Older news items (pre-2010) brought over from the old website
Amphetamine use in adolescence may impair adult working memory
Rats exposed to high doses of amphetamines at an age that corresponds to the later years of human adolescence showed significant declines in working memory as adults, long after the exposure. The researchers tested two types of amphetamine exposure: intermittent (a steady dose every other day) and "binge-escalation," in which increasing amounts of the drug were given over a period of four days, followed by a simulated binge – a high dose every two hours for eight hours on the fifth day. The type of exposure did not make a significant difference.
Stanis, J.J. et al. 2009. Amphetamine-induced deficits in a working memory task are more significant in drug-exposed adolescent rats than drug-exposed adults. Presented October 21 at the annual meeting of the Society for Neuroscience in Chicago.
http://www.eurekalert.org/pub_releases/2009-10/uoia-aui101909.php
Amphetamines and cocaine can damage the brain’s ability to learn from new experiences
A rat study suggests that amphetamines and cocaine can damage the brain’s ability to learn from new experiences. Rats were given either amphetamine, cocaine, or saline for 20 days, and then half were moved to new cages containing multiple levels with ramps, bridges, and a climbing chain; tunnels; and toys that were rearranged once a week to encourage continued exploration of the environment. After three and a half months, the rats who received saline solutions and had lived in a stimulating environment had a greater number of neuronal connections than those who remained in their usual environment. Rats given either amphetamines or cocaine, however, did not respond to the complex environment with a similar growth in neuronal connection.
[2385] Kolb, B., Gorny G., Li Y., Samaha A-N., & Robinson T. E.
(2003). Amphetamine or cocaine limits the ability of later experience to promote structural plasticity in the neocortex and nucleus accumbens.
Proceedings of the National Academy of Sciences. 100(18), 10523 - 10528.
http://www.eurekalert.org/pub_releases/2003-08/niod-aoc082503.php
Amphetamine helps or hinders cognitive function depending on your genes
Everyone inherits two copies of the catecho-O-methyltransferase (COMT) gene, that codes for the enzyme that metabolizes neurotransmitters like dopamine and norepinephrine. It comes in two common versions. One version, met, contains the amino acid methionine at a point in its chemical sequence where the other version, val, contains a valine. Depending on the mix of variants inherited, a person's COMT genes can be typed met/met, val/val, or val/met. People with the val/val variant appear to have reduced prefrontal dopamine activity and less efficient prefrontal information processing, along with slightly increased risk for schizophrenia. People with val/met have more efficient prefrontal function, and people with met/met the most efficient.
In a recent imaging study, 27 volunteers (10 val/val, 11 val/met, and 6 met/met) performed a variety of cognitive tasks that involved working memory and executive functioning, after taking either amphetamine or a placebo. Since amphetamine boosts dopamine activity in the prefrontal cortex, the researchers predicted that the drug would enable val/val types to boost their low level of dopamine and perform better on cognitive tasks that depend on the prefrontal cortex. On the other hand, those with met/met should be hindered by amphetamine. The study confirmed these predictions - val/val subjects on amphetamine performed comparably to met/met types in normal conditions, while met/met subjects on amphetamine performed worse than subjects with val/val types in normal conditions.
Amphetamines and other drugs that affect prefrontal dopamine systems are used to treat Attention Deficit Hyperactivity Disorder (ADHD), and other psychiatric illnesses, and some people respond better than others to these medications. About 15-20% of individuals in populations of European ancestry have the met/met COMT gene type.
[1292] Mattay, V. S., Goldberg T. E., Fera F., Hariri A. R., Tessitore A., Egan M. F., et al.
(2003). Catechol O-methyltransferase val158-met genotype and individual variation in the brain response to amphetamine.
