Fig. 5.
Activation of dopamine receptors in response to meth is involved in reduction in gap junctional communication and increased opening of connexin hemichannels. Mixed cultures of human neurons and astrocytes were analyzed for gap junctional communication by dye coupling and opening of hemichannels by dye uptake. (a) Dopamine receptor blockers SCH23390 (SCH, 10 μM; specific D1 antagonist) and flupenthixol (Flu, 1 μM; non-specific dopamine receptor blocker) prevented the decrease in gap junctional communication (GJC) induced by meth (meth+SCH or meth+Flu, respectively) in astrocytes (white bars) and neurons (bars with cross lines). Addition of SCH or Flu to control cells did not affect dye coupling. The gap junction/hemichannel blocker 18-alpha-glycyrrhetinic acid (AGA) was used as control (18-α-glycyrrhetinic acid, a GJ blocker). (b) D1 and D2 like dopamine receptors are involved in opening of connexin hemichannels induced for meth treatment. Opening of connexin hemichannels was not blocked by D1 antagonist (SCH23390, SCH) or D2 antagonist (Eticlopride, Eti). However, flupenthixol (Flu, 1 μM; nonspecific dopamine receptor blocker) blocked the opening of connexin hemichannels induced by meth. Lanthanum (La+3) was used as a positive control of blocking. (*p < 0.05 as compared to control conditions, #p < 0.05 as compared to meth-treated conditions, &p < 0.05 as compared to SCH or Flu–treated conditions. n = 4)