According to Gould, (2010). different studies have shown the negative effects of drug use on working memory: Morphine has been shown to impair working memory (Friswell et al.,2008); polydrug users who preferred cocaine or heroin, continued to have cognitive impairments, including working memory, up to five months into abstinence (VerdejoGarcía, and Pérez-García, 2007); methylenedioxymethamphetamine (MDMA, ecstasy) caused working memory impairment even two and a half years after cessation of use (Thomasius et al., 2006); also in abstinence, cessation of nicotine causes deficits in working memory (Kenney and Gould, 2008); as does cessation of alcohol (Moriyama et al., 2006). Nicotine is linked to poor cognitive functioning in middle age men and women, and during abstinence, the severity of decreases in cognitive performance predicts relapse (Patterson et al., 2010; Rukstalis et al., 2005, as cited by Gould, 2010). Ecstasy increases the dopamine and serotonin levels, and stimulates norepinephrine production, and through continued use, can stunt natural production of these neurotransmitters. MDMA affects working memory and visual recall in the hippocampus. Abusers can have memory lapses and impairment without being aware of it (Futures of Palm Beach, 2016).
Verbal memory is simply memory for words. Chronic amphetamine and …show more content…
Plasticity is the reshaping of the communication pathways between neurons, and may contribute to the formation of drug stimulus associations, as well as explain their persistence. Cellular and molecular studies have pointed to the similar pathways involved with learning and memory and with drug addiction including LTP and LTD (Nestler, 2001, as cited by Volkow, 2002). Addictive drugs have been shown to modify LTP and LTD at glutamatergic synapses in the ventral tegmental area of the NAc (Jones et al., 2000; Nicola et al., 2000, as cited by Nestler,
Verbal memory is simply memory for words. Chronic amphetamine and …show more content…
Plasticity is the reshaping of the communication pathways between neurons, and may contribute to the formation of drug stimulus associations, as well as explain their persistence. Cellular and molecular studies have pointed to the similar pathways involved with learning and memory and with drug addiction including LTP and LTD (Nestler, 2001, as cited by Volkow, 2002). Addictive drugs have been shown to modify LTP and LTD at glutamatergic synapses in the ventral tegmental area of the NAc (Jones et al., 2000; Nicola et al., 2000, as cited by Nestler,