Adenosine receptor antagonists potentiate dopamine receptor agonist-induced rotational behavior in 6-hydroxydopamine-lesioned rats.

Adenosine receptor antagonists, DMPX, PACPX and theophylline, produce contralateral rotations in unilateral 6-hydroxydopamine-lesioned rats. DMPX and theophylline markedly increase rotations produced by bromocriptine (a dopamine D2 receptor agonist) and/or SKF38393A (a dopamine D1 receptor agonist). All of these effects are inhibited by CGS21680C (an adenosine A2 receptor agonist).

Implantation of genetically modified mesencephalic fetal cells into the rat striatum.

Transplantation of dopamine (DA) cells into the rat model of hemiparkinsonism induced by intranigral 6-hydroxydopamine (6-OHDA) injections has so far focused mainly on DA replacement via a pump-like mechanism. In the present study, we employed a model of hemiparkinsonism that uses an intrastriatal approach to lesioning the nigrostriatal DA pathway to assess the possibility of using cell transplantation to cause regeneration of that system. Toward that end, we transplanted two types of cells on the side of the 6-OHDA-induced lesions: 1) nonmodified fetal mesencephalic cells and 2) fetal mesencephalic cells that have been infected with a retrovirus vector containing a PKC beta 1 cDNA.

Absence of tolerance to the excitatory effects of benzodiazepines: clonazepam-evoked shaking behavior in the rat.

Select benzodiazepine (BDZ) agonists, such as clonazepam, evoke wet-dog shakes (WDS) in the rat, a behavior which may be influenced by serotonergic drugs. To further study the role of serotonin (5-HT) and BDZ receptors in BDZ-induced WDS, we injected adult rats daily for 21 days with clonazepam and measured WDS and 5-HT1, 5-HT2, and BDZ receptors. Clonazepam 5 mg/kg upregulated 5-HT1 and 5-HT2 receptors in frontal cortex, but not in brainstem or spinal cord, compared to vehicle controls, without a change in BDZ receptors.

Sham transplantation protects against 6-hydroxydopamine-induced dopaminergic toxicity in rats: behavioral and morphological evidence.

Administration of the neurotoxin 6-hydroxydopamine (6-OHDA) to rat brain causes biochemical and neuroanatomical changes to the nigrostriatal dopaminergic pathway similar to those observed in Parkinson's disease (PD). Although the cause of PD is unknown, it has been hypothesized that the neurodegenerative changes seen in PD might result from exposure to a neurotoxin. Therefore, strategies for limiting neurotoxin-induced dopaminergic damages, like those caused by 6-OHDA, may be of both clinical and basic interest.

The functional significance of neonatal 5,7-dihydroxytryptamine lesions in the rat: response to selective 5-HT1A and 5-HT2,1C agonists.

To study the involvement of serotonin (5-HT) receptor subtypes in behavioral supersensitivity following neonatal 5,7-dihydroxytryptamine (5,7-DHT) lesions, we measured acute behavioral responses to a single dose of selective 5-HT1A (8-OH-DPAT) or 5-HT2,1C (DOI) agonist compared to 5-hydroxytryptophan (5-HTP) in rats injected with 5,7-DHT intraperitoneally or intracisternally 14 weeks earlier. Only intraperitoneal 5,7-DHT injection resulted in brainstem 5-HT hyperinnervation, but cortical 5-HT depletions were also less. Effects of DOI, such as shaking behavior and forepaw myoclonus, were enhanced by 5,7-DHT lesions made intracisternally not intraperitoneally, whereas 8-OH-DPAT-evoked behaviors, such as forepaw myoclonus and head weaving, were enhanced more by the intraperitoneal route.