Changes in brain somatostatin in memory-deficient rats: comparison with cholinergic markers

Matsuoka, Naoki; Yamazaki, Mayako; Yamaguchi, Isamu

doi:10.1016/0306-4522(94)00628-i

Cited by 48 publications

(22 citation statements)

References 54 publications

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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%

Role of the somatostatin system in contextual fear memory and hippocampal synaptic plasticity

Kluge¹,

Stoppel²,

Szinyei³

et al. 2008

Learn. Mem.

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Somatostatin has been implicated in various cognitive and emotional functions, but its precise role is still poorly understood. Here, we have made use of mice with somatostatin deficiency, based upon genetic invalidation or pharmacologically induced depletion, and Pavlovian fear conditioning in order to address the contribution of the somatostatin system to associative fear memory. The results demonstrate an impairment of foreground and background contextual but not tone fear conditioning in mice with targeted ablation of the somatostatin gene. These deficits were associated with a decrease in long-term potentiation in the CA1 area of the hippocampus. Both the behavioral and the electrophysiological phenotypes were mimicked in wild-type mice through application of the somatostatin-depleting substance cysteamine prior to fear training, whereas no further deficits were observed upon application in the somatostatin null mutants. These results suggest that the somatostatin system plays a critical role in the acquisition of contextual fear memory, but not tone fear learning, and further highlights the role of hippocampal synaptic plasticity for information processing concerning contextual information.

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Section: Discussionmentioning

confidence: 99%

Role of the somatostatin system in contextual fear memory and hippocampal synaptic plasticity

Kluge¹,

Stoppel²,

Szinyei³

et al. 2008

Learn. Mem.

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“…Thus, we propose that inhibition of IRAP in the central nervous system extends the half-life of endogenous neuropeptides that potentiate memory. For example, vasopressin, substance P, and somatostatin, known substrates for IRAP (18), play important roles in cognitive function (26,27). It is tempting to speculate that their functions may be enhanced by inhibition of IRAP.…”

Section: Discussionmentioning

confidence: 99%

Evidence That the Angiotensin IV (AT4) Receptor Is the Enzyme Insulin-regulated Aminopeptidase

Albiston¹,

McDowall²,

Matsacos³

et al. 2001

Journal of Biological Chemistry

418

363

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Central infusion of angiotensin IV or its more stable analogues facilitates memory retention and retrieval in normal animals and reverses amnesia induced by scopolamine or by bilateral perforant pathway lesions. These peptides bind with high affinity and specificity to a novel binding site designated the angiotensin AT 4 receptor. Until now, the AT 4 receptor has eluded molecular characterization. Here we identify the AT 4 Central infusions of the hexapeptide VYIHPF (angiotensin IV, Ang IV) 1 or its more stable analogues, Nle 1 -Ang IV andNorleucinal Ang IV, facilitate memory retention and retrieval in rats in the passive avoidance and Morris water maze paradigms (1-3). In two rat models of amnesia, induced by the muscarinic antagonist, scopolamine, or bilateral perforant pathway lesion, the Ang IV analogues reversed the memory deficits detected utilizing the Morris water maze paradigm (3, 4). Enhancement of long term memory by Ang IV has also been demonstrated in species as distant as crabs (5). Angiotensin IV and its analogues enhance long term potentiation in both the dentate gyrus in vivo (6) and the CA1 region of the hippocampus in vitro (7), possibly via actions at the post-synaptic terminal. We have also shown that Ang IV enhances K ϩ -evoked acetylcholine release from rat hippocampal slices (8).The actions of Ang IV and its analogues are mediated by the angiotensin AT 4 receptor, defined by an international nomenclature committee (9) as the high affinity binding site specific for Ang IV (10). The AT 4 receptor has since been shown to bind with nanomolar affinity the decapeptide, LVVYPWTQRF (LVV-H7), isolated from sheep cerebral cortex (19).Although first identified in bovine adrenal, the receptor is widely distributed throughout the brain and peripheral organs (11). In the central nervous system, its distribution is highly conserved in guinea pig (12), macaque monkey (13), and human (14) brains. AT 4 receptors occur in high levels in the basal nucleus of Meynert, in the CA1 to CA3 regions of Ammon's horn in the hippocampus, and throughout the neocortex, areas important for cognitive processing. Despite the dramatic central effects of Ang IV and the abundance of the receptor in the central nervous system, the identity of the AT 4 receptor and the mechanism by which its ligands mediate their actions were unknown. MATERIALS AND METHODSProtein Purification-AT 4 receptors in bovine adrenal membranes (16 mg of membrane protein) were cross-linked to the photoactivatable analogue of Ang IV, [ 125 I]Nle 1 -BzPhe 6 -Gly 7 -Ang IV as described previously (15). Cross-linked membranes were solubilized in solubilization buffer (1% CHAPS, 20 mM Tris-HCl, pH 7.5, 5 mM EDTA) with shaking at room temperature for 48 h, and insoluble material was pelleted by centrifugation at 100,000 ϫ g for 1 h at 4°C. Non-cross-linked membranes (48 mg of protein) were solubilized and centrifuged similarly, and the supernatant was combined with that from cross-linked membranes. Solubilized membrane proteins were applied to a 1-ml DEAE fas...

