1988
DOI: 10.1016/0014-2999(88)90536-5
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Somatostatin and SMS 201-995 reverse the impairment of cognitive functions induced by cysteamine depletion of brain somatostatin

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Cited by 53 publications
(20 citation statements)
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“…Moreover, intracerebroventricular application of somatostatin facilitated memory and comprised a mitigating effect upon experimentally induced retrograde amnesia (Vecsei et al 1983(Vecsei et al , 1984Lamirault et al 2001). Also, depletion of somatostatin through application of cysteamine (Szabo and Reichlin 1981) impaired hippocampus-dependent memory performance in a variety of tasks including passive and active avoidance learning (Bakhit and Swerdlow 1986;Haroutunian et al 1987;Schettini et al 1988;DeNoble et al 1989;Vecsei and Widerlov 1990;Matsuoka et al 1994), as well as water and radial maze paradigms (Fitzgerald and Dokla 1989;Matsuoka et al 1995;Guillou et al 1998). However, some studies indicate opposite effects of intrahippocampal injections of cysteamine on hippocampusdependent tasks (Guillou et al 1998(Guillou et al , 1999.…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, intracerebroventricular application of somatostatin facilitated memory and comprised a mitigating effect upon experimentally induced retrograde amnesia (Vecsei et al 1983(Vecsei et al , 1984Lamirault et al 2001). Also, depletion of somatostatin through application of cysteamine (Szabo and Reichlin 1981) impaired hippocampus-dependent memory performance in a variety of tasks including passive and active avoidance learning (Bakhit and Swerdlow 1986;Haroutunian et al 1987;Schettini et al 1988;DeNoble et al 1989;Vecsei and Widerlov 1990;Matsuoka et al 1994), as well as water and radial maze paradigms (Fitzgerald and Dokla 1989;Matsuoka et al 1995;Guillou et al 1998). However, some studies indicate opposite effects of intrahippocampal injections of cysteamine on hippocampusdependent tasks (Guillou et al 1998(Guillou et al , 1999.…”
Section: Discussionmentioning
confidence: 99%
“…In support of this are the observations that the concentration of somatostatin in the brain (Davies et al 1980) and cerebrospinal fluid (Atack et al 1988) is reduced in patients with Alzheimer's dementia, neuritic plaques contain somatostatin (Morrison et al 1985), neurofibrillary tangles have been identified in somatostatinergic neurons (Roberts et al 1985) and a strict correlation has been demonstrated between somatostatin levels and cognitive performance in patients affected by Alzheimer's disease (Tamminga et al 1987). In animal models, depletion of rat brain somatostatin by cysteamine administration (a thiol-containing agent the action of which mimics the natural decline in somatostatin content in aged animals (Florio et al 1991)) caused memory loss as assessed by many different behavioural paradigms, including active and passive avoidance tests (Vecsei et al 1984, Harotunian et al 1987, Schettini et al 1988a, Florio et al 1988, the Morris swim test (Fitzgerald & Dokla 1989) and the eight-arm radial maze (Sessions et al 1989).…”
Section: Introductionmentioning
confidence: 98%
“…In a similar paradigm, the SRIFdepleting substance cysteamine, impaired the learning performance of rats in an active avoidance behavior model (VĂšcsei et al 1984). SRIF could also reverse the impairment of cognitive functions induced by cysteamine depletion of brain SRIF (Schettini et al 1988). Dournaud et al(1996) suggest that frontal somatostatinergic interneurons are likely to participate in learning behavior and in the regulation of spatial amnesic processes.…”
Section: -Srif Receptor Induced By Diazepam Was Accompanied By a Decrmentioning
confidence: 98%
“…Nabeshima et al (1990) suggest that benzodiazepines induce disruptive effects on learning and memory through their recognition site on the GABA receptor and that benzodiazepine-induced learning and memory impairment of is, at least in part, the result of the dysfunction of the cholinergic neuronal system. However, because of the important role of brain tetradecapeptide somatostatin (SRIF) in the cognitive functions of rats (Cacabelos et al 1988;Dournaud et al 1996;Matsuoka et al 1994;Schettini et al 1988;VĂšcsei et al 1984;), and interaction between somatostatinergic and GABAergic neuronal systems (Boyano-AdĂĄnez et al 1995;Hendry et al 1984;Kawaguchi and Kubota 1998;Llorens-Cortes et al 1992;Xie and Sastry 1992) it is possible to assume that the somatostatinergic system is implicated in the mechanism of action of diazepam. SRIF is widely distributed in the central nervous system (CNS) and peripheral tissues (see Reichlin 1983).…”
Section: -Srif Receptor Induced By Diazepam Was Accompanied By a Decrmentioning
confidence: 99%