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1.  Amphetamine locomotor sensitization and conditioned place preference in adolescent male and female rats neonatally treated with quinpirole 
Behavioural Pharmacology  2011;22(4):374-378.
Neonatal quinpirole treatment has been shown to produce an increase of dopamine D2 - like receptor sensitivity that persists throughout the animal's lifetime. The objective was to analyze the effects of neonatal quinpirole treatment on effects of amphetamine in adolescent rats using locomotor sensitization and conditioned place preference (CPP) procedures. Sprague-Dawley rats were treated with quinpirole (1mg/kg) or saline from postnatal days (P)1-11 and raised to adolescence. For locomotor sensitization, animals were given amphetamine (1mg/kg) or saline every second day from P35-47 and placed into a locomotor arena. In females, neonatal quinpirole treatment enhanced amphetamine locomotor sensitization compared to quinpirole-free controls sensitized to amphetamine. Males demonstrated sensitization to amphetamine, but this was muted compared to females and unaffected by neonatal quinpirole. For CPP, animals were conditioned for eight consecutive days (P32-39) with amphetamine (1mg/kg) or saline and a drug-free preference test was performed at P40. Neonatal quinpirole enhanced time spent in the amphetamine-paired context compared to quinpirole-free controls conditioned with amphetamine, but only female controls conditioned with amphetamine spent more time in the drug-paired context compared to saline-treated controls. Increased D2 -like receptor sensitivity appears to have enhanced the behavioral effects of amphetamine, but these effects were more prevalent in adolescent females compared to males.
doi:10.1097/FBP.0b013e328348737b
PMCID: PMC3327891  PMID: 21753255
Neonatal; quinpirole; Dopamine D2-like receptors; locomotor sensitization; conditioned place preference; adolescence; rat
2.  Accelerated turnover of taste bud cells in mice deficient for the cyclin-dependent kinase inhibitor p27Kip1 
BMC Neuroscience  2011;12:34.
Background
Mammalian taste buds contain several specialized cell types that coordinately respond to tastants and communicate with sensory nerves. While it has long been appreciated that these cells undergo continual turnover, little is known concerning how adequate numbers of cells are generated and maintained. The cyclin-dependent kinase inhibitor p27Kip1 has been shown to influence cell number in several developing tissues, by coordinating cell cycle exit during cell differentiation. Here, we investigated its involvement in the control of taste cell replacement by examining adult mice with targeted ablation of the p27Kip1 gene.
Results
Histological and morphometric analyses of fungiform and circumvallate taste buds reveal no structural differences between wild-type and p27Kip1-null mice. However, when examined in functional assays, mutants show substantial proliferative changes. In BrdU incorporation experiments, more S-phase-labeled precursors appear within circumvallate taste buds at 1 day post-injection, the earliest time point examined. After 1 week, twice as many labeled intragemmal cells are present, but numbers return to wild-type levels by 2 weeks. Mutant taste buds also contain more TUNEL-labeled cells and 50% more apoptotic bodies than wild-type controls. In normal mice, p27 Kip1 is evident in a subset of receptor and presynaptic taste cells beginning about 3 days post-injection, correlating with the onset of taste cell maturation. Loss of gene function, however, does not alter the proportions of distinct immunohistochemically-identified cell types.
Conclusions
p27Kip1 participates in taste cell replacement by regulating the number of precursor cells available for entry into taste buds. This is consistent with a role for the protein in timing cell cycle withdrawal in progenitor cells. The equivalence of mutant and wild-type taste buds with regard to cell number, cell types and general structure contrasts with the hyperplasia and tissue disruption seen in certain developing p27Kip1-null sensory organs, and may reflect a compensatory capability inherent in the regenerative taste system.
doi:10.1186/1471-2202-12-34
PMCID: PMC3110126  PMID: 21507264

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