Research reportEffects of LY231617 and angiotensin IV on ischemia-induced deficits in circular water maze and passive avoidance performance in rats
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Cited by (63)
Cognitive benefits of angiotensin IV and angiotensin-(1–7): A systematic review of experimental studies
2018, Neuroscience and Biobehavioral ReviewsCitation Excerpt :Thus, i.c.v. treatment is potentially more effective given that it produces more global effects due to diffusion, is easier to perform consistently among animals, and can be done in larger doses. Further, in rats, Ang IV appears to exert beneficial effects when given 5–15 min prior to learning (Wright et al., 1996; Braszko et al., 1988), immediately after learning (Golding et al., 2010; Tchekalarova et al., 2001aa,b), or 5–30 min prior to testing (Braszko et al., 2006; Paris et al., 2013; Wright et al., 1993). However, the Kerr et al. (2005) study administered Ang IV some 30, 90, and 180 min following training, which may have been simultaneously outside the optimal window for Ang IV to exert its hypothesized consolidation-enhancing effects around the time of training, as well as too far away from the testing time for its recognition-enhancing effects.
The development of small molecule angiotensin IV analogs to treat Alzheimer's and Parkinson's diseases
2015, Progress in NeurobiologyCitation Excerpt :The AngIV analog, Nle1-AngIV, has shown promise in overcoming the memory impairments evidenced by several dementia animal models. Treatment with Nle1-AngIV reverses memory deficits due to: (1) application of the cholinergic muscarinic receptor antagonist scopolamine (Pederson et al., 2001); (2) kainic acid-induced lesions of the hippocampus (Stubley-Weatherly et al., 1996); (3) perforant path knife-cuts (Wright et al., 1999); (4) ischemia resulting from transient four-vessel occlusion (Wright et al., 1996b); and (5) embolic stroke due to carotid artery injection of microspheres (Faure et al., 2006). Consistent with these behavioral results, brain binding sites for [125I] AngIV have been autoradiographically localized in structures known to mediate cognitive processing including the neocortex, hippocampus, and basal nucleus of Meynert (Chai et al., 2000; Harding et al., 1992; Wright and Harding, 2009).
Central administration of angiotensin IV rapidly enhances novel object recognition among mice
2013, NeuropharmacologyCitation Excerpt :Consistent with this, central administration of Ang IV induced cognitive improvements equivalent to Ang II in rats (Braszko et al., 1988), and the blockade of AT4 receptors produced deficits in spatial learning (Wilson et al., 2009; Wright et al., 1999). Agonism of AT4 receptors has been reported to promote hippocampal long-term potentiation (LTP; Kramár et al., 2001; Wayner et al., 2001), spatial learning (Lee et al., 2004; Wright et al., 1999), and the restoration of spatial cognitive function following a variety of central insults (Stubley-Weatherly et al., 1996; Wright et al., 1996, 1999; Pederson et al., 2001). In the present investigation, we assessed the dose–response relationship of Ang IV-enhanced learning and memory using a truncated version of the novel object recognition task.
Brain renin-angiotensin-A new look at an old system
2011, Progress in NeurobiologyCitation Excerpt :A number of studies indicate that AngIV, and AngIV analogues such as Nle1-AngIV, can facilitate long-term potentiation, learning, and memory consolidation (Albiston et al., 2004a,b; Braszko et al., 1988; Kramár et al., 2001; Wright et al., 1999). Most importantly studies using various dementia models to test the efficacy of Nle1-AngIV have demonstrated that acute application reversed deficits initiated by: (1) treatment with scopolamine (Pederson et al., 2001); (2) kainic acid injections into the hippocampus (Stubley-Weatherly et al., 1996); (3) perforant path cuts (Wright et al., 1999); and (4) ischemia resulting from transient four vessel occlusion (Wright et al., 1996b). Consistent with these behavioral and electrophysiological results, brain binding sites for [125I]-AngIV have been autoradiographically localized in structures that mediate cognitive processing including the neocortex, hippocampus, and basal nucleus of Meynert (Chai et al., 2000; Harding et al., 1992; Wright and Harding, 2009).