Next, the researchers gave the flies a single dose of cocaine then monitored the activity of tyrosine decarboxylase (TDC), an enzyme that normally shows a spike in activity
after cocaine exposure.
Not exact matches
A prospective cohort study found the SIDS rate to be significantly increased for infants exposed in utero to methadone (OR: 3.6 [95 % CI: 2.5 — 5.1]-RRB-, heroin (OR: 2.3 [95 % CI: 1.3 — 4.0]-RRB-, methadone and heroin (OR: 3.2 [95 % CI: 1.2 — 8.6]-RRB-, and
cocaine (OR: 1.6 [95 % CI: 1.2 — 2.2]-RRB-, even
after controlling for race / ethnicity, maternal age, parity, birth weight, year of birth, and maternal smoking.229 In addition, a meta - analysis of studies that investigated an association between in utero
cocaine exposure and SIDS found an increased risk of SIDS to be associated with prenatal
exposure to
cocaine and illicit drugs in general.230
In these images of rat brains, differences in gene expression of genes for fibroblast growth factor 2 (FGF2, top set) and dopamine 2 receptor (D2, bottom sett) can be seen in rats of two breeds before (left) and
after (right)
cocaine exposure.
«These experiments with cell type - specific pharmacology provide direct evidence for the necessity of NMDA - Rs in dopamine neurons for the synaptic plasticity observed 3 - 5 hours
after exposure to
cocaine in vitro, leaving open the molecular explanation for the potentiation AMPA - Rs that occurs
after many days of NMDA - R inactivity in dopamine neurons in vivo.
There was some evidence for an effect of
exposure status (i.e., maternal
cocaine or opiate use during pregnancy) on parenting stress, although this effect was not significant
after controlling for maternal psychopathology (BSI scores).