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. 2005 Jun 1;25(22):5389–5396. doi: 10.1523/JNEUROSCI.0955-05.2005

Figure 6.

Figure 6.

Intra-VTA perfusions of CRF increased glutamate levels in cocaine-experienced rats but not in drug-naive rats (A); this effect was blocked by α-helical CRF (B) and by the sodium channel blocker TTX (C). Perfusion of CRF (10 μm) increased glutamate levels in cocaine-experienced rats, whether tested 1, 7, or 21 d after withdrawal from 14 to 18 d of cocaine self-administration (n = 7-8 per withdrawal day). This effect of CRF was not observed in rats with a history of saline self-administration (cocaine-naive groups) that were tested 1 d after their last training day (n = 7). Basal glutamate levels in the cocaine-experienced rats were 2493 ± 379, 3438 ± 921, and 2920 ± 547 nm for withdrawal days 1, 7, and 21, respectively. Basal levels in the cocaine-naive rats were 2019 ± 454 nm. *p < 0.05, significant difference from the cocaine-naive group (Fig. 5A). Coperfusions of α-helical CRF (1 μm) or TTX (0.1 μm) blocked the CRF-induced glutamate release. *p < 0.05, significant difference from the α-helical CRF plus CRF or the TTX plus CRF groups (B, C), which were tested in the 1-d-withdrawal condition.