Agmatine decreases long-term potentiation via α2-adrenergic receptor and imidazoline type 1 receptor in the hippocampus

• 발행기관: 대한생리학회-대한약리학회
• 저자명: Wonseok Chang Jihua An Sang Hyun Jang Moonil Kim Sun Seek Min
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제29권 제5호, 593~601쪽, 전체 9쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2025.09.01

국문 초록

Agmatine, a decarboxylation product of L-arginine, has been proposed as a novel neurotransmitter/neuromodulator with diverse neuroprotective and antidepressant-like effects. Although its therapeutic potential has been explored, the precise mechanisms by which agmatine modulates synaptic transmission and plasticity in the hippocampus remain unclear. In this study, we investigated the effects of agmatine on the induction and maintenance of long-term potentiation (LTP) in the CA1 region of mouse hippocampal slices, its ability to counteract amyloid-β (Aβ1-42)-induced LTP impairment, and the receptor systems involved. Bath application of agmatine significantly suppressed the maintenance phase of LTP. Notably, agmatine reversed Aβ-induced deficits in LTP, suggesting a protective effect against synaptic dysfunction. Pharmacological experiments demonstrated that these effects were mediated via α2-adrenergic and imidazoline type I receptors. Paired-pulse facilitation and input–output analyses revealed that agmatine did not alter presynaptic release probability but selectively modulated postsynaptic transmission, particularly under AMPA receptor blockade, indicating a potential regulation of NMDA receptor-mediated signaling. Together, these findings suggest that agmatine modulates hippocampal synaptic plasticity through receptor-specific, postsynaptic mechanisms, and highlight its potential as a therapeutic agent against synaptic impairments in neurodegenerative diseases.

목차

INTRODUCTION

METHODS

RESULTS

DISCUSSION

REFERENCES

키워드

Agmatine Amyloid beta-peptides Imidazoline receptors (I1 subtype) Long-term potentiation Receptors adrenergic alpha-2 Synaptic plasticity