Kisspeptin-10 potentiates miniature excitatory postsynaptic currents in the rat supraoptic nucleus.
Yokoyama. Toru T; Minami. Kouichiro K; Terawaki. Kiyoshi K; Miyano. Kanako K; Ogata. Junichi J; Maruyama. Takashi T; Takeuchi. Mamoru M; Uezono. Yasuhito Y; Ueta. Yoichi Y
Key Findings
- Kisspeptin‑10 raises the frequency of miniature excitatory postsynaptic currents in supraoptic nucleus neurons in a dose‑dependent way
- The increase is blocked by a kisspeptin receptor antagonist and a PKC inhibitor
- Amplitude of the currents is unchanged, indicating a presynaptic effect
Practical Outcomes
- The study shows a basic mechanism of how kisspeptin‑10 can influence brain circuits that regulate vasopressin, but it offers no direct guidance for human dosing or performance enhancement. For biohackers, it’s mainly a piece of foundational science rather than an actionable protocol.
Summary
In rats, a short form of the hormone‑related peptide kisspeptin‑10 makes certain brain cells that control water balance fire more often, but it doesn’t change how strong each signal is. This effect depends on the kisspeptin receptor and a signaling pathway called PKC.
Abstract
Kisspeptin is the natural ligand of the G protein-coupled receptor -54 and plays a major role in gonadotropin-releasing hormone secretion in the hypothalamus. Kisspeptin-10 is an endogenous derivative of kisspeptin and has 10 -amino acids. Previous studies have demonstrated that central administration of kisspeptin-10 stimulates the secretion of arginine vasopressin (AVP) in male rats. We examined the effects of kisspeptin-10 on- excitatory synaptic inputs to magnocellular neurosecretory cells (MNCs) including AVP neurons in the supraoptic nucleus (SON) by obtaining in vitro whole-cell patch-clamp recordings from slice preparations of the rat brain. The application of kisspeptin-10 (100 nM-1 μM) significantly increased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in a dose-related manner without affecting the amplitude. The kisspeptin-10-induced potentiation of the mEPSCs was significantly attenuated by previous exposure to the kisspeptin receptor antagonist kisspeptin-234 (100 nM) and to the protein kinase C inhibitor bisindolylmaleimide I (20 nM). These results suggest that kisspeptin-10 participates in the regulation of synaptic inputs to the MNCs in the SON by interacting with the kisspeptin receptor.
Study Information
pubmed
2014
2014-08-15T00:00:00.000Z
10.1016/j.brainres.2014.08.020
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