Proceedings of the National Academy of Sciences of the United States of America. 100(10), 6186 - 6191.
http://www.eurekalert.org/pub_releases/2003-05/niom-gep050703.php
Long-lasting changes in attention and motor skills after heavy stimulant abuse
A study of 50 pairs of twins, in which one of each pair had a history of cocaine or methamphetamine abuse, and the other had no history of drug abuse, found that the twin with a history of stimulant abuse performed significantly worse on several tests of attention and motor skills than did the one who had never used drugs, even after at least a year had passed since any drugs had been taken. Abusers did, however, outperform their twin on visual vigilance, a test measuring the ability to pay attention over time.
[1163] Toomey, R., Lyons M. J., Eisen S. A., Xian H., Chantarujikapong S., Seidman L. J., et al.
(2003). A Twin Study of the Neuropsychological Consequences of Stimulant Abuse.
Arch Gen Psychiatry. 60(3), 303 - 310.
http://www.eurekalert.org/pub_releases/2003-04/niod-sot040903.php
Methamphetamine abuse may permanently impair cognitive function
Methamphetamine abuse damages the nerve endings of human brain cells containing the chemical messenger dopamine. A recent study has found that methamphetamine-damaged brain cells may recover after prolonged abstinence from the drug. However, the extent of recovery may not be sufficient to restore full cognitive function, particularly in those who are did long-time, heavy users of the drug.
[1223] Ding, Y-S., Logan J., Volkow N. D., Chang L., Wang G-J., Fowler J. S., et al.
(2001). Loss of Dopamine Transporters in Methamphetamine Abusers Recovers with Protracted Abstinence.
J. Neurosci.. 21(23), 9414 - 9418.
http://www.eurekalert.org/pub_releases/2001-12/niod-ise112801.php
http://www.eurekalert.org/pub_releases/2001-12/bnl-bsa112901.php
Prenatal exposure
One hit of crystal meth can cause birth defects
A mouse study has found that a single prenatal dose of methamphetamine (speed) can cause long-term neurodevelopmental problems in babies, especially reduced motor coordination.
[1003] Jeng, W., Wong A. W., Ting-A-Kee R., & Wells P. G.
(2005). Methamphetamine-enhanced embryonic oxidative DNA damage and neurodevelopmental deficits.
Free Radical Biology & Medicine. 39(3), 317 - 326.
http://www.eurekalert.org/pub_releases/2005-07/uot-oho072605.php
Cognitive development affected in babies exposed prenatally to cocaine
In the first study to use measures of both the mothers’ self report of their prenatal drug use, and infant meconium, which provided a physical measure of the amount of drug exposure, 415 cocaine-exposed infants born in Cleveland were compared to non-exposed infants on cognitive and motor development until age 2. Infants were tested at 6.5, 12 and 24 months. Mental retardation in the cocaine-exposed children at age 2 was 4.89 times higher than would be expected in the general population. The percentage of children with mild delays requiring intervention was almost double the rate of the high risk, non-cocaine group. The study also found that tobacco exposure had significant negative effects on infant development.
[390] Singer, L. T., Arendt R., Minnes S., Farkas K., Salvator A., Kirchner L. H., et al.
(2002). Cognitive and Motor Outcomes of Cocaine-Exposed Infants.
JAMA. 287(15), 1952 - 1960.
http://www.eurekalert.org/pub_releases/2002-04/cwru-a2y041602.php
Cocaine may permanently damage learning abilities in developing fetuses
Two recent studies investigating the effect of pre-natal exposure to cocaine in rats suggest that children exposed to cocaine while in the womb may have permanent changes to the part of the brain that helps control attention and memory, leading to learning deficits and symptoms that are very much like attention deficit hyperactivity disorder.
[1270] Morrow, B. A., Elsworth J. D., & Roth R. H.
(2002). Male rats exposed to cocaine in utero demonstrate elevated expression of Fos in the prefrontal cortex in response to environment.
Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology. 26(3), 275 - 285.
[264] Morrow, B. A., Elsworth J. D., & Roth R. H.
(2002). Prenatal cocaine exposure disrupts non-spatial, short-term memory in adolescent and adult male rats.
Behavioural Brain Research. 129(1-2), 217 - 223.
http://www.eurekalert.org/pub_releases/2002-02/yu-ucd021802.php