Improvement by dynorphin A (1–13) of galanin‐induced impairment of memory accompanied by blockade of reductions in acetylcholine release in rats

Hiramatsu, Masayuki; Mori, Hidefumi; Murasawa, Hiroyasu; Kameyama, Tsutomu

doi:10.1111/j.1476-5381.1996.tb15396.x

Cited by 31 publications

(25 citation statements)

References 52 publications

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“…Indeed, Dyn A degrades slower than Dyn B in extracts of several brain structures (Sandin et al, 1997). The facilitatory effects of Dyn A on memory retention in the PA task, sensitivity to the kantagonist and the dose dependence are in an agreement with previous reports Hiramatsu et al, 1996Hiramatsu et al, , 1998Ukai et al, 1997). k-Opioid agonists induce dysphoria in humans and endogenous dynorphins mediate aversive reactions in animals (Kreek et al, 2002;Shippenberg et al, 2001).…”

Section: Discussionsupporting

confidence: 78%

Big Dynorphin, a Prodynorphin-Derived Peptide Produces NMDA Receptor-Mediated Effects on Memory, Anxiolytic-Like and Locomotor Behavior in Mice

Kuzmin

Madjid

Terenius

et al. 2005

Neuropsychopharmacol

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Effects of big dynorphin (Big Dyn), a prodynorphin-derived peptide consisting of dynorphin A (Dyn A) and dynorphin B (Dyn B) on memory function, anxiety, and locomotor activity were studied in mice and compared to those of Dyn A and Dyn B. All peptides administered i.c.v. increased step-through latency in the passive avoidance test with the maximum effective doses of 2.5, 0.005, and 0.7 nmol/animal, respectively. Effects of Big Dyn were inhibited by MK 801 (0.1 mg/kg), an NMDA ion-channel blocker whereas those of dynorphins A and B were blocked by the k-opioid antagonist nor-binaltorphimine (6 mg/kg). Big Dyn (2.5 nmol) enhanced locomotor activity in the open field test and induced anxiolytic-like behavior both effects blocked by MK 801. No changes in locomotor activity and no signs of anxiolytic-like behavior were produced by dynorphins A and B. Big Dyn (2.5 nmol) increased time spent in the open branches of the elevated plus maze apparatus with no changes in general locomotion. Whereas dynorphins A and B (i.c.v., 0.05 and 7 nmol/animal, respectively) produced analgesia in the hot-plate test Big Dyn did not. Thus, Big Dyn differs from its fragments dynorphins A and B in its unique pattern of memory enhancing, locomotor-and anxiolytic-like effects that are sensitive to the NMDA receptor blockade. The findings suggest that Big Dyn has its own function in the brain different from those of the prodynorphin-derived peptides acting through k-opioid receptors.

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Section: Discussionsupporting

confidence: 78%

Big Dynorphin, a Prodynorphin-Derived Peptide Produces NMDA Receptor-Mediated Effects on Memory, Anxiolytic-Like and Locomotor Behavior in Mice

Kuzmin

Madjid

Terenius

et al. 2005

Neuropsychopharmacol

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“…The ACE is a promiscuous enzyme; apart from Ang II and bradykinin, a number of other neuropeptide substrates have been reported for ACE, including substance P, neurotensin, dynorphin and enkephalin. 110 Some of these neuropeptide substrates have memory-enhancing properties; substance P, after peripheral or central application, has reinforcing and memory-facilitating effects inducing place preference 111,112 and avoidance learning; 113,114 dynorphins have an improving role in memory-impairment paradigms, such as basal forebrain lesions 115 and mecamylamine-induced 116 and galanin-induced impairment 117 of learning and memory.…”

Section: Memory-enhancing Effect Of Aceismentioning

confidence: 99%

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

2009

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Since their inception, angiotensin-converting enzyme (ACE) inhibitors have been used as first-line therapy for the treatment of cardiovascular and renal diseases. They restore the balance between the vasoconstrictive salt-retentive and hypertrophy-causing peptide angiotensin II (Ang II) and bradykinin, a vasodilatory and natriuretic peptide. As ACE is a promiscuous enzyme, ACE inhibitors alter the metabolism of a number of other vasoactive substances. ACE inhibitors decrease systemic vascular resistance without increasing heart rate and promote natriuresis. They have been proven effective in the treatment of hypertension, and reduce mortality in congestive heart failure and left ventricular dysfunction after myocardial infarction. They inhibit ischemic events and stabilize plaques. Furthermore, they delay the progression of diabetic nephropathy and neuropathy and act as antioxidants. Ongoing studies have elucidated protective roles for them in both memory-related disorders and cancer. INTRODUCTIONIn recent years, stressful and fiercely competitive lifestyles and food habits have compounded the problems of hypertension. Long-standing and stressful, progressively rising hypertension can lead to many disorders, including myocardial infarction (MI), cerebrovascular events, congestive heart failure, peripheral arterial insufficiency, premature mortality 1 and renal dysfunction leading to glomerulosclerosis and kidney artery aneurysm. 2 A number of therapies are available, but angiotensin-converting enzyme (ACE) inhibitors have been the preferred first-line therapy for hypertension, congestive heart failure, left ventricular (LV) systolic dysfunction and MI. 3,4 ACE inhibitors (ACEis) have been in use for the past two decades, and the interest in them is still growing. Recently, the discovery of domain-selective ACEis and new members of the renin-angiotensin system (RAS) (that is, angiotensin-converting enzyme 2) have again fueled the interest of researchers. Some new studies have expanded the already impressive clinical profile of ACEis. This review traces some already known and new facets of ACE inhibition and introduces new advances in the designing of a new generation of ACEis.

