Depletion of somatostatin-like immunoreactivity in the rat central nervous system by cysteamine

Sagar, S.M.; Landry, Donald W.; Wj, Millard; Badger, TM; Arnold, Marcel; Jb, Martin

doi:10.1523/jneurosci.02-02-00225.1982

Cited by 163 publications

(36 citation statements)

References 22 publications

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“…Ablation in SST ‫מ/מ‬ mice and pre-training depletion with cysteamine, in particular due to its long half-life (Sagar et al 1982), are likely to interfere with somatostatinergic processes during both memory acquisition and memory consolidation (Abel and Lattal 2001;Anagnostaras et al 2001;Rodrigues et al 2004). In our experiments, only pre-training, but not immediate post-training, infusion of cysteamine selectively interfered with contextual fear memory formation.…”

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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“…in rats pretreated with cysteamine (Cys), which depletes endogenous somatostatin (SRIH) stores [17]. Reportedly, SRIH participates in the inhibitory control of gastric acid secretion, and binding sites for the GHS have been detected on hypothalamic SRIH neurons [18].…”

Section: Introductionmentioning

confidence: 99%

Evidence for a Central Inhibitory Role of Growth Hormone Secretagogues and Ghrelin on Gastric Acid Secretion in Conscious Rats

Sibilia

Pagani²,

Guidobono³

et al. 2002

Neuroendocrinology

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We examined the possible central and peripheral effects of synthetic growth hormone secretagogues (GHS), hexarelin (Hexa) and EP 40737 (D-Thr-D-Trp (2-Me)-Ala- Trp-D-Phe-Lys-NH₂), and of their endogenous counterpart, ghrelin, on gastric acid secretion. The compounds were administered intracerebroventricularly (i.c.v.) or subcutaneously (s.c.) in conscious male rats and the volume of gastric secretion and gastric acid output were examined 3 h after pylorus ligation (Shay-test). Central Hexa, EP 40737 and ghrelin administration (from 0.1 pmol to 1 nmol/rat, i.c.v.) significantly inhibited gastric acid secretion. The maximum inhibitory effect on gastric acid output was detected at the dose of 10 pmol/rat, i.c.v. for Hexa (–51.3%), of 100 pmol/rat, i.c.v. for EP 40737 (–70%) and of 1 pmol/rat, i.c.v. for ghrelin (–60%). All peptides were less effective at the highest dose used (1 nmol/rat, i.c.v.). Hexa, EP 40737 and ghrelin injected s.c. did not modify gastric acid secretion. The inhibitory action of Hexa on gastric acid secretion seems to involve brain somatostatinergic system since Hexa (10 pmol/rat, i.c.v.) did not inhibit gastric acid secretion in rats pretreated (4 h before) with cysteamine (300 mg/kg, s.c.), a depletor of endogenous somatostatin. These results show that synthetic GHS and ghrelin exert a central long-lasting inhibitory effect on gastric acid secretion in conscious pylorus-ligated rats. The fact that very low doses of ghrelin and GHS inhibit gastric secretion, provide evidence for a tonic inhibitory role of the peptides in the central control of gastric secretory function.

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“…Furthermore in vitro studies using pituitary tumor cells have demonstrated that somatostatin can direc tly inhibit ACTH secretion [I, 12, 14, 20. 21], Somatostatin may thus be one of many factors regulating pituitary ACTH secretion (see review by Axelrod and Reisine [I]).To determine whether somatostatin systems might play a role in the dexamethasone-induced suppression of the HPA axis in vivo, the effect of pretreatment with cys teamine, a drug which reduces somatostatin levels [2,16,24,26,28,29,31], on the dexamethasone-induced sup pression of plasma corticosterone levels was investigated in the rat. …”

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confidence: 99%

Effects of Systemic and Intracerebroventricular Cysteamine on Dexamethasone-Induced Suppression of Corticosterone Levels in the Rat

Radke

Vincent²

1988

Neuroendocrinology

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To investigate whether somatostatin systems plays a significant role in the regulation of the hypothalamic-pituitary-adrenal axis, the effects of cysteamine, a drug which reduces somatostatin levels, on the dexamethasone-induced suppression of plasma corticosterone levels were examined in the rat. Male Long Evans rats were handled daily for 1 week prior to receiving a standard dexamethasone suppression test. On the 1st day, rats received a 9.00 a.m. saline injection and blood samples were taken from the tail at 1.00 p.m. On the 2nd day, rats received dexamethasone or saline at 9.00 a.m. and a second blood sample was taken at 1.00 p.m. Experimental groups were pretreated with systemic injections of cysteamine, 5 min or 14 h, prior to receiving dexamethasone. Additional groups, previously implanted with guide cannulae, were given an infusion of cysteamine or saline into the lateral ventricle 14 h prior to dexamethasone. Circulating corticosterone levels were determined by radioimmunoassay. Rats were sacrificed immediately following each experiment and the hypothalamus dissected and assayed for levels of somatostatin immunoreactivity. The results of the first experiment showed that dexamethasone (10 µg/kg) alone reduced plasma corticosterone levels from control values (174 + 36 ng/ml) to undetectable levels ( < 25 ng/ml). Pretreatment with cysteamine 5 min prior to dexamethasone, while having no significant effect on basal corticosterone levels, completely blocked the dexamethasone-induced suppression of corticosterone levels. Similar observations were obtained with rats pretreated with cysteamine 14 h prior to dexamethasone. In contrast, intracerebroventricular cysteamine pretreatment did not block the dexamethasone-induced suppression of corticosterone levels. These results add further evidence in support of an involvement of somatostatin systems in the regulation of the hypothalamic-pituitary-adrenal axis.

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Depletion of somatostatin-like immunoreactivity in the rat central nervous system by cysteamine

Cited by 163 publications

References 22 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 for a Central Inhibitory Role of Growth Hormone Secretagogues and Ghrelin on Gastric Acid Secretion in Conscious Rats

Effects of Systemic and Intracerebroventricular Cysteamine on Dexamethasone-Induced Suppression of Corticosterone Levels in the Rat

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