Absence of meningeal mast cells in the Mitf mutant mouse

Sabaté San José, Alba; Petersen, Petur Henry

doi:10.3389/fncel.2024.1337621

Cited by 2 publications

(1 citation statement)

References 41 publications

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“…Interestingly, Mitf mi-vga9/+ mice, which are phenotypically similar to C57BL/6J (i.e., black coat color, normal eyes, melanocytes and mast cells presence), showed a trend of reduced olfactory ability. This suggests that the effect is primary, rather than secondary due to Mitf pleiotropy, and indicates a dosage effect associated with the Mitf mutation, which is in accordance with previous studies (Atacho et al, 2020; Ingason et al, 2019; Sabaté San José & Petersen, 2024).…”

Section: Resultssupporting

confidence: 92%

Reduction in olfactory ability in agingMitfmutant mice without neurodegeneration

Mechmet,

Steingrímsson,

Henry Petersen

2024

Preprint

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Age-related decline occurs in most brain structures and sensory systems. An illustrative case is olfaction, where the olfactory bulb (OB) undergoes deterioration with age, resulting in reduced olfactory ability. Decline in olfaction is also associated with early symptoms of neurodegenerative diseases including Alzheimer’s disease (AD) and Parkinson’s disease (PD). However, the underlying reasons are unclear. The microphthalmia-associated transcription factor (MITF) is expressed in the projection neurons (PNs) of the OB – the mitral and tufted (M/T) cells. Primary M/T cells fromMitfmutant mice show hyperactivity, potentially attributed to reduced expression of a key potassium channel subunit,Kcnd3/Kv4.3. This influences intrinsic plasticity, an essential mechanism involving the non-synaptic regulation of neuronal activity. As neuronal hyperactivity often precedes neurodegenerative conditions, the current study aimed to determine whether the absence ofMitfhas degenerative effects during aging. AgedMitfmutant mice showed reduced olfactory ability without inflammation. However, an increase in the expression of potassium channel subunit genes in the OB suggests that during aging compensatory mechanisms lead to stabilization.Significance statementThis study highlights the age-related decline in olfaction and elucidates compensatory mechanisms mediated by potassium channels. These findings improve our comprehension of the processes underlying age-related changes in olfaction.

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Section: Resultssupporting

confidence: 92%

Reduction in olfactory ability in agingMitfmutant mice without neurodegeneration

Mechmet,

Steingrímsson,

Henry Petersen

2024

Preprint

View full text Add to dashboard Cite

show abstract

Reduction in the olfactory ability in aging Mitf mutant mice without evidence of neurodegeneration

Mechmet,

Steingrímsson,

Petersen

2024

Front. Aging

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Age-related decline occurs in most brain structures and sensory systems. An illustrative case is olfaction. The olfactory bulb (OB) undergoes deterioration with age, resulting in reduced olfactory ability. A decline in olfaction is also associated with early symptoms of neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). However, the underlying reasons are unclear. The microphthalmia-associated transcription factor (MITF) is expressed in the projection neurons (PNs) of the OB–the mitral and tufted (M/T) cells. Primary M/T cells from Mitf mutant mice show hyperactivity, potentially attributed to the reduced expression of a key potassium channel subunit, Kcnd3/Kv4.3. This influences intrinsic plasticity, an essential mechanism involving the non-synaptic regulation of neuronal activity. As neuronal hyperactivity often precedes neurodegenerative conditions, the current study aimed to determine whether the absence of Mitf causes degenerative effects during aging. Aged Mitf mutant mice showed reduced olfactory ability without inflammation. However, an increase in the expression of potassium channel subunit genes in the OBs of aged Mitfmi-vga9/mi-vga9 mice suggests that during aging, compensatory mechanisms lead to stabilization.

show abstract

Absence of meningeal mast cells in the Mitf mutant mouse

Cited by 2 publications

References 41 publications

Reduction in olfactory ability in agingMitfmutant mice without neurodegeneration

Reduction in olfactory ability in agingMitfmutant mice without neurodegeneration

Reduction in the olfactory ability in aging Mitf mutant mice without evidence of neurodegeneration

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