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1.
Fig. 2.

Fig. 2. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

CCK-8 and leptin stimulate CART release in a dose-dependent manner. A: NG neurons stimulated with CCK-8 (0.1–100 nM) for 2 h exhibited a significant increase in CART release at 1, 10, and 100 nM. B: leptin significantly stimulated CART release at 1, 10, and 100 nM. Data are representative of 5 independent experiments. *P < 0.05 indicates statistical significance from unstimulated control.

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.
2.
Fig. 6.

Fig. 6. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

Silencing the EGR-1 gene inhibits leptin plus CCK-8 synergistic stimulation of CART release. A: 80% of the synergistic CCK/leptin-stimulated CART release was significantly inhibited by silencing the EGR-1 gene in NG neurons transfected with EGR-1 siRNA. Data are representative of 5 independent experiments; *P < 0.05, significantly different from unstimulated control; **P < 0.05, significantly different from CCK/leptin-stimulated CART release. B: representative CART RT-PCR confirms that silencing the EGR-1 gene results in decreased CART mRNA expression 5 days after transfection of cultured NG neurons. C: representative EGR-1 RT-PCR confirms that EGR-1 siRNA inhibits both control and CCK/leptin-stimulated EGR-1 expression. D: representative EGR-1 immunoblot confirms >80% inhibition of EGR-1 expression 5 days after transfection with EGR-1 siRNA, n = 5.

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.
3.
Fig. 3.

Fig. 3. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

CCK-8 and leptin potentiate CART release via low-affinity CCKARs. NG neurons were stimulated for 2 h with leptin (0.1 nM) and CCK-8 (0.1 nM) alone and in combination. Neither leptin nor CCK-8 increased CART release; however, when combined, leptin (L) and CCK-8 (C) caused a significant 2.27 ± 0.21-fold increase in CART release. The synergistic CCK/leptin-stimulated CART release was inhibited >70% by the CCK-OPE analog (100 nM), which acts as a low-affinity CCKAR antagonist. Data are representative of 5 independent experiments, n = 5 rats. *P < 0.05, significantly different from unstimulated control; **P < 0.05, significantly different from CCK/leptin-stimulated CART release.

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.
4.
Fig. 4.

Fig. 4. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

Silencing the phosphatidylinositol 3-kinase (PI3K) and SRC genes inhibits CCK-8 and leptin synergistically stimulated CART release. A: 70% of the synergistic CCK/leptin-stimulated CART release was significantly inhibited by silencing the PI3K gene in NG neurons transfected with PI3K small interfering RNA (siRNA). B: representative Western blot confirms inhibition of PI3K expression in NG neurons transfected with PI3K siRNA. C: 79% of the CCK/leptin synergistic CART release was significantly inhibited by silencing the SRC gene. D: representative Western blot confirms inhibition of SRC expression in NG neurons transfected with SRC siRNA. Bars represent means ± SE from 5 independent experiments; *P < 0.05 compared with unstimulated controls (con); **P < 0.05 compared with CART stimulated by CCK-8 (1 nM) and leptin (1 nM).

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.
5.
Fig. 5.

Fig. 5. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

Silencing the STAT gene, but not the Erk1/2 genes inhibits CCK-8 and leptin synergistically stimulated CART release. A: 90% of the CCK/leptin synergistic CART release was significantly inhibited by silencing the STAT3 gene. B: representative Western blot confirms inhibition of STAT3 expression in NG neurons transfected with retroviral STAT3 short hairpin RNA (shRNA). C: CCK/leptin-stimulated CART release was not inhibited by silencing the Erk1/2 gene. D: representative Western blot confirms inhibition of Erk1/2 expression by Erk1/2 siRNA. Bars represent means ± SE from 5 independent experiments; *P < 0.05 compared with unstimulated controls; **P < 0.05 compared with CART stimulated by CCK-8 (1 nM) and leptin (1 nM).

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.
6.
Fig. 1.

