Heart rhythm · 2025
Excitability properties of cardiac calbindin neurons: Identifying a unique neuronal population.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Lizot Guénaëlle, Bescond Jocelyn, De Koninck Yves, Chahine Mohamed, Bois Patrick, Faivre Jean-François, Chatelier Aurélien
Аннотация
BACKGROUND: The intrinsic cardiac nervous system is a complex system that plays a critical role in the regulation of cardiac physiologic parameters and has been shown to contribute to cardiac arrhythmias. To date, several types of neurons with distinct neurochemical and electrophysiologic phenotypes have been identified. However, no study has correlated the neurochemical phenotype to a specific electrophysiologic behavior. Calbindin-D28k, a calcium-binding protein, is expressed in numerous cardiac neurons.
OBJECTIVE: Given that changes in neuronal excitability have been associated with arrhythmia susceptibility and that calbindin expression has been associated with modulations of neuronal excitability, our objective was to assess whether the cardiac calbindin neuronal population has specific properties that could be involved in cardiac regulation and arrhythmias.
METHODS: By using a Cre-Lox mouse model to specifically target calbindin neurons with a fluorescent reporter, we characterized the neurochemical and electrophysiologic phenotype of this cardiac neuronal population.
RESULTS: Calbindin neurons exhibit a specific neurochemical expression profile and a larger soma with shorter neurite length compared with other neurons. This was combined with a distinct electrophysiologic signature characterized by a lower excitability with a predominantly phasic profile associated to a lower N-type calcium current density.
CONCLUSION: Calbindin cardiac neurons display distinct neurochemical, morphologic, and electrophysiologic properties, resembling the cardiac neuronal remodeling observed in pathologic processes such as heart failure. Therefore, we believe that this specific neuronal population deserves investigation in the context of cardiac diseases.
OBJECTIVE: Given that changes in neuronal excitability have been associated with arrhythmia susceptibility and that calbindin expression has been associated with modulations of neuronal excitability, our objective was to assess whether the cardiac calbindin neuronal population has specific properties that could be involved in cardiac regulation and arrhythmias.
METHODS: By using a Cre-Lox mouse model to specifically target calbindin neurons with a fluorescent reporter, we characterized the neurochemical and electrophysiologic phenotype of this cardiac neuronal population.
RESULTS: Calbindin neurons exhibit a specific neurochemical expression profile and a larger soma with shorter neurite length compared with other neurons. This was combined with a distinct electrophysiologic signature characterized by a lower excitability with a predominantly phasic profile associated to a lower N-type calcium current density.
CONCLUSION: Calbindin cardiac neurons display distinct neurochemical, morphologic, and electrophysiologic properties, resembling the cardiac neuronal remodeling observed in pathologic processes such as heart failure. Therefore, we believe that this specific neuronal population deserves investigation in the context of cardiac diseases.