The effect of leptin on the tonic secretion of gonadotropins in the female rats.

OBJECTIVES: This study is an attempt to determine, the in vivo action of leptin on this hypophysiotropic hypothalamic area, by evaluating the concentrations of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in the serum. METHODS: The experiments were done by stereotaxic injection of recombinant rat leptin (rrleptin) into the third cerebral ventricle (V3) of adult female Wistar rats. Subjects were divided into five groups. Group A included normal intact animals. In Group B, the rats were stereotaxically administered with rrleptin in the V3. The rats, in Groups C, D and E, were subjected to electrolytic lesion of the arcuate nucleus (ARC), of the ventromedial nucleus (VMH) and of both of these hypothalamic nuclei, respectively. Immediately after the electric lesion, they were intracranially injected with rrleptin. Blood samplings for serum LH and FSH levels estimation were performed three times: 1) just before any stereotaxic procedure, 2) six hours, and 3) twenty-four hours after leptin administration. RESULTS: The results showed that serum LH levels increased dramatically in group B, six hours after leptin administration. The LH levels in Groups C, D and E presented the same pattern with a lower peak. The FSH levels were doubled six hours after leptin administration in all groups without any exception. Both LH and FSH serum levels reverted to the initial basic levels after 24 hours. DISCUSSION: The significant conclusion derived from this study is that ARC and VMH, which are responsible for controlling the tonic secretion of gonadotropins, respond in a different way for the FSH and LH secretion. This also suggests that some other mechanism(s) or factor(s) may additionally participate in the control of the tonic component of FSH secretion.

Neuroprotection by lamotrigine in a rat model of neonatal hypoxic-ischaemic encephalopathy.

Hypoxic-ischaemic (HI) encephalopathy is a severe complication of perinatal asphyxia and remains a frequent cause of a variety of brain disorders with long-term effects on the patients' life. The associated brain damage is strongly related to the toxic action of excitatory amino acids, especially glutamate and aspartate. Lamotrigine is an anti-epileptic drug that blocks the voltage-gated sodium channels of the presynaptic neuron and inhibits the release of glutamate. In the present study a well-established model of perinatal asphyxia in 7-d-old rats was used to investigate the effect of lamotrigine on HI-induced damage to different hippocampal brain structures, since disruption of this brain area is thought to play a key role in schizophrenia and epilepsy. Therefore, a combination of ischaemia, induced by unilateral occlusion of the left common carotid artery, followed by exposure to a 1-h period of hypoxia, was carried out in neonatal 7-d-old rats. Immediately after the insult, lamotrigine was given i.p. The histological outcome in the hippocampus was conducted and the tissue levels of glutamate, aspartate, GABA, and glutamine in the same area were determined. A remarkable reduction of HI-evoked damaged neurons in most of the investigated hippocampal regions was noted after lamotrigine administration. Furthermore, lamotrigine decreased the asphyxia-induced hippocampal tissue levels of glutamate and aspartate. Immediately after perinatal asphyxia GABA levels were enhanced, while levels of glutamine were decreased. Lamotrigine administration did not affect either GABA or glutamine levels. These results suggest a neuroprotective effect of lamotrigine in this particular animal model of neonatal HI encephalopathy.