TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal Neurons

TRPM4 is a non-selective cation channel activated by intracellular calcium and permeable to monovalent cations. This channel participates in the control of neuronal firing, neuronal plasticity, and neuronal death. TRPM4 depolarizes dendritic spines and is critical for the induction of NMDA receptor-...

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Main Authors: Denise Riquelme, Oscar Cerda, Elias Leiva-Salcedo
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-04-01
Series:Frontiers in Neuroanatomy
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fnana.2021.643287/full
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author Denise Riquelme
Oscar Cerda
Oscar Cerda
Elias Leiva-Salcedo
author_facet Denise Riquelme
Oscar Cerda
Oscar Cerda
Elias Leiva-Salcedo
author_sort Denise Riquelme
collection DOAJ
description TRPM4 is a non-selective cation channel activated by intracellular calcium and permeable to monovalent cations. This channel participates in the control of neuronal firing, neuronal plasticity, and neuronal death. TRPM4 depolarizes dendritic spines and is critical for the induction of NMDA receptor-dependent long-term potentiation in CA1 pyramidal neurons. Despite its functional importance, no subcellular localization or expression during postnatal development has been described in this area. To examine the localization and expression of TRPM4, we performed duplex immunofluorescence and patch-clamp in brain slices at different postnatal ages in C57BL/6J mice. At P0 we found TRPM4 is expressed with a somatic pattern. At P7, P14, and P35, TRPM4 expression extended from the soma to the apical dendrites but was excluded from the axon initial segment. Patch-clamp recordings showed a TRPM4-like current active at the resting membrane potential from P0, which increased throughout the postnatal development. This current was dependent on intracellular Ca2+ (ICAN) and sensitive to 9-phenanthrol (9-Ph). Inhibiting TRPM4 with 9-Ph hyperpolarized the membrane potential at P14 and P35, with no effect in earlier stages. Together, these results show that TRPM4 is expressed in CA1 pyramidal neurons in the soma and apical dendrites and associated with a TRPM4-like current, which depolarizes the neurons. The expression, localization, and function of TRPM4 throughout postnatal development in the CA1 hippocampal may underlie an important mechanism of control of membrane potential and action potential firing during critical periods of neuronal development, particularly during the establishment of circuits.
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spelling doaj.art-133702131508400a9ab5f52bcbd090042022-12-21T19:58:23ZengFrontiers Media S.A.Frontiers in Neuroanatomy1662-51292021-04-011510.3389/fnana.2021.643287643287TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal NeuronsDenise Riquelme0Oscar Cerda1Oscar Cerda2Elias Leiva-Salcedo3Departamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, ChilePrograma de Biología Celular y Molecular, ICBM, Facultad de Medicina, Universidad de Chile, Santiago, ChileMillennium Nucleus of Ion Channel-Associated Diseases, Santiago, ChileDepartamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago, ChileTRPM4 is a non-selective cation channel activated by intracellular calcium and permeable to monovalent cations. This channel participates in the control of neuronal firing, neuronal plasticity, and neuronal death. TRPM4 depolarizes dendritic spines and is critical for the induction of NMDA receptor-dependent long-term potentiation in CA1 pyramidal neurons. Despite its functional importance, no subcellular localization or expression during postnatal development has been described in this area. To examine the localization and expression of TRPM4, we performed duplex immunofluorescence and patch-clamp in brain slices at different postnatal ages in C57BL/6J mice. At P0 we found TRPM4 is expressed with a somatic pattern. At P7, P14, and P35, TRPM4 expression extended from the soma to the apical dendrites but was excluded from the axon initial segment. Patch-clamp recordings showed a TRPM4-like current active at the resting membrane potential from P0, which increased throughout the postnatal development. This current was dependent on intracellular Ca2+ (ICAN) and sensitive to 9-phenanthrol (9-Ph). Inhibiting TRPM4 with 9-Ph hyperpolarized the membrane potential at P14 and P35, with no effect in earlier stages. Together, these results show that TRPM4 is expressed in CA1 pyramidal neurons in the soma and apical dendrites and associated with a TRPM4-like current, which depolarizes the neurons. The expression, localization, and function of TRPM4 throughout postnatal development in the CA1 hippocampal may underlie an important mechanism of control of membrane potential and action potential firing during critical periods of neuronal development, particularly during the establishment of circuits.https://www.frontiersin.org/articles/10.3389/fnana.2021.643287/fullTRPM4ICANhippocampusCA1pyramidal neurons
spellingShingle Denise Riquelme
Oscar Cerda
Oscar Cerda
Elias Leiva-Salcedo
TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal Neurons
Frontiers in Neuroanatomy
TRPM4
ICAN
hippocampus
CA1
pyramidal neurons
title TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal Neurons
title_full TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal Neurons
title_fullStr TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal Neurons
title_full_unstemmed TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal Neurons
title_short TRPM4 Expression During Postnatal Developmental of Mouse CA1 Pyramidal Neurons
title_sort trpm4 expression during postnatal developmental of mouse ca1 pyramidal neurons
topic TRPM4
ICAN
hippocampus
CA1
pyramidal neurons
url https://www.frontiersin.org/articles/10.3389/fnana.2021.643287/full
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AT eliasleivasalcedo trpm4expressionduringpostnataldevelopmentalofmouseca1pyramidalneurons