DRD1

(redirected from DRD1A)

DRD1

A gene on chromosome 5q35.1 that encodes G protein-coupled dopamine receptor D1, which is the most abundant dopamine receptor in the CNS. D1 dopamine receptors stimulate adenylyl cyclase and activate cyclic AMP-dependent protein kinases; they regulate neuronal growth and development, mediate some behavioural responses, and modulate dopamine receptor D2-mediated events.
References in periodicals archive ?
Espadas et al., "Associative learning and CA3-CA1 synaptic plasticity are impaired in [D.sub.1]R null, [Drd1a.sup.-/-] mice and in hippocampal siRNA silenced Drd1a mice," The Journal of Neuroscience: The Official Journal of the Society for Neuroscience, vol.
In the prestroke period, genetic and epigenetic factors (such as genotype for DRD1a and DRD2; Sieber et al., 2014); demographic factors (such as younger age or female gender; Alajbegovic et al., 2014; El Husseini et al., 2012); prior medical history of depression, stroke, or vascular disease (Allan et al., 2013; Andersen et al., 1995); and the relative strength of a patient's social support network (Ayerbe et al., 2011) interact.
The Drd1a gene was also significant: P = .038, [[eta].sup.2] = .181.
Drd1a genes were significantly downregulated in the PTSD-midazolam group compared to the nonstressedmidazolam + L-theanine group concurrent with the results of another study exploring the effects of stress on the mouse prefrontal cortex transcriptome, demonstrating a deregulation of the Drd1a gene in chronic mild stress exposed subjects [36].
Amygdalar genes that were changed across treatment groups also were related to psychological conditions such as depression (Drd2), stress enhanced fear learning (Gabra4), chronic mild stress (Drd1a), and anxiety, mood disorders, and psychoses (Htr3a).
Espadas et al., "Associative learning and CA3-CA1 synaptic plasticity are impaired in D 1R null, Drd1a-/- mice and in hippocampal siRNA silenced Drd1a mice," Journal of Neuroscience, vol.
The molecular markers foriDG include increased expression of dopamine receptor D1A (Drd1a) and decreased expression of tryptophan 2, 3-dioxygenase (Tdo2) and desmoplakin (Dsp) in the DG of mutant mice[1].
Molecular markers for the iDG phenotype were demonstrated in mice with pilocarpine-induced seizures, including dysregulated gene/protein expression of calretinin/calbindin, as well as hallmark alterations in other iDG markers such as Drd1a, Tdo2, and Dsp.