Figure 4.

α1-AR LTD (as measured in the dlBNST) is induced independently of evoked glutamatergic synaptic activity but dependent on L-type voltage gated calcium channels (VGCCs). (a) To address the involvement of presynaptic stimulation the stimulus was turned off prior to 100 µM methoxamine application and turned back on 2 min post α1-AR agonist removal. This did not disrupt LTD expression. (N = 7). (a inset) To control for the lack of stimulation interleaved experiments were run without the presence of agonist (N = 5). (b) To assess the role of N-methyl-d-aspartate receptor (NMDAR) activation α1-AR LTD experiments were performed in whole cell voltage clamp (−70 mV holding potential) and DL-APV (100 µM) was included throughout the duration of the experiment (N = 5). (c) The L-type calcium channel blocker nimodipine (10 µM) prevented the induction of α1-AR LTD by 100 µM methoxamine, however it did not prevent a significant transient depression. (N = 7) (d) To verify that α1-AR LTD does not require mGluR5 signaling we applied 100 µM methoxamine in the mGluR5 antagonist MPEP (10 µM; N = 5). (e) Paired pulse ratios do not change in response to methoxamine (10 or 100 µM) in dlBNST (N = 11).