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Effects of excitotoxic median raphe lesions on scopolamine-induced working memory deficits in inhibitory avoidance
Emine Babar1, Enver Melik, Tuncay Ozgünen
1Department of Physiology, Division of Neurophysiology, Medical Faculty, Cukurova University, Balcalí-Adana, Turkey. ebabar@mail.cu.edu.tr
Abstract:
The aim of the present study was to investigate the effects of excitotoxic damage of the serotonergic cell bodies in the median raphe nucleus (MRN) on the scopolamine-induced working memory deficits in a single-trial light/dark inhibitory avoidance task. Rats were given 1 mg/kg of scopolamine hydrobromide (intraperitonal, i.p.) or saline before the inhibitory avoidance training, in which initial preference to the dark compartment (escape latency) was used to measure nonmnemonic behaviors, and response latency to enter the dark compartment immediately after the shock was used to measure working memory. It was found that scopolamine significantly reduced escape latencies in sham-lesioned rats, whereas it had no effect in the rats with MRN lesions. Although MRN lesion per se did not alter response latency, it prevented scopolamine-induced decrease in this parameter. These results suggest that the antagonistic interactive processes between serotonergic projections of the MRN and the muscarinic cholinergic system modulate nonmnemonic attentional component of working memory formation in the inhibitory avoidance.
Insights
Damage to the median raphe nucleus (MRN) serotonin cells prevented scopolamine-induced working memory deficits in rats. This suggests serotonin pathways modulate attention in memory tasks.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Pharmacology
Background:
- Working memory deficits are often induced by cholinergic system disruption.
- The median raphe nucleus (MRN) plays a role in modulating cognitive functions.
- Serotonergic and cholinergic systems interact in complex ways within the brain.
Purpose of the Study:
- To investigate the impact of damaging serotonergic cell bodies in the MRN on scopolamine-induced working memory deficits.
- To explore the interaction between the serotonergic system and the cholinergic system in a specific memory task.
Main Methods:
- Excitotoxic lesions of the MRN were induced in rats.
- Scopolamine hydrobromide was administered to induce memory deficits.
- A single-trial light/dark inhibitory avoidance task was used, measuring escape latency and response latency.
- Sham-lesioned rats served as controls.
Main Results:
- Scopolamine reduced escape latencies in sham-lesioned rats, indicating nonmnemonic behavioral changes.
- Scopolamine had no effect on escape latencies in MRN-lesioned rats.
- MRN lesions prevented the scopolamine-induced decrease in response latency, which measures working memory.
- MRN lesions alone did not affect response latency.
Conclusions:
- The serotonergic projections from the MRN are crucial for the expression of scopolamine-induced working memory deficits.
- Antagonistic interactions between the MRN serotonergic system and the muscarinic cholinergic system modulate the attentional component of working memory.
- These findings highlight the role of serotonin in attention and memory processes affected by cholinergic disruption.
