ArticleMolecular neurobiology2026
Kisspeptin System: A Modulator of Neuroinflammation and Behaviour in Temporal Lobe Epileptic Rats.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Temporal lobe epilepsy (TLE) is the most prevalent form of drug-resistant epilepsy and is driven by persistent neuroinflammatory cascades wherein interactions between inflammatory mediators and hormones play a crucial role. Kisspeptin (Kiss1), a neuropeptide known to modulate synaptic transmission in the hippocampus, has an unclear role in pathophysiology of epilepsy. To investigate this, a lithium-pilocarpine TLE rat model was established. Expression profiles of Kiss1, Kiss1r, and key neuroinflammatory molecules were assessed in the hippocampus, anterior temporal lobe (ATL), and neocortex at the transcript and protein levels. Neuroinflammatory markers were correlated with the expression of Kiss1 and its receptor under epileptic conditions. The cellular localization of Kiss1r with microglia (Iba1), astrocytic (Gfap), and neuronal (NeuN) markers was examined in TLE. Additionally, kisspeptin-10 (Kp-10) was administered to TLE rats, and its effects on cytoarchitecture, neuroinflammation, and long-term memory were evaluated. The results demonstrated significant downregulation of Kiss1 and Kiss1r mRNA across brain regions (P < 0.05). At the protein level, Kiss1 was significantly downregulated in the hippocampus and ATL but remained unchanged in the neocortex. Kiss1r levels increased in the hippocampus, decreased in the ATL, and remained unchanged in the neocortex. Kp-10 administration led to restoration of cellular alterations in the hippocampus of TLE rats. Kp-10 treatment upregulated the levels of anti-inflammatory cytokine Il-10 in the hippocampus and ATL. A downregulation in the levels of pro-inflammatory cytokine Il-1β in the hippocampus, but no alteration in ATL was seen upon Kp-10 treatment. Novel object recognition test indicated improved memory discrimination in Kp-10-treated TLE rats. These findings suggest that chronic neuroinflammation in TLE disrupts the kisspeptin signalling system, further aggravating disease pathology. Conversely, exogenous Kp-10 administration attenuated neuroinflammation, enhanced cognitive function and survival rate, highlighting a potential neuroprotective role of kisspeptin in TLE pathogenesis.
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