Archival ReportVaried Access to Intravenous Methamphetamine Self-Administration Differentially Alters Adult Hippocampal Neurogenesis
Section snippets
Animals, Bromodeoxyuridine Injections, and Tissue Preparation
Adult male Wistar rats (Charles River, Wilmington, Massachusetts), weighing 250–300 g at the start of the experiment, were housed two/cage in a temperature-controlled vivarium under a reversed light/dark cycle (lights off 10:00 am–10:00 pm). Food and water were available ad libitum, except during the food training period. Rats were subjected to methamphetamine self-administration (6 hours long access [LgA group; n = 6], 1 hour short access [ShA group; n = 9], or 1 hour intermittent short access
Methamphetamine Self-Administration Alters Proliferation, Maturation, and Survival of Hippocampal Progenitor
Intermittent and daily access models of intravenous methamphetamine self-administration were used to investigate methamphetamine-induced alterations in adult hippocampal neurogenesis (Figure 1). Total methamphetamine intake was significantly different in each access group [intake over 49 days: I-ShA, 7.8 ± .01 mg/kg; ShA, 20.6 ± .03 mg/kg; LgA, 128.7 ± .44 mg/kg; F(2,20) = 84960, p < .0001], and methamphetamine self-administration during the first hour was considerably higher in LgA versus ShA
Discussion
The self-administration data from the I-ShA, ShA, and LgA rats provide evidence that distinct patterns of methamphetamine intake might be related to human patterns of methamphetamine abuse: recreational, chronic, and dependent. Given that experimenter-administered methamphetamine in rodents decreases hippocampal-dependent memory (42), that methamphetamine-dependent individuals show hippocampal dysfunction (2), and that hippocampal behavior is partly maintained by the generation of new
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2022, Neurocircuitry of AddictionHippocampal neurogenesis interferes with extinction and reinstatement of methamphetamine-associated reward memory in mice
2021, NeuropharmacologyCitation Excerpt :In turn, promotion of HN could weaken the above-mentioned drugs-associated reward memory by facilitating drug extinction and inhibiting drug reinstatement (Castilla-Ortega et al., 2016b; Kibaly et al., 2019). However, as for METH addiction, Mandyam et al. observed that intermittent access to METH significantly promoted HN in the HIP (Mandyam et al., 2008), whereas other research groups observed opposite effect (Bento et al., 2011; Dong et al., 2018; Kochman et al., 2009; Venkatesan et al., 2011). More importantly, the outcome of promotion and/or inhibition of HN on METH-associated reward memory has not been investigated yet.
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