A novel diketopiperazine improves functional recovery given after the onset of 6-OHDA-induced motor deficit in rats.

Krishnamurthi RV, Mathai S, Kim AH, Zhang R, Guan J

British journal of pharmacology16 Jan 2009Cited by 10 (Europe PMC)

PMID19154439PMCIDPMC2697702DOI10.1111/j.1476-5381.2008.00064.xPepBankPUB-19154439

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study5

5 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In rats with striatal lesions, early NNZ‑2591 treatment reduced motor deficit versus saline.
In plain wordsIn rats with striatal lesions, early NNZ‑2591 treatment reduced motor deficit versus saline.
Peptide
NNZ-2591
Outcome
DecreaseMotor deficit after early treatment
Study
ratsn: not reported in source
6-hydroxydopamine-induced unilateral striatal lesion
Comparator
Saline
Outcome group
Exercise and physical function · Nervous system and cognition
Studied dose
20 ng.day(-1) · intracerebroventricular · 3 daysAs given in this study (rats).
Source sentences
Summary
Cyclo-L-glycyl-L-2-allylproline given 2 h after the lesion reduced the degree of motor deficit compared with the saline-treated group.
3 context sentences(design, population, supporting numbers)
Summary · context
To examine its protective effect, either NNZ-2591 (20 ng.day(-1)) or saline was given intracerebroventricularly for 3 days starting 2 h after 6-hydroxydopamine (6-OHDA) induced unilateral striatal lesion.
Summary · context
The present studies were designed to examine both the neuroprotective and neurotrophic actions of NNZ-2591 on neurochemical and behavioural changes in a rat model of Parkinson's disease.
Summary · context
Behavioural and neurochemical outcomes were examined using the adjusting step test and immunohistochemical staining.
Report a problemFND-1915443901
02AnimalAnimal study (in vivo)Efficacy outcome
In rats with striatal lesions, delayed NNZ‑2591 treatment significantly improved motor function from week 7 onwards versus saline.
In plain wordsIn rats with striatal lesions, delayed NNZ‑2591 improved motor function from week 7 onwards versus saline.
Peptide
NNZ-2591
Outcome
IncreaseMotor function after delayed treatment
Study
ratsn: not reported in source
6-hydroxydopamine-induced unilateral striatal lesion
Comparator
Saline
Outcome group
Exercise and physical function · Nervous system and cognition
Studied dose
0.2, 1 and 5 mg.day(-1) · subcutaneous · 14 daysAs given in this study (rats).
Source sentences
Summary
Delayed treatment with NNZ-2591, initiated after the onset of motor deficit, significantly improved motor function from week 7 onwards compared with the saline-treated group.
3 context sentences(design, population, supporting numbers)
Summary · context
In a subsequent experiment either NNZ-2591 (0.2, 1 and 5 mg.day(-1), s.c.) or saline was administered daily for 14 days starting 2 weeks after the lesion.
Summary · context
The present studies were designed to examine both the neuroprotective and neurotrophic actions of NNZ-2591 on neurochemical and behavioural changes in a rat model of Parkinson's disease.
Summary · context
Behavioural and neurochemical outcomes were examined using the adjusting step test and immunohistochemical staining.
Report a problemFND-1915443902
03AnimalAnimal study (in vivo)Mechanism
In rats with striatal lesions, early NNZ‑2591 treatment did not alter nigrostriatal dopamine depletion versus saline.
In plain wordsIn rats with striatal lesions, early NNZ‑2591 did not change dopamine depletion versus saline.
Peptide
NNZ-2591
Outcome
No significant changeNigrostriatal dopamine depletion after early treatment
Study
ratsn: not reported in source
6-hydroxydopamine-induced unilateral striatal lesion
Comparator
Saline
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
20 ng.day(-1) · intracerebroventricular · 3 daysAs given in this study (rats).
Source sentences
Summary
Neither treatment regime altered nigrostriatal dopamine depletion.
3 context sentences(design, population, supporting numbers)
Summary · context
To examine its protective effect, either NNZ-2591 (20 ng.day(-1)) or saline was given intracerebroventricularly for 3 days starting 2 h after 6-hydroxydopamine (6-OHDA) induced unilateral striatal lesion.
Summary · context
The present studies were designed to examine both the neuroprotective and neurotrophic actions of NNZ-2591 on neurochemical and behavioural changes in a rat model of Parkinson's disease.
Summary · context
Behavioural and neurochemical outcomes were examined using the adjusting step test and immunohistochemical staining.
Report a problemFND-1915443903
04AnimalAnimal study (in vivo)Mechanism
In rats with striatal lesions, delayed NNZ‑2591 treatment did not alter nigrostriatal dopamine depletion versus saline.
In plain wordsIn rats with striatal lesions, delayed NNZ‑2591 did not change dopamine depletion versus saline.
Peptide
NNZ-2591
Outcome
No significant changeNigrostriatal dopamine depletion after delayed treatment
Study
ratsn: not reported in source
6-hydroxydopamine-induced unilateral striatal lesion
Comparator
Saline
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Studied dose
0.2, 1 and 5 mg.day(-1) · subcutaneous · 14 daysAs given in this study (rats).
Source sentences
Summary
Neither treatment regime altered nigrostriatal dopamine depletion.
3 context sentences(design, population, supporting numbers)
Summary · context
In a subsequent experiment either NNZ-2591 (0.2, 1 and 5 mg.day(-1), s.c.) or saline was administered daily for 14 days starting 2 weeks after the lesion.
Summary · context
The present studies were designed to examine both the neuroprotective and neurotrophic actions of NNZ-2591 on neurochemical and behavioural changes in a rat model of Parkinson's disease.
Summary · context
Behavioural and neurochemical outcomes were examined using the adjusting step test and immunohistochemical staining.
Report a problemFND-1915443904
05AnimalAnimal study (in vivo)Mechanism
In rats with striatal lesions, NNZ‑2591 significantly enhanced doublecortin-positive neuroblast expression in the sub-ventricular zone versus saline.
In plain wordsIn rats with striatal lesions, NNZ‑2591 increased doublecortin-positive neuroblast expression versus saline.
Peptide
NNZ-2591
Outcome
IncreaseDoublecortin-positive neuroblasts
Study
ratsn: not reported in source
6-hydroxydopamine-induced unilateral striatal lesion
Comparator
Saline
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated
Source sentences
Summary
NNZ-2591 significantly enhanced the expression of doublecortin-positive neuroblasts in the sub-ventricular zone.
2 context sentences(design, population, supporting numbers)
Summary · context
The present studies were designed to examine both the neuroprotective and neurotrophic actions of NNZ-2591 on neurochemical and behavioural changes in a rat model of Parkinson's disease.
Summary · context
Behavioural and neurochemical outcomes were examined using the adjusting step test and immunohistochemical staining.
Report a problemFND-1915443905

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
27 Oct 2026, 18:20 UTC
Study results updated
Version 1
27 Oct 2026, 16:32 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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