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Section: Electroconvulsive Therapy (Ect) Is a Highly Effective Treatmmentioning

confidence: 99%

“…The role of receptors in learning and memory is more complex. While agonists may impair memory in a dose-dependent fashion (Colombo et al, 1992), From they may also ameliorate memory deficits due to disruption of cholinergic transmission (Hiramatsu et al 1996).Repeated ECS stimulates the release of proenkephalin and proopiomelanocortin ( ␤ -endorphin) (Tortella et al 1989) and results in increased abundance of mRNA for preproenkepohalin in the hypothalmus and hippocampus (Yoshikawa et al 1985;Xie et al 1989;Simmons and Chavkin 1996). In the perforant pathway, projecting from entorhinal cortex to the hippocampal dentate gyrus, repeated ECS results in increased enkephalin immunostaining.…”

mentioning

confidence: 99%

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Naloxone in the Prevention of the Adverse Cognitive Effects of ECT A Within-Subject, Placebo Controlled Study

Prudic¹,

Fitzsimons

Nobler

et al. 1999

Neuropsychopharmacology

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Electroconvulsive therapy (ECT) is a highly effective treatment for major depression, but is also associated with characteristic cognitive side effects. Several reports document that endogenous opioids and their receptors are activated by electroconvulsive shock (ECS) and that naloxone in doses sufficient to block endogenous opioid receptors may reverse ECS-induced retrograde amnesia. This placebo-controlled, randomized, within-patient study was conducted to examine the potential of naloxone, given in doses sufficient to block opioid receptors (high dose)Electroconvulsive therapy (ECT) is a highly effective treatment for major depression and a variety of other disorders . However, the cognitive side effects of ECT are the major factor limiting its use. The cognitive consequences of ECT involve a period of postictal disorientation immediately following the induced seizure, as well as a pattern of more sustained neuropsychological deficits, principally anterograde and retrograde amnesia .There is substantial evidence that electroconvulsive shock (ECS) in experimental animals alters the concentrations of endogenous opioid peptides and the density of their receptors (Holaday et al. 1986). Opioids produce effects through at least three different receptors, , ␦ , and (Mansour et al. 1988; Quirion 1988). The receptors and ␦ have been extensively studied, and agonists at these receptors generally interfere with learning and memory, resulting in both anterograde and retrograde amnesia. The role of receptors in learning and memory is more complex. While agonists may impair memory in a dose-dependent fashion (Colombo et al., 1992), From they may also ameliorate memory deficits due to disruption of cholinergic transmission (Hiramatsu et al. 1996).Repeated ECS stimulates the release of proenkephalin and proopiomelanocortin ( ␤ -endorphin) (Tortella et al. 1989) and results in increased abundance of mRNA for preproenkepohalin in the hypothalmus and hippocampus (Yoshikawa et al. 1985;Xie et al. 1989;Simmons and Chavkin 1996). In the perforant pathway, projecting from entorhinal cortex to the hippocampal dentate gyrus, repeated ECS results in increased enkephalin immunostaining. In contrast, the release of dynorphin appears to be more complex. While increased dynorphin immunostaining has been found in limbic and basal ganglia structures, chronic ECS results in decreased levels in the mossy fiber axons of the dentate granule cells (Kanamatsu et al. 1986;Lasön et al. 1992). Overall, it appears that repeated ECS results in widespread increased synthesis and release in the proenkephalin system, and large decreases in the prodynorphin system in the hippocampus. Increased peptide synthesis and release may account for some findings of a sustained decreased density of and ␦ receptors following chronic ECS (Nakata et al. 1985;Crain et al. 1987). In humans, ECT has been found to result acutely in large increases in plasma ␤ -endorphin immunoreactivity (Alexopoulos et al. 1983;Weizman et al. 1987;Young et al. 1991).In a number of models...

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Improvement by dynorphin A (1–13) of galanin‐induced impairment of memory accompanied by blockade of reductions in acetylcholine release in rats

Cited by 31 publications

References 52 publications

Big Dynorphin, a Prodynorphin-Derived Peptide Produces NMDA Receptor-Mediated Effects on Memory, Anxiolytic-Like and Locomotor Behavior in Mice

Big Dynorphin, a Prodynorphin-Derived Peptide Produces NMDA Receptor-Mediated Effects on Memory, Anxiolytic-Like and Locomotor Behavior in Mice

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

Naloxone in the Prevention of the Adverse Cognitive Effects of ECT A Within-Subject, Placebo Controlled Study

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