Hyperpolarization-activated current I h in mouse trigeminal sensory neurons in a transgenic mouse model of familial hemiplegic migraine type-1

Neuroscience ◽  
2017 ◽  
Vol 351 ◽  
pp. 47-64 ◽  
Author(s):  
Francesca Eroli ◽  
Sandra Vilotti ◽  
Arn M.J.M. van den Maagdenberg ◽  
Andrea Nistri
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Sensory Neurons ◽  
Familial Hemiplegic Migraine ◽  
Transgenic Mouse Model ◽  
Hemiplegic Migraine ◽  
Hyperpolarization Activated Current

scholarly journals The Mechanism of Functional Up-Regulation of P2X3 Receptors of Trigeminal Sensory Neurons in a Genetic Mouse Model of Familial Hemiplegic Migraine Type 1 (FHM-1)

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e60677 ◽  
Author(s):  
Swathi K. Hullugundi ◽  
Michel D. Ferrari ◽  
Arn M. J. M. van den Maagdenberg ◽  
Andrea Nistri
Keyword(s):  
Mouse Model ◽  
Sensory Neurons ◽  
Familial Hemiplegic Migraine ◽  
Hemiplegic Migraine ◽  
P2x3 Receptors ◽  
Genetic Mouse Model

scholarly journals Overexpressed NaV1.7 Channels Confer Hyperexcitability to in vitro Trigeminal Sensory Neurons of CaV2.1 Mutant Hemiplegic Migraine Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Riffat Mehboob ◽  
Anna Marchenkova ◽  
Arn M. J. M. van den Maagdenberg ◽  
Andrea Nistri
Keyword(s):  
Sensory Neurons ◽  
Primary Cultures ◽  
Familial Hemiplegic Migraine ◽  
Hemiplegic Migraine ◽  
P2x3 Receptors ◽  
Enhanced Expression ◽  
Clamp Condition ◽  
And Function

Trigeminal sensory neurons of transgenic knock-in (KI) mice expressing the R192Q missense mutation in the α1A subunit of neuronal voltage-gated CaV2.1 Ca2+ channels, which leads to familial hemiplegic migraine type 1 (FHM1) in patients, exhibit a hyperexcitability phenotype. Here, we show that the expression of NaV1.7 channels, linked to pain states, is upregulated in KI primary cultures of trigeminal ganglia (TG), as shown by increased expression of its α1 subunit. In the majority of TG neurons, NaV1.7 channels are co-expressed with ATP-gated P2X3 receptors (P2X3R), which are important nociceptive sensors. Reversing the trigeminal phenotype with selective CaV2.1 channel inhibitor ω-agatoxin IVA inhibited NaV1.7 overexpression. Functionally, KI neurons revealed a TTX-sensitive inward current of larger amplitude that was partially inhibited by selective NaV1.7 blocker Tp1a. Under current-clamp condition, Tp1a raised the spike threshold of both wild-type (WT) and KI neurons with decreased firing rate in KI cells. NaV1.7 activator OD1 accelerated firing in WT and KI neurons, a phenomenon blocked by Tp1a. Enhanced expression and function of NaV1.7 channels in KI TG neurons resulted in higher excitability and facilitated nociceptive signaling. Co-expression of NaV1.7 channels and P2X3Rs in TGs may explain how hypersensitivity to local stimuli can be relevant to migraine.

Plasma metabolic profiling after cortical spreading depression in a transgenic mouse model of hemiplegic migraine by capillary electrophoresis – mass spectrometry

2015 ◽  
Vol 11 (5) ◽  
pp. 1462-1471 ◽  
Author(s):  
Reinald Shyti ◽  
Isabelle Kohler ◽  
Bart Schoenmaker ◽  
Rico J. E. Derks ◽  
Michel D. Ferrari ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Capillary Electrophoresis ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Metabolic Profiling ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Transgenic Mouse Model ◽  
Metabolic Changes ◽  
Hemiplegic Migraine

Cortical spreading depression-induced brain metabolic changes have been captured in the plasma of a transgenic migraine mouse model using CE-MS.

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