The intriguing effects of ecstasy (MDMA) on cognitive function in mice subjected to a minimal traumatic brain injury (mTBI)

Abstract

The presence of MDMA at the time of mTBI minimizes the alteration of visual and spatial memory of the injured mice. The IGF-1R pathway was activated due to mTBI and MDMA but was not the main contributor to the cognitive improvements. MDMA administration inverted the TH decreases seen after injury. We believe this may be the major cause of the cognitive improvements seen in these mice.

Mild traumatic brain injury-induced hippocampal gene expressions: The identification of target cellular processes for drug development

“…Using the same methodologies other areas of interest of equal scientific importance could readily be evaluated. Prior studies using the same mouse weight drop model of mTBI have illustrated long-lasting cognitive deficits (Zohar et al, 2003; Milman et al, 2005; Edut et al, 2011; Baratz et al, 2011). Parallel studies have illustrated that these cognitive deficits were associated with a diffuse form of injury showing an apoptotic and neurodegenerative pathology in several brain regions associated with learning and memory (Tashlykov et al, 2007; Tweedie et al, 2007; Tashlykov et al, 2009; Rachmany et al, 2013).…”

“…A minimal number of mice were used for the study and all efforts were made to minimize suffering. mTBI was induced as has been described previously (Zohar et al, 2003; Milman et al, 2005; Edut et al, 2011; Baratz et al, 2011), mice (30 - 40 g) were fully anesthetized by exposure to Isoflurane. After full anesthesia was achieved, the animals were placed under the opening of a weight drop device and a weight (30 g) dropped from a height of 80 cm.…”

Longitudinal changes in the DTI measures, anti-GFAP expression and levels of serum inflammatory cytokines following mild traumatic brain injury

“…In vivo studies have failed to show any apparent cell death and tissue damage in mTBI that is commonly found after moderate and severe TBI (Dixon et al, 1991;Scheff et al, 1997;DeFord et al, 2002). Animal models of non-penetrative closed head mTBI have demonstrated resultant cellular dysfunction (Lyeth et al, 1990;Kanayama et al, 1996;Uryu et al, 2002), cognitive and behavioral short-and long-term deficits (Edut et al, 2011;Milman et al, 2005;Rachmany et al, 2013;Tweedie et al, 2007Tweedie et al, , 2013Zohar et al, 2003;Marklund and Hillered, 2011).…”

The nuclear factor erythroid 2-like 2 activator, tert-butylhydroquinone, improves cognitive performance in mice after mild traumatic brain injury

“…TBI induced in mice (Tashlykov et al, 2009) has shown neuronal loss in the hippocampus and associated cognitive deficits and similar results have been found in the rat (Hicks et al, 1993;Smith et al, 1994). Importantly, animal models have shown that closed head injury results in cognitive deficits (Zohar et al, 2003) when evaluated for visual memory (Biegon et al, 2004;Edut et al, 2011), spatial memory (Rubovitch et al, 2010;Baratz et al, 2011), nonspatial memory (Zohar et al, 2011), or anxiety (Edut et al, 2011). A chronic loss of memory, even slight, complicates several other cognitive functions.…”