Consequences of long-term treatment with agomelatine on depressive-like behavior and neurobiological abnormalities in pinealectomized rats.

Previous data have shown that the rat model of melatonin deficit can cause a number of neurobiological aberrations. The aim of the present study was to determine whether the antidepressant drug agomelatine, a MT1/MT2 melatoninergic receptor agonist/5-HT2C receptor antagonist is able to prevent some of the behavioral, biochemical and cellular abnormalities induced by pinealectomy. The injection of agomelatine (40 mg/kg, i.

Effect of endurance training on seizure susceptibility, behavioral changes and neuronal damage after kainate-induced status epilepticus in spontaneously hypertensive rats.

The therapeutic efficacy of regular physical exercises in an animal model of epilepsy and depression comorbidity has been confirmed previously. In the present study, we examined the effects of endurance training on susceptibility to kainate (KA)-induced status epilepticus (SE), behavioral changes and neuronal damage in spontaneously hypertensive rats (SHRs). Male SHRs were randomly divided into two groups.

Effect of long-term caffeine administration on depressive-like behavior in rats exposed to chronic unpredictable stress.

Chronic unpredictable stress (CUS) was used to study the effects of a long-term treatment with either caffeine (8 mg/kg, orally) or desipramine (DMI) (10 mg/kg, intraperitoneally) in Wistar rats. The CUS procedure was applied for 6 weeks. Animals underwent a 2-week drug-free CUS procedure.

Effect of peptide and nonpeptide antagonists of angiotensin II receptors on noradrenaline release in hypothalamus of rats with angiotensin II-induced increase of water intake.

Angiotensin II (Ang II) administered intracerebroventriculary (icv) at a dose that induces drinking behavior in rats significantly increased K(+)-stimulated release of [(3)H] noradrenaline (NA) in hypothalamus without affecting basal [(3)H] NA release. The observed difference between the effects of Ang II on basal and K(+)-stimulated [(3)H]NA release may possibly be due to the fact that peptides are released after increased neuronal activity. It can be suggested that Ang II is important primarily in pathological states and that NA plays a substantial role in the brain Ang II-induced drinking response.

The effects of peptide and nonpeptide antagonists of angiotensin II receptors on the noradrenaline uptake of different brain structures in rats with angiotensin II-induced increase of water intake.

Angiotensin II (ANG II) significantly increased noradrenaline (NA) uptake by cortical, hypothalamic and hippocampal synaptosomes thus activating noradrenergic neurotransmission. ANG II did not affect NA uptake by striatal synaptosomes. The interaction between AT1 receptors and noradrenergic neurons and the involvement of brain noradrenergic neurotransmitter system in ANG II-induced drinking in rats is suggested by the increase of NA uptake in hypothalamus and frontal cortex which are rich in AT1 receptors and are of importance for drinking behavior.