Skip to main content
. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: Neurotoxicology. 2009 Feb 13;30(3):436–444. doi: 10.1016/j.neuro.2009.02.003

Fig 5. TH immunoactivity in striatum, SNpc, and SNpr.

Fig 5

Animals were treated with veh or AP4A (i.c.v.) and then saline or MA (s.c.). THir was analyzed 4 days after injection. (A) In striatum, parenteral administration of MA significantly reduced density of striatal THir. Administration of AP4A did not significantly reduce the loss of THir density in MA – treated rats. (B) In SNpr, MA administration significantly reduced THir density. AP4A significantly increased THir in SNpr in animals receiving MA. (C) In SNpc, MA did not alter the density of TH neurons. There is no significant interaction in TH neuronal density between treatments with AP4A and MA. (D) Typical immunostaining in SNpr. (D1: vehicle+saline; D2: vehicle+MA; D3: AP4A +saline; D4: AP4A +MA). Calibration = 500 μm.