ArticleCommunications biology2025
Synergistic mechanisms of medullary cholinergic-serotonergic pathway interactions in regulating neuronal excitability and locomotor activities.
Article in Communications biology, 2025. 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
Medullary serotonergic (5-HT) neurons play a pivotal role in locomotor initiation. While these neurons receive cholinergic innervation, the functional consequences and underlying mechanisms remain poorly understood. Using ePet-EYFP transgenic mice (P3-P6) and multidisciplinary approaches, we elucidated the mechanisms by which cholinergic signaling regulated medullary 5-HT neuronal activity and locomotor output. Key findings included: (1) acetylcholine (ACh) elicited location-dependent excitatory, inhibitory, or neutral responses in 5-HT neurons, recapitulated by muscarine and abolished by atropine, indicating muscarinic receptor (mAChR)-mediated regulation. (2) 5-HT neurons in parapyramidal region exhibited ACh-induced excitation, whereas those in midline raphe nuclei displayed inhibition. (3) ACh-enhanced excitability was mediated via M3 receptors, whereas ACh-induced suppression depended on M2/M4 receptor activation. (4) In vitro bath application of muscarine to medullary region induced triphasic modulation of fictive locomotion. Blockade of M1/M5 receptors did not affect locomotion, whereas M3 receptor antagonism reduced gait velocity and perturbated locomotor rhythm. Conversely, M2/M4 receptor antagonism increased stepping frequency without altering locomotor pattern. This study provided the first mechanistic dissection of how medullary cholinergic-serotonergic interactions regulated neuronal excitability and locomotion, uncovering distinct mAChR subtype contributions to motor control.
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