Fig. 1. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

Immunostaining of rat nodose ganglia (NG) neurons shows colocalization of leptin receptors (LRb), CCK-A receptors (CCKAR), and cocaine- and amphetamine-regulated transcript (CART). A: representative photomicrograph of a rat NG shows that 36.7 ± 4.4% of the NG neurons stained positive for LRb. B: 55.9 ± 5.1% of the NG neurons stained positive for the CCKAR. C: 24.5 ± 6.3% of the NG neurons stained positive for CART. D: 18.7 ± 2.8% of the NG neurons contained both CCKARs and LRbs. E: 11.5 ± 5.1% contained CART immunoreactivity as well as CCKARs and LRbs. F: histogram shows the percentage of the total number of NG neurons that exhibited immunoreactivities for LRb, CCKAR, CART, or for both receptors and CART, n = 4, scale bar = 50 μm. Data are representative of 4 independent experiments (n = 4 rats).

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.
7.
Fig. 9.

Fig. 9. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

Silencing the STAT3 and CART genes abolishes the effects of CCK-8/leptin on satiety. Feeding studies in rats 5 days after electroporation of NG with control siRNA or CART siRNA (A) and with control siRNA or STAT3 siRNA (B). Rats were fasted overnight and injected with CCK-8 (3.5 μg/kg ip) and leptin (120 μg/kg ip), and, after a 1-h recovery, cumulative food intake was measured for 3 h. Data are representative of 5 independent experiments; *P < 0.05 compared with food intake by control rats that received no treatment to nodose ganglia. C: representative RT-PCR confirms silencing of CART gene expression, 5 days after electroporation of NG. D: representative RT-PCR confirms silencing of STAT3 gene expression, 5 days after electroporation of NG (n = 5).

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.
8.
Fig. 7.

Fig. 7. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

Silencing the EGR-1 gene did not affect neuronal firing evoked by leptin/CCK-8. A: representative nodose ganglia neuron transfected with EGR1 siRNA and identified by the presence of Cy3 marker (red). B: continuous membrane potential recording demonstrates that silencing EGR-1 did not abolish the synergistic leptin (1 nM) and CCK-8 (1 nM) excitatory action in the recorded neuron. The neuronal input resistance was tested every 40 s by injecting 0.5-s, 100-pA negative-amplitude current pulses (negative membrane potential deflections). C: in contrast, continuous membrane potential recording (performed in the same neuron as in shown in B) demonstrates that superfusion of leptin (1 nM) or CCK-8 (1 nM) separately did not produce significant changes in neuronal excitability. These findings are similar to those observed in nontransfected nodose ganglia neurons.

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.
9.
Fig. 8.

Fig. 8. From: Cocaine- and amphetamine-regulated transcript is the neurotransmitter regulating the action of cholecystokinin and leptin on short-term satiety in rats.

Silencing the expression of CART in rat NG inhibited c-Fos expression in the hypothalamus. Representative photomicrographs showing immunostaining of rat hypothalamic c-Fos-positive nuclei stained red. c-Fos expression in rat lateral hypothalamus (LH; A), dorsomedial hypothalamus (DMH; C), paraventricular nucleus (PVN; E), and arcuate nucleus (ARC; G) in response to CCK-8 (3.5 μg/kg) plus leptin (Lep; 120 μg/kg) ip, 5 days after electroporation with control siRNA. Elimination of c-Fos expression in rat LH (B), DMH (D), PVN (F), and ARC (H), 5 days after electroporation of the nodose ganglia with CART siRNA, followed by CCK-8 (3.5 μg/kg) plus leptin (120 μg/kg ip). I: histogram shows the percentage of neurons that exhibited c-Fos immunoreactivities over the total number of neurons in the hypothalamus. Note that silencing of CART in the NG markedly reduced the CCK/leptin-stimulated c-Fos expression in the LH, DMH, PVN, and ARC; *P < 0.05 compared with electroporation with control siRNA. Data are representative of 5 independent experiments, n = 5 rats in each study group.

Andrea Heldsinger, et al. Am J Physiol Gastrointest Liver Physiol. 2012 November 1;303(9):G1042-G1051.

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