Effects of LY231617 and angiotensin IV on ischemia-induced deficits in circular water maze and passive avoidance performance in rats

Jw, Wright; Ja, Clemens; Ja, Panetta; Eb, Smalstig; La, Weatherly; Ea, Kramár; Es, Pederson; Mungall, Bruce A.; Jw, Harding

doi:10.1016/0006-8993(95)01454-3

Cited by 65 publications

(35 citation statements)

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“…Spaced training and massed training on the MWM lead to differences in the retention of spatial learning (Spreng et al, 2002) and it is possible that this condensed training protocol is a more sensitive test of ischemia-related impairments in spatial learning. While studies vary in the reported patterns of performance of ischemic rats across training trials on the MWM task, they consistently report that ischemic rats exhibit significantly weaker spatial biases on probe trials that follow training (Block andSchwarz, 1997,1998;Jaspers et al, 1990;Nelson et al, 1997;Nunn et al, 1994;Wright et al, 1996). Our data confirm this pattern of results with ischemic animals demonstrating a significantly weaker spatial bias on the probe trial.…”

Section: Discussionsupporting

confidence: 81%

“…Transient global ischemia results in severe impairments in performance on hippocampally-dependent spatial learning tasks such as the Morris water maze (Block andSchwarz, 1997,1998;Hagan and Beaughard, 1990;Jaspers et al, 1990;Nelson et al, 1997;Nunn et al, 1994;Olsen et al, 1994;Wright et al, 1996). Ischemia also leads to deficits in working memory as assessed with object and place recognition tasks (Gulinello et al, 2006;Mumby et al, 1996;Plamondon et al, 2006;Wood et al, 1993).…”

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confidence: 99%

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Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Sandstrom

Rowan

2007

Hormones and Behavior

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Estradiol can act to protect against hippocampal damage resulting from transient global ischemia, but little is known about the functional consequences of such neuroprotection. The present study examines whether acute estradiol administered prior to the induction of transient global ischemia protects against hippocampal cell death and deficits in performance on a spatial learning task. Ovariectomized female rats were primed with estradiol benzoate or oil vehicle 48 and 24 hrs prior to experiencing one of three durations of 4-vessel occlusion (0, 5, or 10 min). Performance on the cued and hidden platform versions of the Morris water maze was assessed one week following ischemia. On the cued platform task, neither hormone treatment nor ischemia significantly influenced acquisition. When tested on the hidden platform task, however, oil-treated rats exhibited impairments in spatial learning after either 5 or 10 min of ischemia while estradiol-treated rats showed no impairments after 5 min of ischemia and only mild impairments after 10 min of ischemia. Immediately following behavioral testing, rats were perfused and survival of CA1 pyramidal cells was assessed. Ischemia was associated with the loss of CA1 pyramidal cells but rats that received estradiol prior to ischemia showed less severe damage. Furthermore, the extent of cell loss was correlated with degree of spatial bias expressed on a probe trial following hidden platform training. These findings indicate that acute exposure to estradiol prior to ischemia is both neuroprotective and functionally protective. Keywords estrogen; ischemia; cardiac arrest; hippocampus; neuroprotection; spatial learning; water maze Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemiaTransient global ischemia leads to the dramatic loss of neurons in the CA1 region of the hippocampus in humans (Horn and Schlote, 1992;Tanabe et al., 1999;Taraszewska et al., 2002), non-human primates (Zola-Morgan et al., 1992), and rodents (Pulsinelli et al., 1982). This neuronal damage can be accompanied by severe impairments in cognition. For example, human survivors of ischemic strokes typically exhibit disruptions in performance on tasks requiring attention, learning and memory (Elwan et al., 1994;Volpe et al., 1986; Address Correspondence to: Noah J. Sandstrom, Department of Psychology, Williams College, 18 Hoxsey Street, Williamstown, MA 01267, Phone: 413-597-4107, Fax: 413-597-2085, E-mail: Noah.Sandstrom@williams.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain...

