Impaired decision making on the Balloon Analogue Risk Task as a result of long-term alcohol use.

The Balloon Analogue Risk Task (BART) is an experimental measure of risk taking that has commonly been employed to measure the risk taking behavior of nonclinical populations. Previous research has indicated that the task measures a unique aspect of behavioral disinhibition, but there has not as yet been focus upon the possible impact of other aspects of cognitive processing on performance. The current study investigated the cognitive factors related to performance of the BART in an alcohol-using sample. Seventeen individuals with long-term alcohol use were matched for age and education to a group of 17 nonusing participants. The results indicated that the alcohol-using group pumped the balloons on the BART to a lesser extent than did the nonusing group across all trials on the task. The results indicate that the alcohol-using group made less "optimal" decisions on the BART most notably due to neuropsychological impairment in the domains of immediate memory and executive functioning.

Piracetam, an AMPAkine drug, facilitates memory consolidation in the day-old chick.

Piracetam is an AMPAkine drug that may have a range of different mechanisms at the cellular level, and which has been shown to facilitate memory, amongst its other effects. This series of experiments demonstrated that a 10mg/kg dose of piracetam facilitated memory consolidation in the day-old chick when injected from immediately until 120min after weak training (i.e. using a 20% v/v concentration of methyl anthranilate) with the passive avoidance learning task. Administration of piracetam immediately after training led to memory facilitation which lasted for up to 24h following training. This dose of the AMPAkine was not shown to facilitate memory reconsolidation. These findings support the contention that application of the AMPAkine piracetam facilitates memory using a weak training task, and extend the range of actions previously noted with NMDA-related agents to those which also facilitate the AMPA receptor.

Brain-derived neurotrophic factor facilitates memory consolidation and reconsolidation of a weak training stimulus in the day-old chick.

Recent research has pointed to a role for brain-derived neurotrophic factor (BDNF) in long-term potentiation and memory. The present series of experiments examined the effects of the application of exogenous BDNF on memory consolidation and reconsolidation of a weak training stimulus with the day-old chick, using the passive avoidance learning paradigm. Chicks injected intracranially with 12.5 µg/mL recombinant BDNF immediately after a single-trial training event displayed enhanced retention relative to saline up to 24h post-training. Furthermore, this dose was also shown to enhance retention when administered following initial weak training. Thus, exogenous BDNF was shown to enhance both consolidation and reconsolidation of memory when administered acutely to the day-old chick.

Memantine facilitates memory consolidation and reconsolidation in the day-old chick.

Memantine is a non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist that has been approved for the treatment of the cognitive deficits noted in Alzheimer's disease. While there is a body of research that supports memantine's facilitative action upon memory compromise, this series of studies aimed to investigate the effects of this drug in healthy animals with intact memory functioning. A 0.1 mM dose of memantine injected immediately after a weakly aversive training event (i.e. 20% v/v methyl anthranilate) was found to enhance passive avoidance learning for this event in day-old chicks up to 24 h following training. The same dose of memantine was also observed to enhance memory for the training event when it was administered in conjunction with a reminder trial. These results suggest that memantine is capable of facilitating both memory consolidation as well as memory reconsolidation. It was concluded that memantine's mechanism may involve the short-term or intermediate memory phases of the Gibbs and Ng model of memory, and that the current findings represent enhancement of intact memory, rather than amelioration of memory compromise.