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. Author manuscript; available in PMC: 2011 Apr 15.
Published in final edited form as: Eur J Neurosci. 2010 May 24;31(11):1946–1959. doi: 10.1111/j.1460-9568.2010.07231.x

Fig. 5.

Fig. 5

Small-conductance calcium-dependent potassium channel inhibition enhanced long-term depression (LTD) induction in lateral dorsal striatum (latDS) but not in nucleus accumbens shell (NAS) neurons. (A) Sample traces of field excitatory postsynaptic potential/population spikes (fEPSP/PSs) in latDS neurons recorded before and after high frequency stimulation (HFS) (50 Hz for 2 s, repeated four times, with 15 s between initiation of trains). N2 indicates the postsynaptic field potential, and N1 indicates the presynaptic fiber volley, which was not altered during induction of synaptic plasticity (data not shown) [see also Behnisch & Reymann (1998) and Stackman et al. (2002)]. (A–C) Apamin facilitated the development of HFS-induced LTD in latDS neurons (A and B) but not in NAS neurons (C). In addition, apamin (apa)-facilitated LTD in latDS neurons was inhibited by the CB1 receptor antagonist AM251 (AM) (B) (2 μm) and the dopamine D2 receptor antagonist eticlopride (etic) (B) (1 μm).