Effects of the growth hormone-releasing hormone (GH-RH) antagonist on brain functions in mice.
Telegdy. Gyula G; Tanaka. Masaru M; Schally. Andrew V AV
Key Findings
- MZ‑4‑71 improved memory consolidation in a passive avoidance test
- It fully prevented beta‑amyloid‑induced memory impairment when given before or shortly after the toxin
- The compound showed antidepressant‑like effects in forced swim test and mild anxiolytic effects in a plus‑maze, with no impact on open‑field locomotion
Practical Outcomes
- The results are interesting but not actionable for self‑experimenters; the drug was delivered straight into mouse brains, a method not feasible for humans. More research is needed before considering any dosage or protocol for humans, especially with sermorelin, which is a different peptide.
Summary
In mice, a brain‑injected GH‑releasing hormone blocker called MZ‑4‑71 helped them remember a task better, stopped memory loss caused by a beta‑amyloid peptide, and showed mild anti‑depression and anti‑anxiety effects, without changing general activity. However, the study used direct brain injections in animals, so it doesn’t give clear guidance for people to use this or related peptides like sermorelin in real life.
Abstract
The growth hormone-releasing hormone (GH-RH) antagonist MZ-4-71 has been shown to suppress secretion of GH and insulin-like growth factor-1 (IGF-1) secretion. These findings suggested that GH-RH antagonists could be used for the therapy of disorders characterized by excessive GH secretion. A number of GH-RH antagonists has been synthesized, and shown to suppress the growth of various tumors. However, little is known about the possible action of GR-RH antagonists on brain functions. In the present work, the influence of MZ-4-71 on different aspects of brain function was studied in mice, following its administration into the lateral brain ventricle. The effects tested included the action of MZ-4-71 on passive avoidance learning and on the impairment of the consolidation of a passive avoidance reflex caused by beta-amyloid 25-35, antidepressive action in a forced swimming test, and anxiolytic action on plus-maze and open-field behavior. MZ-4-71 facilitated the consolidation of passive avoidance learning. Beta-amyloid 25-35 administered immediately after the learning trial impaired the consolidation of passive avoidance learning. MZ-4-71 fully blocked this impairment when given simultaneously with or 30min following beta-amyloid 25-35 administration icv. In the forced swimming tests, MZ-47-1 demonstrated antidepressive-like action and in the plus-maze, depending on the dose used it elicited mild anxiolytic action, however, in open-field behavior tests, it displayed no action on locomotion, rearing or grooming. The results demonstrate that MZ-4-71 affects the brain functions: by improving memory consolidation in passive avoidance learning and correcting the impairment of the memory consolidation caused by beta-amyloid 25-35. MZ-4-71 also elicits anxiolytic and antidepressive effects, but it does not influence the open-field activity. Further experimental work with MZ-4-71 is necessary, to determine the possible mechanism of action. The results imply a possible merit of a clinical trial with MZ-4-71 in patients with anxiety, depression and cognitive impairment, as observed in Alzheimer's disease.
Study Information
pubmed
2011
2011-06-06T00:00:00.000Z
10.1016/j.bbr.2011.05.036
34
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