Abstract：
:Thiamine deficiency during embryonic or early postnatal development causes deficits in cerebellum-dependent activities including motor control and procedural memory. Here, we give a detailed description of the changes to A-type current in cultured cerebellar granule neurons exposed to thiamine deficiency in vitro. A-type current in treated neurons was reduced to 51% of that in controls. The remaining A-type current in treated neurons exhibited normal activation kinetics and voltage dependence whereas inactivation was markedly faster. These effects were selective because the delayed-rectifier potassium current density and kinetics were unchanged in thiamine-deficient neurons. A computational model of the cerebellar granule neuron was used to test the impact of these alterations and predicts an increase in excitability that is especially pronounced for synaptic activation. Our results suggest that the loss of A-type potassium conductance leads to hyperactivity in cerebellar granule neurons and may contribute to cell death observed in the granule layer of cerebellum during thiamine-deficiency in vivo.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Cruz JS,Kushmerick C,Moreira-Lobo DC,Oliveira FAdoi
10.1016/j.neuroscience.2012.06.053subject
Has Abstractpub_date
2012-09-27 00:00:00pages
108-14eissn
0306-4522issn
1873-7544pii
S0306-4522(12)00671-9journal_volume
221pub_type
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