Stress-dependent changes in neuroinflammatory markers observed after common laboratory stressors are not seen following acute social defeat of the Sprague Dawley rat

Hueston, Cara M.; Barnum, Christopher J.; Eberle, Jaime A.; Ferraioli, Frank J.; Buck, Hollin M.; Deak, Terrence

doi:10.1016/j.physbeh.2011.03.013

Cited by 57 publications

(53 citation statements)

References 30 publications

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“…Real-time RT-PCR was acquired and subsequently used in Exps. 2–5 (e.g., Blandino et al, 2009; Hueston et al, 2011). Please refer to supplemental text for more detailed methodology concerning measurement of gene expression.…”

Section: Methodsmentioning

confidence: 99%

“…In order to gain greater spatial resolution, the paraventricular nucleus of the hypothalamus (PVN) was examined. In prior studies, the PVN has been shown to be a key hypothalamic nucleus that is responsive to stress-induced alterations in central cytokines (Hueston et al, 2011), with minocyline effectively blocking stress-related increases in PVN IL-1 expression (Blandino et al, 2006). Thus, given the sensitivity of the hypothalamus demonstrated in Exp.…”

Section: Methodsmentioning

confidence: 99%

“…Several cell types within the CNS such as microglia, perivascular and meningeal macrophages (van Dam et al, 1992), astrocytes (Martinez et al, 1992), and neurons (Tringali et al, 1996), have been shown to produce cytokines, with cytokine receptors identified on nearly all cell types within the brain (Vitkovic et al, 2000). Importantly, however, cytokines have been recognized as having roles outside of neuroinflammation, as they are expressed in both neurons and glia during non-pathological conditions (for review see Vitkovic et al, 2000), and are also recruited in response of non-immunogenic stimuli, such as stress (Hueston et al, 2011). …”

Section: Introductionmentioning

confidence: 99%

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Intoxication‐ and Withdrawal‐Dependent Expression of Central and Peripheral Cytokines Following Initial Ethanol Exposure

Doremus-Fitzwater

Buck

Bordner

et al. 2014

Alcoholism Clin & Exp Res

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Background Evidence has emerged demonstrating that ethanol influences cytokine expression within the CNS, although most studies have examined long-term exposure. Thus, the cytokine response to an acute ethanol challenge was investigated, in order to characterize profiles of cytokine changes following acute exposure. Methods Rats pups were injected intraperitoneally (i.p.) with 2-g/kg ethanol and IL-1 mRNA and protein assessed 0, 60, 120, 180, and 240 min post-injection (Exp. 1). In Exps. 2-5, the expression of several cytokines was examined in adult male rats during acute intoxication (3 hr after 4-g/kg ethanol), as well as withdrawal (18 hr post-injection), after i.p. and intragastric (i.g.) ethanol administration. Results Early in ontogeny, acute ethanol significantly decreased brain IL-1 mRNA and protein. Subsequently, when adult rats were examined, significant and temporally dynamic alterations in central and peripheral cytokines were observed following acute i.p. ethanol exposure (4-g/kg). Although cytokine- and region-dependent, central IL-6 expression was generally increased and TNFα decreased during intoxication, whereas IL-1 expression exhibited increases during withdrawal. In the periphery, acute i.p. ethanol elevated expression of all cytokines, with the response growing in magnitude as the time post-injection increased. Following acute i.g. ethanol (4-g/kg), intoxication-related increases in IL-6 expression were again observed in the PVN, although to a lesser extent. Long-term, voluntary, intermittent ethanol consumption resulted in tolerance to the effects of an i.g. ethanol challenge (4-g/kg) on PVN IL-6 expression, whereas these same elevations in IL-6 expression were still seen in the amygdala in rats with a history of moderate ethanol intake. Treatment with minocycline did not significantly attenuate i.p. or i.g. ethanol-induced changes in central cytokine expression. Conclusions Together, these studies provide a foundation for understanding fluctuations in central and peripheral cytokines following acute ethanol as potential contributors to the constellation of neural and behavioral alterations observed during ethanol intoxication and withdrawal.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Intoxication‐ and Withdrawal‐Dependent Expression of Central and Peripheral Cytokines Following Initial Ethanol Exposure

Doremus-Fitzwater

Buck

Bordner

et al. 2014

Alcoholism Clin & Exp Res

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“…Tissue samples were homogenized into Trisol using TissueLyser 2 (Qiagen), extracted with RNeasy mini protocol (Qiagen), normalized, and converted into cDNA using the QuantiTect Reverse Transcription Kit (Qiagen), which included a DNase treatment step. 73 Probed cDNA amplification was performed in a 10 μL reaction consisting of 5 μL of IQ SYBR Green Supermix (Bio-Rad Laboratories, Hercules, CA), 0.5 μL of primer (final concentration 250 nM), 0.5 μL of cDNA template, and 4 μL of RNase-free water run in triplicate in a 384 well plate (BioRad) and captured in real-time using the CFX Real-Time PCR detection system (BioRad). Relative gene expression was quantified using the 2 −ΔCT method, with expression values normalized to 100% of ultimate control values.…”

Section: ■ Conclusionmentioning

confidence: 99%

Effects of 5-HT_1A Receptor Stimulation on D1 Receptor Agonist-Induced Striatonigral Activity and Dyskinesia in Hemiparkinsonian Rats

Dupre

Ostock

George

et al. 2013

ACS Chem. Neurosci.