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Section: Discussionsupporting

confidence: 81%

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confidence: 99%

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Sandstrom

Rowan

2007

Hormones and Behavior

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“…In terms of function, intracranially administered AngIV and its functional analogs facilitate memory in rodent behavior models (Braszko et al, 1988;Wright et al, 1993;Tchekalarova et al, 2001;Lee et al, 2003). AngIV also facilitates reversal of memory shortfalls produced by scopolamine, mecamylamine, abusive alcohol dose, ischemia, as well as by disruption of the perforant path in the hippocampus (Borawska et al, 1989;Wright et al, 1996;Pederson et al, 1998;Albiston et al, 2004a;Olson et al, 2004). AngIV enhances neuronal long-term potentiation in vitro and in vivo (Kramar et al, 2001;Wayner et al, 2001) as well as attenuates PTZinduced seizures (Tchekalarova et al, 2001;Stragier et al, 2006) and protects against cerebral ischemia (Faure et al, 2006a(Faure et al, ,b, 2008.…”

Section: E Distribution Of the Of Angiv Binding Sitesmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli

et al. 2015

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“…In 2001, the hexapeptide angiotensin IV (Ang IV; Val-Tyr-IleHis-Pro-Phe), which improves memory and learning in both rats and mice (Braszko et al, 1988;Wright et al, 1993Wright et al, , 1996Wright et al, , 1999Lee et al, 2004;Gard et al, 2007Gard et al, , 2012Braszko et al, 2008;De Bundel et al, 2009), was demonstrated to inhibit the membrane-bound zinc-dependent insulin-regulated aminopeptidase (EC 3.4.11.3 IRAP,oxytocinase), a member of the M1 family, which is expressed in a diversity of tissues/cells (Albiston et al, 2001;Liao et al, 2006;Saveanu and van Endert, 2012;Nikolaou et al, 2014). There has been dispute in the field as to the target that mediates the memory-enhancing effects of Ang IV, because this hexapeptide has the ability to bind to other proteins (Vanderheyden, 2009;Kawas et al, 2012;Benoist et al, 2014;.…”

Section: Introductionmentioning

confidence: 99%

Binding to and Inhibition of Insulin-Regulated Aminopeptidase by Macrocyclic Disulfides Enhances Spine Density

et al. 2016

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Angiotensin IV (Ang IV) and related peptide analogs, as well as nonpeptide inhibitors of insulin-regulated aminopeptidase (IRAP), have previously been shown to enhance memory and cognition in animal models. Furthermore, the endogenous IRAP substrates oxytocin and vasopressin are known to facilitate learning and memory. In this study, the two recently synthesized 13-membered macrocyclic competitive IRAP inhibitors HA08 and HA09, which were designed to mimic the N terminus of oxytocin and vasopressin, were assessed and compared based on their ability to bind to the IRAP active site, and alter dendritic spine density in rat hippocampal primary cultures. The binding modes of the IRAP inhibitors HA08, HA09, and of Ang IV in either the extended or g-turn conformation at the C terminus to human IRAP were predicted by docking and molecular dynamics simulations. The binding free energies calculated with the linear interaction energy method, which are in excellent agreement with experimental data and simulations, have been used to explain the differences in activities of the IRAP inhibitors, both of which are structurally very similar, but differ only with regard to one stereogenic center. In addition, we show that HA08, which is 100-fold more potent than the epimer HA09, can enhance dendritic spine number and alter morphology, a process associated with memory facilitation. Therefore, HA08, one of the most potent IRAP inhibitors known today, may serve as a suitable starting point for medicinal chemistry programs aided by MD simulations aimed at discovering more drug-like cognitive enhancers acting via augmenting synaptic plasticity.

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Effects of LY231617 and angiotensin IV on ischemia-induced deficits in circular water maze and passive avoidance performance in rats

Cited by 65 publications

References 60 publications

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

Acute pretreatment with estradiol protects against CA1 cell loss and spatial learning impairments resulting from transient global ischemia

International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli

Binding to and Inhibition of Insulin-Regulated Aminopeptidase by Macrocyclic Disulfides Enhances Spine Density

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