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1.
Figure 3

Figure 3. From: Modulation of CGRP-induced light aversion in wildtype mice by a 5HT1B/D agonist.

CGRP-induced light aversion. (A) Time spent in light zone and (B) number of transitions between zones by WT mice during four repeated exposures in light-dark box at 2.7×104 lx. After icv injection, CGRP-treated ( n = 20) mice compared with vehicle (Veh) (, n = 15) spent less time in light (***p < 0.001) and transitioned less (**p < 0.01) at indicated intervals. CGRP-treated mice also spent less time in light and transitioned less compared to pre- and post-treatment (**p < 0.01, ***p < 0.001) as indicated by brackets. Error bars indicate mean ± SEM.

Eric A. Kaiser, et al. J Neurosci. 2012 October 31;32(44):15439-15449.
2.
Figure 1

Figure 1. From: Modulation of CGRP-induced light aversion in wildtype mice by a 5HT1B/D agonist.

Lack of CGRP-induced light-aversion upon naïve exposure of WT mice at low and bright light intensities. Time spent in light zone and number of transitions between zones shown in the left and right panels, respectively. (A) Behavior in low light (5.5×101 lx) after icv injection of CGRP (, n=10) or vehicle (Veh) (, n=10). (B) Behavior in bright light (2.7×104 lx) after icv injection of CGRP (, n=10) or vehicle (, n=10). Observation time indicates the interval over the previous 5 min (e.g. 5 min interval is from 0–5 min). Error bars indicate mean ± SEM.

Eric A. Kaiser, et al. J Neurosci. 2012 October 31;32(44):15439-15449.
3.
Figure 4

Figure 4. From: Modulation of CGRP-induced light aversion in wildtype mice by a 5HT1B/D agonist.

CGRP-induced aversion is dependent on light. (A) Time spent in uncovered (normally light) zone with lights off (~0 lx) during all four exposures. Mice injected with vehicle (Veh) (, n = 10) or CGRP (, n = 10). (B) Time spent in light zone with lights on (2.7×104 lx) or uncovered zone with lights off (~0 lx). Lights were on for first two exposures and off for the last two exposures (Veh, , n = 9; CGRP, , n = 10). After icv injection, CGRP-treated mice compared with vehicle spent similar amount of time in the uncovered zone in both (A) and (B). Brackets marked with symbols indicate a significant difference between treatment and either pre-treatment 2 or post-treatment (CGRP: *p < 0.05; Veh: +p < 0.05, ++p < 0.01, +++p < 0.01). Error bars indicate mean ± SEM.

Eric A. Kaiser, et al. J Neurosci. 2012 October 31;32(44):15439-15449.
4.
Figure 8

Figure 8. From: Modulation of CGRP-induced light aversion in wildtype mice by a 5HT1B/D agonist.

Rizatriptan reduces CGRP effects on transitions and motility. (A) Time resting and (B) vertical activity during four repeated exposures to light-dark box at 2.7×104 lx. After icv injection, CGRP-treated (n = 19) mice compared with vehicle (Veh) (, n = 10) (*p < 0.05, ***p<0.01), co-administration of rizatriptan (Riza) and CGRP (, n = 29) (##p < 0.01), and rizatriptan alone (, n = 29) (^p < 0.05, ^^^ p < 0.001) at indicated intervals. Brackets marked with symbols indicate a significant difference between treatment and either pre-treatment 2 or post-treatment (CGRP: *p < 0.05, ***p < 0.001; Riza + CGRP: #p < 0.05, ##p < 0.01, ###p < 0.001; Riza ^^^ p< 0.001). For resting time in the light zone rizatriptan- and vehicle-treated mice were different (p < 0.05) in post-treatment at the 5 min interval. Error bars indicate mean ± SEM.

Eric A. Kaiser, et al. J Neurosci. 2012 October 31;32(44):15439-15449.
5.
Figure 5

Figure 5. From: Modulation of CGRP-induced light aversion in wildtype mice by a 5HT1B/D agonist.

CGRP has no effect on anxiety-like behavior in an open field test. (A) Schematic of repeated testing paradigm used for the open field test. WT mice were exposed to light-dark box in pre-treatment 1 (Pre1) and pre-treatment 2 (Pre2) exposures under the same conditions used for the light aversion assay; however, during the treatment (Tx) and post-treatment (Post) exposures the dark insert was removed to create an open field. (B) Time in center in at 2.7×104 lx after icv injection of CGRP ( n = 10) or vehicle (Veh) (, n = 10) during the treatment and post-treatment exposures. There were no significant differences between times spent in the center zone. Error bars indicate mean ± SEM.

