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Title 

Thalamic T-type Ca2+ channels mediate frontal lobe dysfunctions caused by a hypoxia-like damage in the prefrontal cortex

Authors 

J KimJ WooY G ParkSu Jin ChaeS JoJ W ChoiH Y JunYoung Il YeomS H ParkK H KimH S ShinD Kim

Publisher 

Society for Neuroscience

Issue Date 

2011

Citation 

Journal of Neuroscience, vol. 31, no. 11, pp. 4063-4073

Abstract 

Hypoxic damage to the prefrontal cortex (PFC) has been implicated in the frontal lobe dysfunction found in various neuropsychiatric disorders. The underlying subcortical mechanisms, however, have not been well explored. In this study, we induced a PFC-specific hypoxia-like damage by cobalt-wire implantation to demonstrate that the role of the mediodorsal thalamus (MD) is critical for the development of frontal lobe dysfunction, including frontal lobe-specific seizures and abnormal hyperactivity. Before the onset of these abnormalities, the cross talk between the MD and PFC nuclei at theta frequencies was enhanced. During the theta frequency interactions, burst spikes, known to depend on T-type Ca(2+) channels, were increased in MD neurons. In vivo knockout or knockdown of the T-type Ca(2+) channel gene (Ca(V)3.1) in the MD substantially reduced the theta frequency MD-PFC cross talk, frontal lobe-specific seizures, and locomotor hyperactivity in this model. These results suggest a two-step model of prefrontal dysfunction in which the response to a hypoxic lesion in the PFC results in abnormal thalamocortical feedback driven by thalamic T-type Ca(2+) channels, which, in turn, leads to the onset of neurological and behavioral abnormalities. This study provides valuable insights into preventing the development of neuropsychiatric disorders arising from irreversible PFC damage.

ISSN 

0270-6474

Link 

http://dx.doi.org/10.1523/JNEUROSCI.4493-10.2011

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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