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Nitric oxide modulates apomorphine-induced recognition memory deficits in rats
Ioannis Gourgiotis1, Nikoletta G Kampouri, Vasiliki Koulouri
1Department of Pharmacology, School of Medicine, University of Thessaly, Larissa, Greece.
Pharmacology, Biochemistry, and Behavior
|June 28, 2012
Summary
Nitric oxide (NO) modulators reversed apomorphine-induced recognition memory deficits in rats. This suggests NO plays a role in dopamine-related cognitive dysfunction.
Area of Science:
- Neuroscience
- Pharmacology
- Cognitive Science
Background:
- Nitric oxide (NO) is a key brain messenger implicated in schizophrenia.
- NO's role in schizophrenia (over or underproduction) remains unclear.
- NO donors or inhibitors can counteract NMDA receptor hypofunction-induced cognitive deficits.
Purpose of the Study:
- To investigate if NO modulators can reverse recognition memory impairments caused by dopamine dysfunction.
- To examine the effects of NO donors and NOS inhibitors on apomorphine-induced memory deficits in rats.
Main Methods:
- Rats were tested using the novel object recognition test (NORT).
- Apomorphine was administered to induce recognition memory impairments.
- NO donors (molsidomine, SNP) and NOS inhibitors (L-NAME, 7-NI) were used to assess their effects.
Main Results:
- Apomorphine dose-dependently impaired recognition memory in rats.
- Both NO donors and NOS inhibitors reversed the apomorphine-induced memory deficits.
- These findings highlight the sensitivity of dopamine dysfunction-related cognitive deficits to NO modulation.
Conclusions:
- Apomorphine administration leads to dose-dependent recognition memory impairment.
- Nitric oxide modulation can effectively reverse cognitive deficits associated with dopamine dysfunction.
- This study provides evidence for NO's role in regulating memory processes affected by dopamine.
