Aphonia induced by simultaneous bilateral ischemic infarctions of the putamen nuclei: a case report and review of the literature.

Introduction: Isolated aphonia induced by acute stroke is a rare phenomenon with only a few cases reported in the literature.

Case Presentation: We report an unusual case of a 44-year-old African-American man with a history of hypertension, smoking and cocaine use who developed acute aphonia secondary to simultaneous ischemic infarctions of the bilateral putamen nuclei.

Conclusion: We describe the clinical presentation of acute aphonia induced by bilateral putamen nuclei ischemic infarctions, correlating clinical symptoms with injury localization.

Cheiro-Oral syndrome secondary to thalamic infarction: a case report and literature review.

Introduction: Small thalamic infarcts can present with a variety of sensory deficits that can be difficult to diagnose clinically because of their seemingly disconnected manifestations.

Case Report: Here we report a case of a 55-year-old man presenting with the clinical findings of Cheiro-Oral syndrome, a pure sensory thalamic lacunar syndrome that clinically presents with contralateral sensory deficits of the fingers and hemimouth.

Conclusions: This report highlights both common and unusual clinical presentations of isolated thalamic infarctions, correlating clinical symptomatology with anatomic localization.

Cav 1.3 L-type Ca ( 2+) channels mediate long-term adaptation in dopamine D2L-mediated GluA1 trafficking in the dorsal striatum following cocaine exposure.

AMPA receptor (AMPAR) plasticity at glutamatergic synapses in the mesostriatal dopaminergic pathway has been implicated in persistent cocaine-induced behavioral responses; however, the precise mechanism underlying these changes remains unknown. Utilizing cocaine psychomotor sensitization in mice we find that repeated cocaine results in a basal reduction of Ser 845 GluA1 and cell surface GluA1 levels in the dorsal striatum (dStr) following a protracted withdrawal period, an adaptation that is dependent on Cav 1.3 channels but not those expressed in the VTA.

Molecular switch from L-type Ca v 1.3 to Ca v 1.2 Ca2+ channel signaling underlies long-term psychostimulant-induced behavioral and molecular plasticity.

L-type Ca(2+) channel (LTCC)-activated signaling cascades contribute significantly to psychostimulant-induced locomotor sensitization; however, the precise contribution of the two brain-specific subunits Ca(v)1.2 and Ca(v)1.3 remains mostly unknown.

L-type Ca2+ channels mediate adaptation of extracellular signal-regulated kinase 1/2 phosphorylation in the ventral tegmental area after chronic amphetamine treatment.

L-type Ca2+ channels (LTCCs) play an important role in chronic psychostimulant-induced behaviors. However, the Ca2+ second messenger pathways activated by LTCCs after acute and recurrent psychostimulant administration that contribute to drug-induced molecular adaptations are poorly understood. Using a chronic amphetamine treatment paradigm in rats, we have examined the role of LTCCs in activating the mitogen-activated protein (MAP) kinase pathway in the ventral tegmental area (VTA), a primary target for the reinforcing properties of psychostimulants.