Skip to main content
. Author manuscript; available in PMC: 2022 Oct 14.
Published in final edited form as: Neurobiol Dis. 2015 Feb 4;76:67–76. doi: 10.1016/j.nbd.2015.01.003

Figure 3. H2 antagonism is more effective at blocking the histamine induced increase in ChI firing in dyskinetic 6-OHDA lesioned mice.

Figure 3

(A) 1 μM histamine increases action potential firing rate among ChIs located in the lesioned hemisphere of 6-OHDA lesioned mice, both chronically treated with vehicle and with L-DOPA. A1 shows sample traces (Scale: 1 mV, 1 s for A1 and B1). A2 shows a histogram of average firing rates. (Vehicle: n = 6; L-DOPA: n = 8). (B) In chronic vehicle-treated animals, pre-application of 1μM famotidine had no effect on the histamine induced increase in firing rate. In dyskinetic L-DOPA treated animals however, 1μM famotidine inhibited the histamine induced increase in ChI firing. (Vehicle: n = 16; L-DOPA: n = 10. Data were analyzed using Student's t-test. * p < 0.05). (C) Summary data illustrating that pre-application of 1 μM famotidine inhibits the histamine induced increase in action potential firing in chronic L-DOPA treated animals but not vehicle-treated animals. Dotted line indicates peak histamine induced increase in firing rate, normalized for each treatment group. Bars represent percent change of the histamine response while in the presence of famotidine (* p < 0.05 between treatment groups. Error bars represent ± SEM). (D) Pre-application of both H1 and H2 receptor antagonists completely occlude the excitatory effects of histamine. (n = 3) (E) Famotidine blocked the histamine induced excitation in dyskinetic mice in the presence of synaptic excitatory (DNQX, APV) and inhibitory (GABA) antagonists (Vehicle: n = 7; L-DOPA: n = 5. * p < 0.05 between treatment groups).