Enhancement of basal and pentylenetetrazol (PTZ)-stimulated dopamine release in the brain of freely moving rats by PTZ-induced kindling
✍ Scribed by Laura Dazzi; Mariangela Serra; Maria Luisa Porceddu; Angela Sanna; M. Francesca Chessa; Giovanni Biggio
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 135 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0887-4476
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✦ Synopsis
The effects of pentylenetetrazol (PTZ)-induced kindling on the activity of mesocortical, mesoaccumbens, and nigrostriatal dopaminergic neurons was investigated with the transversal microdialysis technique in freely moving rats. Four days after the last chronic administration of PTZ, the basal extracellular concentrations of dopamine in the prefrontal cortex, nucleus accumbens, and striatum of kindled rats were significantly increased (176, 136, 149%, respectively) relative to those of animals chronically treated with saline. Moreover, dopamine output was markedly more sensitive to the effect of a challenge injection of PTZ (20 mg/kg ip) in the prefrontal cortex (193 vs. 150%, relative to basal values), the nucleus accumbens (136 vs. 14%), and the striatum (150 vs. 135%) of kindled rats relative to that in the control animals.
Because kindled rats and their controls are habituated to handling, the neurochemical mechanisms that underlie the effects of chemical kindling on the sensitivity of dopaminergic neurons to PTZ were investigated by comparing the effects of an acute administration of PTZ (20 mg/kg ip) between naive and handling-habituated animals. The sensitivity of dopamine output to PTZ in naive rats was markedly greater than that in handling-habituated animals for the prefrontal cortex (183 vs. 150%) and nucleus accumbens (135 vs. 14%), but not for the striatum (135 vs. 132%). These results indicate that PTZ kindling enhances the basal activity and the sensitivity to PTZ of dopamine neurons in rat brain and suggest that mesocortical, mesoaccumbens, and nigrostriatal dopaminergic neurons contribute to the central alterations associated with experimental epilepsy.