Intracerebroventricular effects of angiotensin II on a step-through passive avoidance task in rats

Souza, Fernando Andrade; Sanchis‐Segura, Carles; Fukada, Sandra Yasuyo; Bortoli, Valquiria C. de; Zangrossi, Hélio; Oliveira, Ana Maria de

doi:10.1016/j.nlm.2003.08.006

Cited by 15 publications

(6 citation statements)

References 12 publications

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“…In the same direction, Amph detrimental effects (regarding ROS, inflammatory cytokines and dopaminergic degeneration) were described in limbic areas, whereas they were not detected in HPC (Belcher, O'Dell, & Marshall, ; Dietrich et al, ; Jiang et al, ; Tan et al, ; Valvassori et al, ). On the contrary, vascular, glial, and oxidative markers increase have been described in HPC after higher doses of Amph or a very short time after the last administration (i.e., after 24 hr), suggesting time‐ and dose‐dependent alterations (Che et al, ; Hodes, Lifschytz, Rosen, Cohen Ben‐Ami, & Lichtstein, ; de Souza et al, ). Since the main long‐lasting effect of Amph exposure is DA neurotransmission imbalance, PFC regional susceptibility could be triggered by its greater dopaminergic innervation (Sofuoglu, ).…”

Section: Discussionmentioning

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: Discussionmentioning

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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“…For example, some have shown that angiotensin II improves avoidance memory (60–63), while others using similar learning paradigms have shown that angiotensin II impairs or has no effect on learning and memory (60; 64–66). Given that one of the main aims of the current study was to further understand the role of the renin-angiotensin system in the fear response, we utilized Pavlovian fear conditioning, a robust animal model for assessing memory in fear learning in both animals and humans.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin Type 1 Receptor Inhibition Enhances the Extinction of Fear Memory

Marvar

Goodman

Fuchs

et al. 2014

Biological Psychiatry

103

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Background The current effective treatment options for posttraumatic stress disorder (PTSD) are limited and therefore the need to explore new treatment strategies is critical. Pharmacological inhibition of the renin-angiotensin system is a common approach to treat hypertension and emerging evidence highlights the importance of this pathway in stress and anxiety. A recent clinical study from our laboratory provides evidence supporting a role for the renin-angiotensin system in the regulation of the stress response in patients diagnosed with PTSD. Methods Using an animal model of PTSD and the selective angiotensin receptor type 1 (AT1) antagonist losartan, we investigated the acute and long-term effects of AT1 receptor inhibition on fear memory and baseline anxiety. Following losartan treatment, we performed classical Pavlovian fear conditioning pairing auditory cues with footshocks and examined extinction behavior, gene expression changes in the brain as well as neuroendocrine and cardiovascular responses. Results Following cued fear conditioning, both acute and 2-week administration of losartan enhanced the consolidation of extinction memory but had no effect on fear acquisition, baseline anxiety, blood pressure and neuroendocrine stress measures. Gene expression changes in the brain were also altered in mice treated with losartan for 2 weeks, in particular reduced amygdala AT1 receptor and bed nucleus stria terminalis c-Fos mRNA levels. Conclusions These data suggest that AT1 receptor antagonism enhances the extinction of fear memory and therefore maybe a beneficial therapy for PTSD patients who have impairments in extinction of aversive memories.

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“…112 Angiotensin II antagonist injection before and after a conditioned avoidance test facilitated learning and retention. 112,113 It acts directly on central RAS receptors to enhance associative memory and learning, possibly with a differential effect on acquisition, storage, and recall. 113 In support of earlier findings, Gard and colleagues 106 demonstrated that ACE inhibitors have cognitive enhancing effects, and they enhance learning in rats.…”

Section: Mechanism By Which Hypertension Affects Cognitive Functionmentioning

confidence: 99%

“…112,113 It acts directly on central RAS receptors to enhance associative memory and learning, possibly with a differential effect on acquisition, storage, and recall. 113 In support of earlier findings, Gard and colleagues 106 demonstrated that ACE inhibitors have cognitive enhancing effects, and they enhance learning in rats. This evidence supports the view that the RAS system, which is central to the pathogenesis of hypertension, may also have an additional but important role in cognitive processing that is independent of its effects on blood pressure.…”

Section: Mechanism By Which Hypertension Affects Cognitive Functionmentioning

confidence: 99%

Hypertension and Cognitive Function

Obisesan¹

2009

Clinics in Geriatric Medicine

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Intracerebroventricular effects of angiotensin II on a step-through passive avoidance task in rats

Cited by 15 publications

References 12 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

Angiotensin Type 1 Receptor Inhibition Enhances the Extinction of Fear Memory

Hypertension and Cognitive Function

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