Skip to main content
. Author manuscript; available in PMC: 2019 May 17.
Published in final edited form as: Mol Cell Neurosci. 2014 Aug 6;62:30–41. doi: 10.1016/j.mcn.2014.08.001

Fig. 5. The effect of leptin is presynaptic and dependent on neurotensin (NTS).

Fig. 5.

A) Whole cell current-clamp recordings from an LHA orexin-GI neuron in a brain slice. Leptin significantly reduced the change in membrane potential (MP) and input resistance (IR) normally associated with decreased glucose (G; top 2 traces; n = 16). The neurotensin receptor antagonist (SR142948, 1 μM) blocked the effect of leptin on the glucose sensitivity of this orexin-GI neuron (bottom trace; N = 5). B and C) Bars represent the % change in MP and IR when glucose was lowered from 2.5 to 0.1 mM in the presence or absence of leptin when either the neurotensin receptor antagonist (B) or TTX (C) was present. There was no significant effect of leptin on the response to decreased glucose in the presence of the neurotensin antagonist (Student’s t-test, P > 0.05; n = 5). Similarly, leptin had no effect on glucose sensitivity in the presence of TTX (n = 6). Post-recording single cell (sc) RT-PCR indicated orexin but not leptin receptor expression in LHA orexin-GI neurons (n = 4). Data were analyzed by paired t-test. nsd: no significant difference. N values are indicated within bars.