Somatostatin receptors and the modulation of adenylyl cyclase activity in Alzheimer's disease.

Cowburn, Richard F.; Fowler, Christopher; Garlind, Anita; Alafuzoff, Irina; Nilsson, Lars; Winblad, Bengt; Bergström, Lena

doi:10.1136/jnnp.54.8.748

Cited by 19 publications

(10 citation statements)

References 16 publications

(2 reference statements)

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“…However, the capacity of SRIF to inhibit basal or forskolin‐stimulated AC activity in cortical membranes was significantly lower in the Aβ25–35‐treated rats as compared with control rats. This may be as a result of the observed loss of SRIF receptors in these rats, as previously demonstrated by (Cowburn et al . 1991) in the temporal cortex of patients with AD.…”

Section: Discussionsupporting

confidence: 78%

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Protective effects of insulin‐like growth factor‐I on the somatostatinergic system in the temporal cortex of β‐amyloid‐treated rats

Aguado-Llera

Arilla‐Ferreiro

Campos‐Barros

et al. 2004

Journal of Neurochemistry

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Insulin-like growth factor-I (IGF-I) has protective effects against b-amyloid (Ab)-induced neuronal cell death. Because alterations of the somatostatinergic system have been described in Alzheimer's disease, we investigated the effects of the Ab peptide and the possible protective role of IGF-I on the somatostatinergic system of the rat temporal cortex and on cell death and phosphorylated (p)-Akt levels in this area. Ab25-35 was administered intracerebroventricularly to male rats via an osmotic minipump over 14 days (300 pmol/day). Another group received a subcutaneous IGF-I infusion (50 lg/kg/day), concomitant with Ab25-35 administration, whereas a third group received IGF-I alone. Ab25-35 significantly decreased the somatostatin (SRIF)-like immunoreactive content and the SRIF receptor density, as a result of a decrease in the levels of the SRIF receptor subtype 2. The inhibitory effect of SRIF on adenylyl cyclase activity was significantly lower after Ab25-35 infusion, whereas the levels of the inhibitory G protein subunit Gia1, Gia2 or Gia3 were unaltered. Cell death was increased and p-Akt levels decreased in Ab25-35-treated animals. IGF-I administration increased immunoreactive IGF-I levels in the temporal cortex and restored all parameters affected by Ab25-35 to baseline values. These findings suggest that IGF-I prevents the deleterious effect of Ab25-35 on the somatostatinergic system.

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Section: Discussionsupporting

confidence: 78%

“…1985), whereas the levels of inhibitory G proteins are preserved. This suggests that the reduction in SRIF‐mediated inhibition of AC activity described in these patients (Cowburn et al . 1991) is related to the reduction in the receptor density.…”

mentioning

confidence: 76%

Protective effects of insulin‐like growth factor‐I on the somatostatinergic system in the temporal cortex of β‐amyloid‐treated rats

Aguado-Llera

Arilla‐Ferreiro

Campos‐Barros

et al. 2004

Journal of Neurochemistry

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“…Regarding the SRIF receptors, several authors (Beal et al, 1985;Bergström et al, 1991;Krantic et al, 1992) have reported a marked loss in the SRIF receptor density in various cortical areas of the AD brain. Cowburn et al (1991) found a reduced SRIF-mediated inhibition of adenylyl cyclase (AC) activity in the superior temporal cortex of AD brains as compared with controls.…”

mentioning

confidence: 99%

Effects of single and continuous administration of amyloid β-peptide (25–35) on adenylyl cyclase activity and the somatostatinergic system in the rat frontal and parietal cortex

et al. 2005

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“…Taken together, the present results suggest that the decrease in SRIH-mediated inhibition of basal AC activity is most probably due to the decrease in the SRIH receptor density. Cowburn et al [25] have shown a preservation of Gi protein-inhibited AC activity in the brains of patients with AD. O’Neill et al [61] also found that Gi protein-inhibited AC activity was unaltered in the frontoparietal cortex of AD patients.…”

Section: Discussionmentioning

confidence: 99%

“…The SRIH receptors, which transduce the SRIH signal, have also been reported by several authors [23, 24] to be markedly reduced in various cortical areas of the AD brain. In addition, Cowburn et al [25] found a reduced SRIH-mediated inhibition of AC activity in the superior temporal cortex of AD brains as compared with controls. Recently, our group demonstrated that i.c.v.…”

Section: Introductionmentioning

confidence: 99%

Sulfadiazine Partially Protects the Rat Temporal Cortex from Amyloid Beta Peptide (25–35)-Induced Alterations of the Somatostatinergic System

et al. 2009

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The aim of this study was to elucidate whether sulfadiazine, shown to improve cognitive capacity in the elderly, can prevent amyloid beta peptide (Aβ) (25–35)-induced impairment of the somatostatinergic system previously reported by our group in rat temporal cortex. Male Wistar rats were thus treated with sulfadiazine (160 mg/kg) or vehicle, via a gastric cannula, twice on the day prior to Aβ(25–35) treatment. On the following day and during 14 days, Aβ(25–35) was administered intracerebroventricularly (i.c.v.) via an osmotic minipump connected to a cannula implanted in the right lateral ventricle (300 pmol/day). Sulfadiazine (80 mg/kg) or vehicle was administered once again the last 2 days of the Aβ(25–35) infusion. All animals were sacrificed by decapitation 24 h after the last sulfadiazine dose. The findings obtained reveal that sulfadiazine partially prevents the decrease in somatostatin (SRIH)-like immunoreactivity content in the temporal cortex of rats infused with Aβ(25–35) during 14 days. In addition, sulfadiazine blocks the Aβ(25–35)-induced reduction in the SRIH receptor density and in SRIH receptor subtype 2 expression. Sulfadiazine treatment also restored the inhibitory effect of SRIH on basal adenylyl cyclase activity back to control values. Altogether, the results suggest that sulfadiazine might have beneficial effects in the early treatment of Alzheimer’s disease.

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Somatostatin receptors and the modulation of adenylyl cyclase activity in Alzheimer's disease.

Cited by 19 publications

References 16 publications

Protective effects of insulin‐like growth factor‐I on the somatostatinergic system in the temporal cortex of β‐amyloid‐treated rats

Protective effects of insulin‐like growth factor‐I on the somatostatinergic system in the temporal cortex of β‐amyloid‐treated rats

Effects of single and continuous administration of amyloid β-peptide (25–35) on adenylyl cyclase activity and the somatostatinergic system in the rat frontal and parietal cortex

Sulfadiazine Partially Protects the Rat Temporal Cortex from Amyloid Beta Peptide (25–35)-Induced Alterations of the Somatostatinergic System

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