ProteinSimple, then boiled at 95 °C for 5 min.…”

Section: Methodsmentioning

confidence: 99%

Rats Lacking Dopamine Transporter Display Increased Vulnerability and Aberrant Autonomic Response to Acute Stress

et al. 2020

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The activity of the hypothalamus–pituitary–adrenal (HPA) axis is pivotal in homeostasis and presides the adaptative response to stress. Dopamine Transporter (DAT) plays a key role in the regulation of the HPA axis. We used young adult female DAT Knockout (KO) rats to assess the effects of DAT ablation (partial, heterozygous DAT+/-, or total, homozygous DAT-/-) on vulnerability to stress. DAT-/- rats show profound dysregulation of pituitary homeostasis, in the presence of elevated peripheral corticosterone, before and after acute restraint stress. During stress, DAT-/- rats show abnormal autonomic response at either respiratory and cardiovascular level, and delayed body temperature increase. DAT+/- rats display minor changes of hypophyseal homeostatic mechanisms. These rats display a similar pituitary activation to that of the control animals, albeit in the presence of higher release of peripheral corticosterone than DAT-/- after stress, and reduced temperature during stress. Our data indicate that DAT regulates the HPA axis at both the central and peripheral level, including autonomic function during stress. In particular, the partial deletion of DAT results in increased vulnerability to stress in female rats, which display central and peripheral alterations that are reminiscent of PTSD, and they might provide new insights in the pathophysiology of this disorder.

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Section: Methodsmentioning

confidence: 99%

Rats Lacking Dopamine Transporter Display Increased Vulnerability and Aberrant Autonomic Response to Acute Stress

et al. 2020

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“…GLT-1 and GLAST are located in astrocytes; they take in the excessive glutamate and maintain normal neurotransmission. PAG is an enzyme located in the presynaptic terminal and catalyses glutamine to glutamate, which could enhance the level of glutamate [33,34]. Therefore, the dysregulation of these regulators could lead to the excessive accumulation of glutamate in the synaptic cleft and eventually induce excitotoxicity [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Naringin provides neuroprotection in CCL2-induced cognition impairment by attenuating neuronal apoptosis in the hippocampus

et al. 2020

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Background: Chemokine CC motif ligand 2 (CCL2) is one of the most widely recognised proinflammatory chemokines in cognitive disorders. Currently, CCL2-targeting drugs are extremely limited. Thus, this study aimed to explore the neuroprotection afforded by naringin in CCL2-induced cognitive impairment in rats. Methods: Before the CCL2 intra-hippocampal injection, rats were treated with naringin for 3 consecutive days via intraperitoneal injection. Two days post-surgery, the Morris water maze (MWM) and novel object recognition (NORT) tests were performed to detect spatial learning and memory and object cognition, respectively. Nissl staining and dUTP nick-end labelling (TUNEL) staining were performed to assess histopathological changes in the hippocampus. Commercial kits were used to measure the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to examine the relative mRNA expression of interleukin 1β, (IL-1β), interleukin 6 (IL-6), glutamate/aspartate transporter (GLAST), glutamate transporter-1 (GLT-1), phosphate-activated glutaminase (PAG), cysteine aspartic acidspecific protease 8 (caspase-8), cysteine aspartic acid-specific protease 3 (caspase-3), cell lymphoma/leukaemia-2 (Bcl-2), and Bcl-2 associated X protein (Bax). Results: In the MWM, the average escape latency and average swimming distance were significantly reduced and the crossing times were increased in the naringin-treated groups, compared with the CCL2 group. The NORT results revealed that, compared with the CCL2 rats, the discrimination index in the naringin-treated rats increased significantly. Nissl and TUNEL staining revealed that naringin protected the structure and survival of the neurons in the CA1 zone of the hippocampus. In the naringin-treated groups, the SOD and GSH-Px activities were increased, whereas the MDA levels were decreased. Furthermore, in the naringin-treated groups, the relative mRNA expression of IL-1β and IL-6 was significantly decreased; GLAST and GLT-1 mRNA expression levels were increased, whereas PAG was decreased. In the naringin-treated groups, the relative mRNA expression levels of caspase-8, caspase-3, and Bax were decreased, whereas that of Bcl-2 was increased.

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Glutamatergic neurotransmission: A potential pharmacotherapeutic target for the treatment of cognitive disorders

Chakraborty

Dey

Gopalakrishnan

et al. 2023

Ageing Research Reviews

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Glutamate-Glutamine Transfer and Chronic Stress-Induced Sex Differences in Cocaine Responses

Cited by 7 publications

References 70 publications

Rats Lacking Dopamine Transporter Display Increased Vulnerability and Aberrant Autonomic Response to Acute Stress

Rats Lacking Dopamine Transporter Display Increased Vulnerability and Aberrant Autonomic Response to Acute Stress

Naringin provides neuroprotection in CCL2-induced cognition impairment by attenuating neuronal apoptosis in the hippocampus

Glutamatergic neurotransmission: A potential pharmacotherapeutic target for the treatment of cognitive disorders

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