Marta Valle León, Ph.D.

@article{pmid29053217,

title = {Behavioral control by striatal adenosine A -dopamine D receptor heteromers},

author = {J Taura and M Valle-León and K Sahlholm and M Watanabe and K Van Craenenbroeck and V Fernández-Dueñas and S Ferré and F Ciruela},

url = {https://pubmed.ncbi.nlm.nih.gov/29053217/},

doi = {10.1111/gbb.12432},

issn = {1601-183X},

year  = {2018},

date = {2018-04-01},

urldate = {2018-04-01},

journal = {Genes Brain Behav},

volume = {17},

number = {4},

pages = {e12432},

abstract = {G protein-coupled receptors (GPCR) exhibit the ability to form receptor complexes that include molecularly different GPCR (ie, GPCR heteromers), which endow them with singular functional and pharmacological characteristics. The relative expression of GPCR heteromers remains a matter of intense debate. Recent studies support that adenosine A receptors (A R) and dopamine D receptors (D R) predominantly form A R-D R heteromers in the striatum. The aim of the present study was evaluating the behavioral effects of pharmacological manipulation and genetic blockade of A R and D R within the frame of such a predominant striatal heteromeric population. First, in order to avoid possible strain-related differences, a new D R-deficient mouse with the same genetic background (CD-1) than the A R knock-out mouse was generated. Locomotor activity, pre-pulse inhibition (PPI) and drug-induced catalepsy were then evaluated in wild-type, A R and D R knock-out mice, with and without the concomitant administration of either the D R agonist sumanirole or the A R antagonist SCH442416. SCH442416-mediated locomotor effects were demonstrated to be dependent on D R signaling. Similarly, a significant dependence on A R signaling was observed for PPI and for haloperidol-induced catalepsy. The results could be explained by the existence of one main population of striatal postsynaptic A R-D R heteromers, which may constitute a relevant target for the treatment of Parkinson's disease and other neuropsychiatric disorders.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid29692729,

title = {Pridopidine Reverses Phencyclidine-Induced Memory Impairment},

author = {Kristoffer Sahlholm and Marta Valle-León and Víctor Fernández-Dueñas and Francisco Ciruela},

url = {https://pubmed.ncbi.nlm.nih.gov/29692729/},

doi = {10.3389/fphar.2018.00338},

issn = {1663-9812},

year  = {2018},

date = {2018-01-01},

urldate = {2018-01-01},

journal = {Front Pharmacol},

volume = {9},

pages = {338},

abstract = {Pridopidine is in clinical trials for Huntington's disease treatment. Originally developed as a dopamine D receptor (DR) ligand, pridopidine displays about 100-fold higher affinity for the sigma-1 receptor (sigma-1R). Interestingly, pridopidine slows disease progression and improves motor function in Huntington's disease model mice and, in preliminarily reports, Huntington's disease patients. The present study examined the anti-amnesic potential of pridopidine. Thus, memory impairment was produced in mice by administration of phencyclidine (PCP, 10 mg/kg/day) for 10 days, followed by 14 days' treatment with pridopidine (6 mg/kg/day), or saline. Finally, novel object recognition performance was assessed in the animals. Mice receiving PCP and saline exhibited deficits in novel object recognition, as expected, while pridopidine treatment counteracted PCP-induced memory impairment. The effect of pridopidine was attenuated by co-administration of the sigma receptor antagonist, NE-100 (10 mg/kg). Our results suggest that pridopidine exerts anti-amnesic and potentially neuroprotective actions. These data provide new insights into the therapeutic potential of pridopidine as a pro-cognitive drug.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}