A previous history of repeated amphetamine exposure modifies brain angiotensin II AT1 receptor functionality

Casarsa, Brenda Solange; Marinzalda, M.Á.; Marchese, Natalia Andrea; Paz, Maria Constanza; Vivas, Laura; Baiardi, Gustavo; Bregonzio, Claudia

doi:10.1016/j.neuroscience.2015.08.027

Cited by 11 publications

(6 citation statements)

References 76 publications

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“…Our previous reports support the AT 1 ‐R involvement in the development of Amph‐induced neuroadaptations at neurochemical, structural, and behavioral levels (Paz, Assis, Cabrera, Cancela, & Bregonzio, ; Paz, Marchese, Cancela, & Bregonzio, ; Occhieppo et al, ). Moreover, a long‐lasting overexpression of functional AT 1 ‐R was observed in DA‐innervated areas after Amph exposure (Paz et al, ), whereas altered AT 1 ‐R functionality was described regarding classical AngII‐elicited actions (Casarsa et al, ). In the present study, we aimed to characterize the pattern of Amph‐induced deleterious effects, over microglia and astrocyte activation along with vascular network organization in PFC and HPC, and how the AT 1 ‐R modulates those effects.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

Marchese

Occhieppo

Basmadjian

et al. 2019

Eur J of Neuroscience

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Amphetamine‐induced neuroadaptations involve vascular damage, neuroinflammation, a hypo‐functioning prefrontal cortex (PFC), and cognitive alterations. Brain angiotensin II, through angiotensin type 1 receptor (AT1‐R), mediates oxidative/inflammatory responses, promoting endothelial dysfunction, neuronal oxidative damage and glial reactivity. The present work aims to unmask the role of AT1‐R in the development of amphetamine‐induced changes over glial and vascular components within PFC and hippocampus. Attention deficit was evaluated as a behavioral neuroadaptation induced by amphetamine. Brain microvessels were isolated to further evaluate vascular alterations after amphetamine exposure. Male Wistar rats were administered with AT1‐R antagonist, candesartan, followed by repeated amphetamine. After one week drug‐off period, animals received a saline or amphetamine challenge and were evaluated in behavioral tests. Afterward, their brains were processed for cresyl violet staining, CD11b (microglia marker), GFAP (astrocyte marker) or von Willebrand factor (vascular marker) immunohistochemistry, and oxidative/cellular stress determinations in brain microvessels. Statistical analysis was performed by using factorial ANOVA followed by Bonferroni or Tukey tests. Repeated amphetamine administration increased astroglial and microglial markers immunoreactivity, increased apoptotic cells, and promoted vascular network rearrangement at the PFC concomitantly with an attention deficit. Although the amphetamine challenge improved the attentional performance, it triggers detrimental effects probably because of the exacerbated malondialdehyde levels and increased heat shock protein 70 expression in microvessels. All observed amphetamine‐induced alterations were prevented by the AT1‐R blockade. Our results support the AT1‐R involvement in the development of oxidative/inflammatory conditions triggered by amphetamine exposure, affecting cortical areas and increasing vascular susceptibility to future challenges.

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Section: Introductionmentioning

confidence: 99%

Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

Marchese

Occhieppo

Basmadjian

et al. 2019

Eur J of Neuroscience

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“…Furthermore, ANG II receptor type 1 blockade attenuates sensitized locomotor activity elicited by repeated amphetamine injections and alters neuronal activation elicited by amphetamine (15,23,24). Interestingly, amphetamine injection followed by a delay period appears to desensitize salt appetite, urine sodium excretion, and plasma renin induced by intracerebroventricular ANG II in mice (5). Here, we show that amphetamine can potentiate the pressor response to ANG II, providing additional evidence for shared neural substrates between the consequences of amphetamine action and ANG II.…”

Section: Discussionmentioning

confidence: 57%

Amphetamine-induced sensitization of hypertension and lamina terminalis neuroinflammation