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Accumulating evidence supports the value of 5-HT 1A receptor (5-HT 1A R) agonists for dyskinesias that arise with long-term L-DOPA therapy in Parkinson's disease (PD). Yet, how 5-HT 1A R stimulation directly influences the dyskinetogenic D1 receptor (D1R)-expressing striatonigral pathway remains largely unknown. To directly examine this, one cohort of hemiparkinsonian rats received systemic injections of Vehicle + Vehicle, Vehicle + the D1R agonist SKF81297 (0.8 mg/kg), or the 5-HT 1A R agonist ±8-OH-DPAT (1.0 mg/kg) + SKF81297. Rats were examined for changes in abnormal involuntary movements (AIMs), rotations, striatal preprodynorphin (PPD), and glutamic acid decarboxylase (GAD; 65 and 67) mRNA via RT-PCR. In the second experiment, hemiparkinsonian rats received intrastriatal pretreatments of Vehicle (aCSF), ±8-OH-DPAT (7.5 mM), or ±8-OH-DPAT + the 5-HT 1A R antagonist WAY100635 (4.6 mM), followed by systemic Vehicle or SKF81297 after which AIMs, rotations, and extracellular striatal glutamate and nigral GABA efflux were measured by in vivo microdialysis. Results revealed D1R agonist-induced AIMs were reduced by systemic and intrastriatal 5-HT 1A R stimulation while rotations were enhanced. Although ±8-OH-DPAT did not modify D1R agonist-induced increases in striatal PPD mRNA, the D1R/5-HT 1A R agonist combination enhanced GAD65 and GAD67 mRNA. When applied locally, ±8-OH-DPAT alone diminished striatal glutamate levels while the agonist combination increased nigral GABA efflux. Thus, presynaptic 5-HT 1A R stimulation may attenuate striatal glutamate levels, resulting in diminished D1R-mediated dyskinetic behaviors, but maintain or enhance striatal postsynaptic factors ultimately increasing nigral GABA levels and rotational activity. The current findings offer a novel mechanistic explanation for previous results concerning 5-HT 1A R agonists for the treatment of dyskinesia.

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“…The original mapping studies in the rat showed that one such area of exclusive ER-β gene expression is the PVN [37,38], implicating an involvement of gonadal steroid modulation in stress-induced inflammatory responses. On the other hand, Pg is a stress-related steroid which is synthesized and released from both the gonad and adrenal cortex [39,40]. To date, however, animal studies have yet to establish a relationship between endogenous gonadal steroid levels and stress-induced changes in cytokine expression.…”

Section: Introductionmentioning

confidence: 99%

Effects of the Estrous Cycle and Ovarian Hormones on Central Expression of Interleukin-1 Evoked by Stress in Female Rats

Arakawa

Hueston

et al. 2014

Neuroendocrinology

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Exposure to stressors such as foot shock (FS) leads to increased expression of multiple inflammatory factors, including the proinflammatory cytokine interleukin-1 (IL-1) in the brain. Studies have indicated that there are sex differences in stress reactivity, suggesting that the fluctuations in gonadal steroid levels across the estrous cycle may play a regulatory role in the stress-induced cytokine expression. The present studies were designed to investigate the role of 17-β-estradiol (E₂) and progesterone (Pg) in regulating the cytokine response within the paraventricular nucleus (PVN) of the hypothalamus through analysis of gene expression with real-time RT-PCR. Regularly cycling female rats showed a stress-induced increase in PVN IL-1 levels during the diestrous, proestrous, and estrous stages. During the metestrous stage, no change in IL-1 levels was seen following FS; however, estrogen receptor (ER)-β levels did increase. Ovariectomy resulted in an increase in PVN IL-1 levels, which was attenuated by treatment with estradiol benzoate (10 or 50 µg), indicating an E₂-mediated anti-inflammatory effect. Ovariectomized rats treated with Pg (500 or 1,250 µg) showed no alteration in IL-1 levels, but Pg did up-regulate ER-β gene expression. The results from the current study implicate a potential mechanism through which high availability of endogenous Pg during the metestrous stage increases ER-β sensitivity, which in turn attenuates the PVN IL-1 response to stress. Thus, the interaction between gonadal steroid hormones and their central receptors may exert a powerful inhibitory effect on neuroimmune consequences of stress throughout the estrous cycle.

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Stress-dependent changes in neuroinflammatory markers observed after common laboratory stressors are not seen following acute social defeat of the Sprague Dawley rat

Cited by 57 publications

References 30 publications

Intoxication‐ and Withdrawal‐Dependent Expression of Central and Peripheral Cytokines Following Initial Ethanol Exposure

Intoxication‐ and Withdrawal‐Dependent Expression of Central and Peripheral Cytokines Following Initial Ethanol Exposure

Effects of 5-HT_1A Receptor Stimulation on D1 Receptor Agonist-Induced Striatonigral Activity and Dyskinesia in Hemiparkinsonian Rats

Effects of the Estrous Cycle and Ovarian Hormones on Central Expression of Interleukin-1 Evoked by Stress in Female Rats

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Stress-dependent changes in neuroinflammatory markers observed after common laboratory stressors are not seen following acute social defeat of the Sprague Dawley rat

Cited by 57 publications

References 30 publications

Intoxication‐ and Withdrawal‐Dependent Expression of Central and Peripheral Cytokines Following Initial Ethanol Exposure

Intoxication‐ and Withdrawal‐Dependent Expression of Central and Peripheral Cytokines Following Initial Ethanol Exposure

Effects of 5-HT1A Receptor Stimulation on D1 Receptor Agonist-Induced Striatonigral Activity and Dyskinesia in Hemiparkinsonian Rats

Effects of the Estrous Cycle and Ovarian Hormones on Central Expression of Interleukin-1 Evoked by Stress in Female Rats

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Effects of 5-HT_1A Receptor Stimulation on D1 Receptor Agonist-Induced Striatonigral Activity and Dyskinesia in Hemiparkinsonian Rats