L-DOPA (Levodopa) is an amino acid precursor of dopamine with antiparkinsonian properties. Levodopa is a prodrug that is converted to dopamine by DOPA decarboxylase and can cross the blood-brain barrier. When in the brain, levodopa is decarboxylated to dopamine and stimulates the dopaminergic receptors, thereby compensating for the depleted supply of endogenous dopamine seen in Parkinson's disease. To assure that adequate concentrations of levodopa reach the central nervous system, it is administered with carbidopa, a decarboxylase inhibitor that does not cross the blood-brain barrier, thereby diminishing the decarboxylation and inactivation of levodopa in peripheral tissues and increasing the delivery of dopamine to the CNS.

L-DOPA 在诱导MPTP帕金森症状的猴子中引起多种异常运动的发展。L-DOPA 给药导致在6-OHDA-损伤大鼠的CdPu中多巴胺D3受体表达的异位。[3] L-DOPA （50 mg/kg）通过激活完整大鼠多巴胺D1/D2受体，增加基底节区整体的内酰胺浓度。L-DOPA 产生日益严重的口-舌自发运动，这些运动在损伤大鼠中可被大麻素激动剂R(+)-WIN55,212-2（1 mg/kg）减缓。[4] L-DOPA 给药逆转了严重损伤大鼠中观察到的D2多巴胺受体上调，提供了L-DOPA 在基底节达到生物活性浓度的证据。[5]

L-DOPA 在诱导MPTP帕金森症状的猴子中引起多种异常运动的发展。L-DOPA 给药导致在6-OHDA-损伤大鼠的CdPu中多巴胺D3受体表达的异位。[3] L-DOPA （50 mg/kg）通过激活完整大鼠多巴胺D1/D2受体，增加基底节区整体的内酰胺浓度。L-DOPA 产生日益严重的口-舌自发运动，这些运动在损伤大鼠中可被大麻素激动剂R(+)-WIN55,212-2（1 mg/kg）减缓。[4] L-DOPA 给药逆转了严重损伤大鼠中观察到的D2多巴胺受体上调，提供了L-DOPA 在基底节达到生物活性浓度的证据。[5]

Briefly, transfected HEK-293 cells, incubated in charcoal-treated Dulbecco's modified Eagle's medium for 24 h, are washed once with Hanks' solution and resuspended in a buffer containing 100 mM NaCl, 1 mM MgCl2, 1 mM EDTA, 1 mM EGTA, 250 mMsucrose, 20 mM Tris-HCl, pH 7.4. Cells are lysed by freezing in liquid nitrogen. Dehydrogenase activity is measured in a final volume of 20 μL containing the appropriate concentration of bile acid, 30 nCi of [3H]cortisol, and unlabeled cortisol to a final concentrations of 50 nM. The reaction is started by mixing cell lysate with the reaction mixture. Alternatively, endoplasmic reticulum microsomes are prepared from transfected HEK-293 cells and incubated with reaction mixture containing various concentrations of cortisol and CDCA. Incubation proceeded for 20 min, and the conversion of cortisol to cortisone is determined by thin layer chromatography (TLC). Because of the inaccuracy of the TLC method at low conversion rates and the end-product inhibition of 11βHSD2 at conversion rates higher than 60-70%, only conversion rates between 10 and 60% are considered for calculation. The inhibitory constant IC50 is evaluated using the curve-fitting program. Results are expressed as means±S.E. and consist of at least four independent measurements.