Eric A. Kaiser, et al. J Neurosci. 2012 October 31;32(44):15439-15449.
6.
Figure 7

Figure 7. From: Modulation of CGRP-induced light aversion in wildtype mice by a 5HT1B/D agonist.

Rizatriptan attenuates CGRP-induced light aversion. (A) Time spent in light zone and (B) number of transitions between zones by WT mice during four repeated exposures to light-dark box at 2.7×104 lx. After icv injection, CGRP-treated ( n = 19) mice compared with vehicle (Veh) (, n = 10) and rizatriptan (Riza) (, n = 29) spent less time in the light and transitioned between zones (CGRP vs. Veh: *p < 0.05, **p < 0.01; vs. Riza: ^p < 0.05, ^^p < 0.01) at indicated intervals. Co-administration of rizatriptan with CGRP (, n = 29) was not statistically different from CGRP in either (A) or (B). Brackets marked with symbols indicate a significant difference between treatment and either pre-treatment 2 or post-treatment (CGRP: *p < 0.05, **p < 0.01, ***p < 0.001; Riza + CGRP: #p < 0.05, ##p < 0.01, ###p < 0.001; Riza ^p < 0.05, ^^ p< 0.01). Error bars indicate mean ± SEM.

Eric A. Kaiser, et al. J Neurosci. 2012 October 31;32(44):15439-15449.
7.
Figure 6

Figure 6. From: Modulation of CGRP-induced light aversion in wildtype mice by a 5HT1B/D agonist.

CGRP decreases motility in the dark zone. (A) Amount of time resting by WT mice during four repeated exposures to light-dark box at 2.7×104 lx. After icv injection, CGRP-treated (, n = 20) mice compared with vehicle (Veh) (, n = 15) rested more (*p < 0.05, **p < 0.01, ***p < 0.001) in the dark zone at indicated intervals. In post treatment, CGRP-treated mice also rested more than vehicle treated mice in the light zone only (* p < 0.05). CGRP-treated mice also rested more compared to pre- and post-treatment (***p < 0.001) as indicated by brackets. (B) Vertical beam breaks, a measure of rearing, by WT mice during four repeated exposures to light-dark box at 2.7×104 lx. After icv injection, CGRP-treated (, n = 20) mice compared with vehicle (Veh) ( n = 15) reared less (*p < 0.05) in the dark zone at indicated intervals. CGRP-treated mice also reared less compared to pre- and post-treatment (*p < 0.05, **p < 0.01, ***p < 0.001) as indicated by brackets. (C) Ambulatory velocity of WT mice during four repeated exposures to light-dark box at 2.7×104 lx. After icv injection, CGRP-treated (, n = 20) mice compared with vehicle (Veh) ( n = 15) were similar. In post-treatment, vehicle-treated mice moved at lower velocity than CGRP-treated mice at the 20 min interval (* p < 0.05). Error bars indicate mean ± SEM.

Eric A. Kaiser, et al. J Neurosci. 2012 October 31;32(44):15439-15449.
8.
Figure 2

Figure 2. From: Modulation of CGRP-induced light aversion in wildtype mice by a 5HT1B/D agonist.

Repeated testing paradigm decreases latency to enter dark or covered zone. (A) Schematic of repeated testing paradigm in which WT mice were exposed to light-dark box four separate times: pre-treatment 1 (Pre1), pre-treatment 2 (Pre2), treatment (Tx), and post-treatment (Post). Each successive exposure occurred on the third day after previous exposure. (B) Latency to enter the dark zone at 2.7×104 lx. Latencies are shown for two cohorts of mice prior to and following icv injection of vehicle (Veh) (, n=14) or CGRP (, n= 20). (C) Latency to enter the covered zone with the lights off (~0 lx) for two cohorts of mice prior to and after injection of vehicle (, n=10) or CGRP (, n=10). In both (B) and (C), vehicle and CGRP-treated mice showed significantly reduced latencies after the first exposure (Veh: +p < 0.05, ++p < 0.01, +++p < 0.001; CGRP: **p < 0.01, ***p < 0.001). Error bars indicate mean ± SEM.

Eric A. Kaiser, et al. J Neurosci. 2012 October 31;32(44):15439-15449.

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