Hurley

Beltz

Guo

et al. 2020

American Journal of Physiology-Regulatory, Integrative and Comp

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Psychomotor stimulants are prescribed for many medical conditions, including obesity, sleep disorders, and attention-deficit/hyperactivity disorder. However, despite their acknowledged therapeutic utility, these stimulants are frequently abused, and their use can have both short- and long-term negative consequences. Although stimulants such as amphetamines acutely elevate blood pressure, it is unclear whether they cause any long-term effects on cardiovascular function after use has been discontinued. Previous work in our laboratory has demonstrated that physiological and psychosocial stressors will produce sensitization of the hypertensive response, a heightened pressor response to a hypertensinogenic stimulus delivered after stressor exposure. Here, we tested whether pretreatment with amphetamine for 1 wk can sensitize the hypertensive response in rats. We found that repeated amphetamine administration induced and maintained sensitization of the pressor response to angiotensin II following a 7-day delay after amphetamine injections were terminated. We also found that amphetamine pretreatment altered mRNA expression for molecular markers associated with neuroinflammation and renin-angiotensin-aldosterone system (RAAS) activation in the lamina terminalis, a brain region implicated in the control of sympathetic nervous system tone and blood pressure. The results indicated amphetamine upregulated mRNA expression underlying neuroinflammation and, to a lesser degree, message for components of the RAAS in the lamina terminalis. However, we found no changes in mRNA expression in the paraventricular nucleus. These results suggest that a history of stimulant use may predispose individuals to developing hypertension by promoting neuroinflammation and upregulating activity of the RAAS in the lamina terminalis.

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“…Increased locomotor activity induced by AMPH challenge is inhibited by AT 1 -R antagonist losartan administration in the caudate putamen of rats [24]. AT 1 -R is also involved in learning and memory alterations induced by amphetamine in rats [25]. These findings hint the potential role of brain RAS components in neuroadaptative changes.…”

Section: Electronic Supplementary Materialsmentioning

confidence: 76%

Brain Renin–Angiotensin System Blockade Attenuates Methamphetamine-Induced Hyperlocomotion and Neurotoxicity

Jiang

Zhu

et al. 2018

Neurotherapeutics

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Methamphetamine (METH) abuse has become a major public health concern worldwide without approved pharmacotherapies. The brain renin-angiotensin system (RAS) is involved in the regulation of neuronal function as well as neurological disorders. Angiotensin II (Ang II), which interacts with Ang II type 1 receptor (AT-R) in the brain, plays an important role as a neuromodulator in dopaminergic transmission. However, the role of brain RAS in METH-induced behavior is largely unknown. Here, we revealed that repeated METH administration significantly upregulated the expression of AT-R in the striatum of mice, but downregulated dopamine D3 receptor (D3R) expression. A specific AT-R blocker telmisartan, which can penetrate the brain-blood barrier (BBB), or genetic deletion of AT-R was sufficient to attenuate METH-triggered hyperlocomotion in mice. However, intraperitoneal injection of AT-R blocker losartan, which cannot penetrate BBB, failed to attenuate METH-induced behavior. Moreover, intra-striatum re-expression of AT with lentiviral virus expressing AT reversed the weakened locomotor activity of AT mice treated with METH. Losartan alleviated METH-induced cytotoxicity in SH-SY5Y cells in vitro, which was accompanied by upregulated expressions of D3R and dopamine transporter. In addition, intraperitoneal injection of perindopril, which is a specific ACE inhibitor and can penetrate BBB, significantly attenuated METH-induced hyperlocomotor activity. Collectively, our results show that blockade of brain RAS attenuates METH-induced hyperlocomotion and neurotoxicity possibly through modulation of D3R expression. Our findings reveal a novel role of Ang II-AT-R in METH-induced hyperlocomotion.

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A previous history of repeated amphetamine exposure modifies brain angiotensin II AT1 receptor functionality

Cited by 11 publications

References 76 publications

Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

Amphetamine-induced sensitization of hypertension and lamina terminalis neuroinflammation

Brain Renin–Angiotensin System Blockade Attenuates Methamphetamine-Induced Hyperlocomotion and Neurotoxicity

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