Figure 1.

Field potential in the jcBNST. A, Coronal brain slices were obtained from the rostral cerebrum of Wistar rats at the level indicated in the diagram (modified from Paxinos and Watson, 1998). st, Stria terminalis; jcBNST, juxtacapsular bed nucleus of the stria terminalis (shown in red); BNSTdl, dorsolateral bed nucleus of the stria terminalis; BNSTdm, dorsomedial bed nucleus of the stria terminalis; BNSTv, ventral bed nucleus of the stria terminalis; ac, anterior commissure; LV, lateral ventricle; ic, internal capsule. The boundary of the jcBNST is in good agreement with Dong et al. (2000) and was operationally defined by the area in which a glutamatergic field potential was readily evoked by stimulation of the stria terminalis. B, Photomicrograph of a brain slice at the level of the BNST demonstrating electrode placements for stimulation (Stim.) and electrophysiological recordings (Rec.). C, Field potential evoked in the jcBNST by stimulation of the stria terminalis in coronal brain slices is characterized by two fast negative components followed by a more variable slow positive deflection (blue trace). The second negative component of the field potential and the positive deflection were abolished by application of the AMPA glutamate receptor inhibitor CNQX in bath (20 μm) (red trace). Blocking GABA_A and GABA_B receptors with bicuculline (30 μm) and SCH50911 (20 μm), respectively, increased the size of the postsynaptic components of the field potential without altering the field morphology (black trace). D, Local application of CNQX by diffusion of the inhibitor included in the recording electrode (25 mm) blocked the second negative and the positive components of the field potential (red trace), suggesting they are postsynaptic responses that originate locally in the jcBNST. E, Bath application of the NMDA inhibitor d-AP-5 (50 μm) had no effect on the field potential (red trace). Stimuli artifacts were removed, and the asterisk indicates their location. F, Delivery of HFS (5 trains at 100 Hz for 1 s at 10 s intervals) resulted in a protracted potentiation of the amplitude of the postsynaptic component of the field potential (sample traces are shown in G). A transient application of either d-AP-5 or the mGluR5 inhibitor MPEP around the time of delivery of HFS (horizontal bar) prevented potentiation of the amplitude of the field potential. However, tetanization during continuous application of the GABA_A and GABA_B inhibitors bicuculline and SCH50911, respectively, resulted in the same degree of potentiation as controls (baseline renormalized). H, Application of either d-AP-5 or the mGluR5 inhibitor MPEP to an established LTP of field potential (horizontal bar) was ineffective.