scholarly journals Vesicular Glutamate Transporter 1 Knockdown in Infralimbic Prefrontal Cortex Augments Neuroendocrine Responses to Chronic Stress in Male Rats

Endocrinology ◽  
2017 ◽  
Vol 158 (10) ◽  
pp. 3579-3591 ◽  
Author(s):  
Brent Myers ◽  
Jessica M McKlveen ◽  
Rachel Morano ◽  
Yvonne M Ulrich-Lai ◽  
Matia B Solomon ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Chronic Stress ◽  
Glutamate Transporter ◽  
Male Rats ◽  
Vesicular Glutamate Transporter ◽  
Neuroendocrine Responses ◽  
Glutamate Transporter 1

scholarly journals Prefrontal Cortex Regulates Chronic Stress-Induced Cardiovascular Susceptibility

2019 ◽  
Author(s):  
Derek Schaeuble ◽  
Amy E.B. Packard ◽  
Jessica M. McKlveen ◽  
Rachel L. Morano ◽  
Sarah Fourman ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Chronic Stress ◽  
Cardiovascular Health ◽  
Ex Vivo ◽  
Glutamate Release ◽  
Glutamate Transporter ◽  
Male Rats ◽  
Projection Neurons ◽  
Autonomic Imbalance ◽  
Glutamate Transporter 1

The medial prefrontal cortex (mPFC) is necessary for appropriate appraisal of stressful information, as well as coordinating visceral and behavioral processes. However, prolonged stress impairs mPFC function and prefrontal-dependent behaviors. Additionally, chronic stress induces sympathetic predominance, contributing to health detriments associated with autonomic imbalance. Previous studies identified a subregion of rodent prefrontal cortex, infralimbic cortex (IL), as a key regulator of neuroendocrine-autonomic integration after chronic stress, suggesting that IL output may prevent chronic stress-induced autonomic imbalance. In the current study, we tested the hypothesis that the IL regulates hemodynamic, vascular, and cardiac responses to chronic stress. To address this hypothesis, a viral-packaged siRNA construct was used to knockdown vesicular glutamate transporter 1 (vGluT1) and reduce glutamate packaging and release from IL projection neurons. Male rats were injected with a vGluT1 siRNA-expressing construct or GFP control into the IL and then remained as unstressed controls or were exposed to chronic variable stress (CVS). IL vGluT1 knockdown increased heart rate and mean arterial pressure (MAP) reactivity, while CVS increased chronic MAP only in siRNA-treated rats. In a separate cohort, CVS and vGluT1 knockdown interacted to impair both endothelial-dependent and endothelial-independent vasoreactivity ex vivo. Furthermore, vGluT1 knockdown and CVS increased histological markers of fibrosis and hypertrophy. Thus, knockdown of glutamate release from IL projection neurons indicates that these cells are necessary to prevent the enhanced sympathetic responses to stress that promote susceptibility to cardiovascular pathophysiology. These findings provide evidence for a neurobiological mechanism mediating the relationship between stress and poor cardiovascular health outcomes.

scholarly journals Effects of Repeated 20-Hz Electrical Stimulation on Functional Recovery Following Peripheral Nerve Injury

2019 ◽  
Vol 33 (9) ◽  
pp. 775-784 ◽  
Author(s):  
Sohee Park ◽  
Cai-yue Liu ◽  
Patricia J. Ward ◽  
Poonam B. Jaiswal ◽  
Arthur W. English
Keyword(s):  
Electrical Stimulation ◽  
Peripheral Nerves ◽  
Treadmill Exercise ◽  
Glutamate Transporter ◽  
Vesicular Glutamate Transporter ◽  
Single Application ◽  
Repeated Applications ◽  
Peripheral Axon ◽  
Glutamate Transporter 1 ◽  
Muscle Responses

One hour of 20-Hz continuous electrical stimulation (ES) applied at the time of injury promotes the regeneration of axons in cut peripheral nerves. A more robust enhancement of peripheral axon regeneration is achieved by 2 weeks of daily treadmill exercise. We investigated whether repeated applications of brief ES (mES) would be more effective in promoting regeneration than a single application. Sciatic nerves of C57B6 mice were cut and repaired by end-to-end anastomosis. At that time and every third day for 2 weeks, the repaired nerve was stimulated for 1 hour at 20 Hz. In controls, injured mice were either untreated or treated with ES only once. Direct muscle responses recorded from reinnervated muscles in awake animals were observed earlier both in mice treated with ES and mES than untreated controls. Their amplitudes increased progressively over the post transection study period, but the rate of this progression was increased significantly only in animals treated once with ES. Monosynaptic H reflexes recovered to pretransection levels in both untreated and singly treated mice but in the animals treated repeatedly, they were maintained at more than twice that of the same reflexes recorded prior to injury. In anatomical analyses, both excitatory and inhibitory synaptic contacts with the cell bodies of injured motoneurons, including those expressing the vesicular glutamate transporter 1 (VGLUT1), were sustained in mice treated repeatedly but not in singly treated or untreated mice. Repeated ES does not enhance the rate of restoration of functional muscle reinnervation and results in the retention of exaggerated reflexes.

scholarly journals Expression of Vesicular Glutamate Transporter-2 in Gonadotrope and Thyrotrope Cells of the Rat Pituitary. Regulation by Estrogen and Thyroid Hormone Status

Endocrinology ◽  
2006 ◽  
Vol 147 (8) ◽  
pp. 3818-3825 ◽  
Author(s):  
Erik Hrabovszky ◽  
Imre Kalló ◽  
Gergely F. Turi ◽  
Katalin May ◽  
Gábor Wittmann ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Thyroid Hormone ◽  
Glutamate Transporter ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Mrna Levels ◽  
Vesicular Glutamate Transporter ◽  
Local Synthesis ◽  
Enhanced Secretion

Immunocytochemical studies of the rat adenohypophysis identified a cell population that exhibits immunoreactivity for type-2 vesicular glutamate transporter (VGLUT2), a marker for glutamatergic neuronal phenotype. The in situ hybridization detection of VGLUT2 mRNA expression in adenohypophysial cells verified that VGLUT2 immunoreactivity is due to local synthesis of authentic VGLUT2. Dual-immunofluorescent studies of the hypophyses from male rats showed the presence of VGLUT2 in high percentages of LH (93.3 ± 1.3%)-, FSH (44.7 ± 3.9%)-, and TSH (70.0 ± 5.6%)-immunoreactive cells and its much lower incidence in cells of the prolactin, GH, and ACTH phenotypes. Quantitative in situ hybridization studies have established that the administration of a single dose of 17-β-estradiol (20 μg/kg; sc) to ovariectomized rats significantly elevated VGLUT2 mRNA in the adenohypophysis 16 h postinjection. Thyroid hormone dependence of VGLUT2 expression was addressed by the comparison of hybridization signals in animal models of hypo- and hyperthyroidism to those in euthyroid controls. Although hyperthyroidism had no effect on VGLUT2 mRNA, hypothyroidism increased adenohypophysial VGLUT2 mRNA levels. This coincided with a decreased ratio of VGLUT2-immunoreactive TSH cells, regarded as a sign of enhanced secretion. The presence of the glutamate marker VGLUT2 in gonadotrope and thyrotrope cells, and its up-regulation by estrogen or hypothyroidism, address the possibility that endocrine cells of the adenohypophysis may cosecrete glutamate with peptide hormones in an estrogen- and thyroid status-regulated manner. The exact roles of endogenous glutamate observed primarily in gonadotropes and thyrotropes, including its putative involvement in autocrine/paracrine regulatory mechanisms, will require clarification.

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