The disruptive effects of methamphetamine on delayed-matching-to-sample performance reflect proactive interference and are reduced by SCH23390

Macaskill, Anne C.; Harrow, Catherine C.; Harper, David N.

doi:10.1016/j.pbb.2014.11.009

Cited by 5 publications

(4 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…DAT is reduced in rats exposed to MA for 10 days, particularly in the striatum, orbitofrontal cortex, dorsolateral prefrontal cortex and amygdala, persisting after abstinence (Hong et al, 2015). Furthermore, animal models have demonstrated that MA exposure impairs spatial learning and memory, (Bigdeli et al, 2015), but that proactive interference (the tendency to repeat previous responses) to WM can be ameliorated with a dopamine D1 receptor antagonist (Macaskill et al, 2015). Additionally, impaired memory in mice that have been exposed to MA is associated with dysfunction in dopamine D1 receptor-extracellular signal-regulated kinase 1/2 (ERK1/2) pathway in the prefrontal cortex, striatum and hippocampus (Nagai and Yamada, 2010).…”

Section: Discussionmentioning

confidence: 99%

Psychological intervention with working memory training increases basal ganglia volume: A VBM study of inpatient treatment for methamphetamine use

Brooks

Burch

Maiorana

et al. 2016

NeuroImage: Clinical

View full text Add to dashboard Cite

BackgroundProtracted methamphetamine (MA) use is associated with decreased control over drug craving and altered brain volume in the frontostriatal network. However, the nature of volumetric changes following a course of psychological intervention for MA use is not yet known.Methods66 males (41 MA patients, 25 healthy controls, HC) between the ages of 18–50 were recruited, the MA patients from new admissions to an in-patient drug rehabilitation centre and the HC via public advertisement, both in Cape Town, South Africa. 17 MA patients received 4 weeks of treatment as usual (TAU), and 24 MA patients completed TAU plus daily 30-minute cognitive training (CT) using an N-back working memory task. Magnetic resonance imaging (MRI) at baseline and 4-week follow-up was acquired and voxel-based morphometry (VBM) was used for analysis.ResultsTAU was associated with larger bilateral striatum (caudate/putamen) volume, whereas CT was associated with more widespread increases of the bilateral basal ganglia (incorporating the amygdala and hippocampus) and reduced bilateral cerebellum volume coinciding with improvements in impulsivity scores.ConclusionsWhile psychological intervention is associated with larger volume in mesolimbic reward regions, the utilisation of additional working memory training as an adjunct to treatment may further normalize frontostriatal structure and function.

show abstract

Section: Discussionmentioning

confidence: 99%

Psychological intervention with working memory training increases basal ganglia volume: A VBM study of inpatient treatment for methamphetamine use

Brooks

Burch

Maiorana

et al. 2016

NeuroImage: Clinical

View full text Add to dashboard Cite

show abstract

“…Harper, Hunt, and Schenk (2006) found that it did so, again consistent with proactive interference as a crucial driver of impairment in DMTS performance caused by MDMA. In general, stimulant-based drugs, including d- amphetamine (Harper, McLean, & Dalrymple-Alford, 1994) and methamphetamine (Macaskill, Harrow, & Harper, 2015) have been found to produce proactive interference. The proactive interference effects of both MDMA and methamphetamine are reduced by administration of the D 1 receptor antagonist SCH23390 (Harper, 2013; Macaskill et al, 2015).…”

mentioning

confidence: 99%

“…It is useful to consider side bias separately from sensitivity to reinforcement because an increase in position bias caused by drug administration might account for some of the impairment in DMTS performance previously observed. As Macaskill et al (2015) noted, proactive interference and side-bias cannot be conclusively separated in the standard DMTS task because proactive interference can manifest as repeated responses on one alternative and thus resemble a side bias. The procedure used in the current study allowed the impact of MDMA administration on side bias to be isolated and quantified.…”

mentioning

confidence: 99%

The effect of MDMA on sensitivity to reinforcement rate.

Lie¹,

Macaskill²,

Harper³

2016

Behavioral Neuroscience

Self Cite

View full text Add to dashboard Cite

Administration of (±)3,4-methylenedioxymethamphetamine (MDMA) causes memory errors by increasing proactive interference. This might occur because MDMA alters sensitivity to reinforcement. The current 2 experiments investigated this directly by assessing the acute (Experiment 1) and chronic (Experiment 2) effects of MDMA on sensitivity to reinforcement. We presented 5 pairs of concurrent variable interval schedules within each session and calculated sensitivity to reinforcement for 3 acute doses of MDMA. In contrast to the related drug, d-amphetamine, and in spite of producing reductions in response rate, MDMA did not reduce sensitivity to reinforcement rate. Chronic administration of a fixed dose of MDMA following each session reduced response rate but did not affect sensitivity to reinforcement rate. In combination with previous research, these results indicate that related drugs may have different effects on sensitivity to reinforcement and that these effects should be considered when interpreting disruptions to operant task performance caused by drug administration. (PsycINFO Database Record

