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Agomelatine is a nootropic compound with the potential to elicit antidepressant effects by acting as a melatonergic agonist for MT1 and MT2 receptors, as well as serotonergic antagonist for 5-HT2C receptors. Previous research has found that agomelatine improves symptoms of depression related to unpredictable stress by affecting the levels of brain-derived neurotrophic factor in the hippocampus [1].
Main Research Findings
1) Treatment with agomelatine was found to prevent comorbid depression by suppressing inflammatory signaling in a model of acquired epilepsy.
2) Treatment with agomelatine was found to have antidepressant effects on test subjects without eliciting any adverse effects on sexual behavior or development.
Selected Data
1) Previous research has found that depression is the most frequent psychiatric disorder that accompanies temporal lobe epilepsy. The research team of Tchekalarova et al examined the effects of treatment with the nootropic, agomelatine, on the symptoms of depression related to epilepsy. For the purpose of this study, adult male Wistar rats weighing 200-230 grams each were utilized. The test subjects were housed 3-4 to a cage and were maintained under standard laboratory conditions with free access to food and water. Status epilepticus was induced in the rats through an injection of kainate acid, following the injection the rats were kept in individual cages in order for the research team to monitor and record occurrences of spontaneous motor seizures through the use of 24 hour video recording and EEG monitoring [2].
Kainate acid was intraperitoneally injected at a dose of 5 mg/kg, followed by a half-dose of 2.5 mg/kg, 1 hour later. A modified Racine’s scale was used in order for the researchers to monitor the intensity of the seizures. Class I and class II partial seizures characterized by immobility, facial automatism, head nodding, and wet-dog shakes were not scored. Additional injections of kainate acid were based on the detection of class III seizures defined by forelimb clonus with lordotic posture, class IV seizures defined by rearing and continued forelimb clonus, and class V seizures defined by forelimb clonus and loss of posture. Seizure intensity determined whether a half-dose of kainate acid should be injected or whether administered should be discontinued. The onset of status epilepticus was characterized by the occurrence of >9 sustained motor seizures per hour; onset typically required between 3 and 4 doses of kainate acid [2].
After kainate acid-induction of status epilepticus, the animals were randomly divided into four different experimental treatment groups. Group 1 included control rats treated with the vehicle substance, hydroxyethyl cellulose; group 2 included control rats treated with agomelatine; group 3 included rats injected with kainate acid and treated with a hydroxyethyl cellulose; and group 4 included rats injected with kainate acid and treated with agomelatine. Agomelatine was intraperitoneally injected at a dose of 40 mg/kg dissolved in hydroxyethyl cellulose, 1 hour after status epilepticus was induced via kainate acid. After the first initial dose of the nootropic, all surviving test subjects included in the group administered both kainate acid and agomelatine continued treatment for 10 weeks receiving the same 40 mg/kg dose on a daily basis. It is important to mention that the neuroprotective effects of agomelatine was shown to be most potent within 1 hour of administration [2].
Agomelatine is a nootropic compound with the potential to elicit antidepressant effects by acting as a melatonergic agonist for MT1 and MT2 receptors, as well as serotonergic antagonist for 5-HT2C receptors. Previous research has found that agomelatine improves symptoms of depression related to unpredictable stress by affecting the levels of brain-derived neurotrophic factor in the
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