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“…Although there is ample evidence for the importance of acetylcholine in hippocampal-dependent mnemonic tasks (Blokland, 1996), the possible role of SRIF in mnemonic functions has also been demonstrated. Cysteamine has been shown to impair hippocampal-sensitive spatial learning when administered systemically (Matsuoka et al, 1995) or infused directly into the hippocampus (Guillou et al, 1998). Experiments using intrahippocampal injections of SS or cysteamine have provided evidence that both facilitatory and impairing effects can be observed, depending on the task used (Lamirault et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…In particular, intrahippocampal injections of SS-14 have been shown to enhance the rate of acquisition of a spatial discrimination task in the eightarm radial maze (Guillou et al, 1998). In contrast, both intrahippocampal and systemic injections of cysteamine, a depleter of SS-14 stores, was found to slow down the rate of acquisition in the radial-arm maze (Sessions et al, 1989;Guillou et al, 1998) and water maze (Fitzgerald and Dokla, 1989;Matsuoka et al, 1995) spatial tasks.…”

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confidence: 99%

A vitamin A-free diet results in impairment of the rat hippocampal somatostatinergic system

2006

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Abstract-Previous studies have revealed the presence of retinoid specific receptors in the hippocampus and have demonstrated that vitamin A deficiency produces a severe deficit in spatial learning and memory which are linked to a proper hippocampal functioning. It is also well known that the tetradecapeptide somatostatin binds to specific receptors in the hippocampus and, when injected into this brain area, facilitates the acquisition of spatial tasks. In addition, depletion of somatostatin by cysteamine impairs acquisition of these tasks. Taken together, these studies support the idea that the hippocampal somatostatinergic system might be regulated by vitamin A. Hence, we evaluated the effects of vitamin A deprivation and subsequent administration of vitamin A on the rat hippocampal somatostatinergic system. Rats fed a vitamin A-free diet exhibited a significant reduction of somatostatin-like immunoreactivity content in the hippocampus whereas the somatostatin mRNA levels were unaltered. Vitamin A deficiency increased the somatostatin receptor density and its dissociation constant. Functional Gi activity as well as the capacity of somatostatin to inhibit basal and forskolin-stimulated adenylyl cyclase activity was decreased in vitamin A deficiency rats as compared with the control animals. All these parameters were fully restored when vitamin A was replaced in the diet. Furthermore, we found that the Gi␣ 1 , Gi␣ 2 and Gi␣ 3 protein levels were unaltered in hippocampal membranes from rats fed a vitamin A-free diet whereas subsequent vitamin A administration to these rats caused a significant increase in the levels of Gi␣1 and Gi␣2. Altogether, the present findings suggest that dietary vitamin A levels modulate the somatostatinergic system in the rat hippocampus.

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Changes in brain somatostatin in memory-deficient rats: comparison with cholinergic markers

Cited by 48 publications

References 54 publications

Role of the somatostatin system in contextual fear memory and hippocampal synaptic plasticity

Role of the somatostatin system in contextual fear memory and hippocampal synaptic plasticity

Evidence That the Angiotensin IV (AT4) Receptor Is the Enzyme Insulin-regulated Aminopeptidase

A vitamin A-free diet results in impairment of the rat hippocampal somatostatinergic system

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