sfn2001

Gadd CA, Murtra P, Hall CN, Gana M, Webber MJ, De Felipe C, Hunt SP (2001) NK1-expressing neurons critical for morphine reward behaviors in mice: C-fos expression and ablation of NK1-expressing neurons. Neuroscience 2001 Abstracts 224.13. Society for Neuroscience, San Diego, CA.

Summary: We have previously shown using conditioned place preference (CPP) that mice lacking the preferred receptor for substance P (NK1) show an absence of the rewarding response to morphine as well as reduced conditioned place aversion and physical withdrawal signs following chronic opiate treatment (Nature 405, 180-183). To locate those regions of the brain in which NK1-expressing neurons are crucial for opiate-mediated reward behavior, we examined the expression of c-Fos following acute (10 mg/kg IP) and chronic (increasing doses from 10 to 100 mg/kg IP) morphine administration, and following CPP to morphine (7.5 mg/kg) in wild-type and NK1 knockout mice. The expression of c-Fos in the brains of mice treated with chronic or acute morphine treatment was similar in both genotypes. Moreover, NK1-expressing neurons in the striatum and nucleus accumbens (NAc) were never seen to co-express c-Fos immunoreactivity. In contrast, the expression of c-Fos following the CPP protocol was significantly different between genotypes with a reduced number of c-Fos positive neurons in NK1 knockout mice in the amygdala and hippocampus but not in the NAc or dorsomedial striatum (DMS). We next investigated the effects of selective ablation of NK1 expressing neurons by injecting substance P-saporin into these regions. Our results suggest that destruction of these cells in the amygdala but not in the NAc or DMS causes a reduction in CPP to morphine without affecting anxiety levels or locomotor activity.

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Camara AL, Pereira EF, Alkondon M, Randall WR, Castro NG, Cintra WM, Albuquerque EX (2001) Septal innervation of the hippocampus regulates expression α7 nicotinic receptors in CA1 and CA3 pyramidal neurons. Neuroscience 2001 Abstracts 145.1. Society for Neuroscience, San Diego, CA.

Summary: To investigate the effects of septal innervation on expression of α7 nicotinic receptors (nAChRs) in CA1 and CA3 pyramidal neurons in the hippocampus, the patch-clamp technique and confocal microscopy were applied to organotypic hippocampal cultures and septal-hippocampal co-cultures. In the co-cultures, septal fibers labeled with DiI were visualized in the hippocampus. Field stimulation of septal fibers also resulted in postsynaptic currents that could be recorded from CA1 and CA3 pyramidal neurons in the hippocampus. These currents had glutamatergic, GABAergic and cholinergic components. The latter originated most likely from the septal cholinergic neurons that were labeled in situ with the cholinergic marker Cy3-192 IgG. α7 nAChRs in the somatodendritic region of CA1 and CA3 pyramidal neurons in the hippocampus in cultures and co-cultures were activated by the α7 nAChR agonist choline, which elicited type IA currents, and were visualized by labeling with rhodamine-conjugated α-bungarotoxin (Rho-α-BGT). After 21 days in vitro, the amplitude of type IA currents was substantially smaller in pyramidal neurons in septal-hippocampal co-cultures than in hippocampal oragnotypic cultures. Labeling of the somatodendritic region of hippocampal pyramidal neurons with Rho-α-BGT was also less intense in the organotypic co-cultures than in cultures. These results suggest that functional septal innervation of the hippocampus regulates the expression of α7 nAChRs in hippocampal pyramidal neurons.

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