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. 2011 Dec 14;31(50):18479–18491. doi: 10.1523/JNEUROSCI.4785-11.2011

Figure 6.

Figure 6.

Increased ERK1/2 phosphorylation following glycemic challenges is dependent on intact catecholaminergic inputs to the neuroendocrine PVH. a–c, Insulin (a, c) or 2-DG (b, c) significantly increased mean (+SEM) pERK1/2-IR compared with saline (Sal) in the PVHmpd of sham (MSAP)-lesioned rats. Catecholaminergic denervation of the PVH (as assessed by DBH immunocytochemistry) completely abolished pERK1/2 responses to both challenges (a, c). Partial lesions abolished the pERK1/2 response to insulin (a, c) but not 2-DG (b, c). An asymmetric lesion in the PVH of an insulin-injected animal (a) produced a correspondingly asymmetric pERK1/2 response. **p < 0.001, ***p < 0.0001. ns, Not significant. Numbers below the bars (c) are the number of samples per group. Scale bars, 100 μm.