The ACTH 4-9 analog, H-Met((O2)-Glu-His-Ph-D-Lys-Phe-OH (Or 2766), attenuates in rats CO2-induced amnesia for a one-trial passive avoidance step-through response when administered prior to the retrieval test but not when given prior to acquisition. Even a dose of 0.001 mug/rat Org 2766 yields an anti-amnesic effect. In this respect Org 2766 is more active than the ACTH fragment ACTH 4-10. An anti-amnesic effect was also obtained when Org 2766 was administered orally. ACTH 4-10 (100 mug/rat) has to be given SC within 8 hr of the retrieval test in order to be effective. A similar time span of effectiveness was observed when Org 2766 was SC injected in a dose of 0.1 mug/rat. The anti-amnesic effect of ACTH 4-10 remains when the time interval between acquisition and retrieval is extended beyond the usual 24 hr. The same appeared to be true for SC ADMINISTERED Org 2766. It is suggested that ACTH-like peptides, and particularly the orally active Org 2766, may be helpful in the treatment of deficient mental performance.

Download full-text PDF

Source
http://dx.doi.org/10.1016/0091-3057(76)90328-2DOI Listing

Publication Analysis

Top Keywords

org 2766
28
acth 4-10
12
orally active
8
active acth
8
acth 4-9
8
4-9 analog
8
0
8
retrieval test
8
org
7
acth
6

Similar Publications

Interventions for preventing neuropathy caused by cisplatin and related compounds.

Cochrane Database Syst Rev

March 2014

Department of Neurology, University of Michigan, 1C325/0032 University Hospital, 1500 E. Medical Center Drive, Box 0316, Ann Arbor, USA, MI 48109-0032.

Background: Cisplatin and several related antineoplastic drugs used to treat many types of solid tumours are neurotoxic, and most patients completing a full course of cisplatin chemotherapy develop a clinically detectable sensory neuropathy. Effective neuroprotective therapies have been sought.

Objectives: To examine the efficacy and safety of purported chemoprotective agents to prevent or limit the neurotoxicity of cisplatin and related drugs.

View Article and Find Full Text PDF

Interventions for preventing neuropathy caused by cisplatin and related compounds.

Cochrane Database Syst Rev

February 2011

Department of Neurology, University of Michigan, 1C325/0032 University Hospital, 1500 E. Medical Center Drive, Box 0316, Ann Arbor, USA, MI 48109-0032.

Background: Cisplatin and several related antineoplastic agents used to treat many types of solid tumors are neurotoxic, and most patients completing a full course of cisplatin chemotherapy develop a clinically detectable sensory neuropathy. Effective neuroprotective therapies have been sought.

Objectives: To examine the efficacy of purported chemoprotective agents to prevent or limit the neurotoxicity of cisplatin and related agents.

View Article and Find Full Text PDF

Interventions for preventing neuropathy caused by cisplatin and related compounds.

Cochrane Database Syst Rev

January 2007

University of Michigan, Department of Neurology, 1C325/0032 University Hospital, 1500 E. Medical Center Drive, Box 0316, Ann Arbor, MI 48109-0032, USA.

Background: Cisplatin and several related antineoplastic agents used to treat many types of solid tumors are neurotoxic, and most patients completing a full course of cisplatin chemotherapy develop a clinically detectable sensory neuropathy. Effective neuroprotective therapies have been sought.

Objectives: To examine the efficacy of purported chemoprotective agents to prevent or limit the neurotoxicity of cisplatin and related agents among human patients.

View Article and Find Full Text PDF

Future opportunities in preventing cisplatin induced ototoxicity.

Cancer Treat Rev

August 2006

Department of Pharmacy and Pharmacology, Slotervaart Hospital/The Netherlands Cancer Institute, P.O. Box 90440, 1006 BK Amsterdam, The Netherlands.

Cisplatin is one of the most commonly used cytotoxic agents. Ototoxicity is an important and dose-limiting side-effect of cisplatin therapy. It is believed that cisplatin suppresses the formation of endogenous anti-oxidants that normally prevent the inner ear against reactive oxygen species (ROS).

View Article and Find Full Text PDF

In the present study, the temporal and spatial alterations of adrenocorticotropic hormone (ACTH) immunoreactivity in the gerbil hippocampus after 5 min transient forebrain ischemia were investigated as followed up 7 days after ischemic insult, and the effects of ACTH after ischemic insult were also investigated 4 days after ischemic insult. The ectopic expression of ACTH (1-24 fragments) immunoreactive neurons in the cornus ammonis 1 (CA1) region of hippocampus and hilar region of the dentate gyrus 1 day after the ischemic insult was observed. Judging from the double immunofluorescence study, these neurons contain GABA.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!