show abstract

“…In vitro assay and in vivo microdialysis demonstrate that acute MDMA administration leads to pronounced increases in extracellular DA in the prefrontal cortex (PFC), striatum, nucleus accumbens (Nacc) and hippocampus (HPS) (Baumann et al, 2008;Crespi, Mennini, & Gobbi, 1997;Gough, Ali, Slikker, & Holson, 1991;Johnson et al, 1986;Shankaran & Gudelsky, 1998) and it has been suggested that the repeated use of MDMA may lead to a sensitised DA response that contributes to the transition from use to abuse (Schenk, 2011). The idea that DA may play a role in MDMA-induced memory deficits (Harper, 2013;Rozas et al, 2012) is in line with research suggesting that potent DA exerting drugs, such as methamphetamine (METH) and cocaine, also appear to impair memory via DA mechanisms (Macaskill, Harrow, & Harper, 2015;Shoblock, Maisonneuve, & Glick, 2003;Tomasi et al, 2007), and corroborates the large body of literature demonstrating that intact DA mechanisms, involving activation of D1-like receptors in mesocorticolimbic pathways, are required for normal memory function (Goldman-Rakic & Williams, 1995;Nai et al, 2010;Valentim Jr, Gontijo, Peres, Rodriques, & Nakamura-Palacios, 2009;Vijayraghavan, Wang, Birnbaum, Williams, & Arnsten, 2007).…”

mentioning

confidence: 89%

Behavioural and Neurochemical Effects of Acute (±) 3,4 methylenedioxymethamphetamine (MDMA) in the Dopamine D1 Receptor Mutant Rat

Squire¹

View full text Add to dashboard Cite

<p>Rationale: (±) 3,4-methylenedioxymethamphetamine (MDMA; ‘ecstasy’) is a recreationally abused psychostimulant that leads to detrimental effects on memory performance. MDMA’s acute effects on memory are often attributed to a working memory impairment resulting from compromised serotonin systems. However, recent evidence from non-human animal experimental studies suggests that acute MDMA may impair memory performance through an MDMA-induced increase in dopamine (DA) release, leading to overstimulation of DA D1 receptors. The overstimulation of D1 receptors during acute MDMA exposure is thought to indirectly impair memory by increasing a subject’s susceptibility to proactive interference, leading to a perseverative pattern of responding during memory tasks. Objective: This project investigates the hypothesis that acute MDMA impairs memory performance via overstimulation of D1 receptors. The acute actions of MDMA will be assessed using DA D1 mutant (DAD1-/-) rats which possess a selective down-regulation in functional DA D1 receptors. On the basis that acute MDMA impairs memory function via overstimulation of D1 receptors it is predicted that, compared to control rats, DAD1-/- rats will be protected from the acute memory deficits caused by MDMA. Due to the novelty of the DAD1-/- rat model, prior to the assessment of the acute effects of MDMA on memory performance in these rats, behavioural and neurochemical characterisations will be conducted. Methods: Firstly, a behavioural characterisation was conducted to explore the tendencies of DAD1-/- rats, compared to controls, in a drug free state. Behaviours relevant for motivation and reward, movement, and memory were the focus of the behavioural investigation due to evidence suggesting a role for D1-like receptors in these functions. Secondly, a neurochemical assessment of DAD1-/- and controls rats in response to MDMA (3 mg/kg) was assayed using c-fos expression, a marker for neuronal activity, in several brain regions with known DA innervation. Thirdly, to assess the acute effects of MDMA on memory performance, DAD1-/- and control rats were trained on a spatial working memory T-maze task, delayed non-matching to position (DNMTP), over 25 sessions. Once trained, rats were administered either MDMA (1.5, 2.25 and 3 mg/kg) or saline fifteen minutes prior to testing on DNMTP, with all subjects experiencing all drug doses three time each. In addition, to further investigate the hypothesis that overstimulation of D1 receptors impairs memory performance, the effects of a D1 receptor agonist, SKF 81297 (0.5, 1, 1.5, 3, 4.5 mg/kg) on DNMTP performance were also assessed. Results: The behavioural characterisation revealed that DAD1-/- rats are capable of performing many behaviours relevant for reward processing, movement and memory function. However, DAD1-/- rats were impaired with regard to some reward-related behaviours, such as the acquitision of lever pressing for sugar pellets. The assessment of c-fos expression demonstrated that DAD1-/- rats express less c-fos in the medial prefrontal cortex, striatum and nucleus accumbens compared to control rats following MDMA administration. Lastly, the effects of acute MDMA administration on memory performance were tested. During the third block of MDMA administration, control rats demonstrated decreased accuracy on the DMNTP task at both the 2.25 and 3 mg/kg doses. The decrease in accuracy during MDMA exposure in control rats was driven by an increase in perseverative errors. On the contrary, DAD1-/- rats were not impaired on the DNMTP task following acute MDMA at any of the doses tested. Administration of SKF 81297 did not lead to any systematic changes in performance, but at the 3 mg/kg dose DAD1-/- rats displayed increased accuracy compared to control rats. Conclusions: DAD1-/- rats were protected from an MDMA-induced decrease in accuracy on the DNMTP task compared to control rats. This finding challenges the assumption that MDMA’s acute effects on memory performance are wholly due to serononergic mechanisms. Specifically, the current study provides evidence for the hypothesis that acute MDMA exposure impairs memory performance in rats.</p>

show abstract

The disruptive effects of methamphetamine on delayed-matching-to-sample performance reflect proactive interference and are reduced by SCH23390

Cited by 5 publications

References 34 publications

Psychological intervention with working memory training increases basal ganglia volume: A VBM study of inpatient treatment for methamphetamine use

Psychological intervention with working memory training increases basal ganglia volume: A VBM study of inpatient treatment for methamphetamine use

The effect of MDMA on sensitivity to reinforcement rate.

Behavioural and Neurochemical Effects of Acute (±) 3,4 methylenedioxymethamphetamine (MDMA) in the Dopamine D1 Receptor Mutant Rat

Contact Info

Product

Resources

About