Aging and individual differences in rapid two-choice decisions

The effects of aging on performance were examined in signal detection, letter discrimination, brightness discrimination, and recognition memory, with each subject tested on all four tasks. Ratcliff’s (1978) diffusion model was fit to the data for each subject for each task, and it provided a good account of accuracy and the distributions of correct and error response times. The model’s analysis of the components of processing showed that aging had three main effects: The nondecision components of processing were slower and the decision criteria were more conservative for 60- to 74-year-old and 75- to 85-year-old subjects than for college students, but the quality of the evidence on which decisions were based was as good for the older subjects as for college students on some of the tasks. Individual differences among subjects in components of processing tended to be preserved across the tasks, as was shown by strong correlations across the tasks in the parameters of the model that represent the components of processing. For example, if the evidence on which a subject’s decisions were based was good in one task, it tended to be good in all four tasks.     

Two mutations preventing PDZ-protein interactions of GluR1 have opposite effects on synaptic plasticity

The regulated trafficking of GluR1 contributes significantly to synaptic plasticity, but studies addressing the function of the GluR1 C-terminal PDZ-ligand domain in this process have produced conflicting results. Here, we resolve this conflict by showing that apparently similar C-terminal mutations of the GluR1 PDZ-ligand domain result in opposite physiological phenotypes during activity- and CamKII-induced synaptic plasticity.     

Hippocampal train stimulation modulates recall of fear extinction independently of prefrontal cortex synaptic plasticity and lesions

It has been shown that long-term potentiation (LTP) develops in the connection between the mediodorsal thalamus (MD) and the medial prefrontal cortex (mPFC) and between the hippocampus (HPC) and the mPFC following fear extinction, and correlates with extinction retention. However, recent lesion studies have shown that combined lesions of the MD and mPFC do not interfere with extinction learning and retention, while inactivation of the dorsal HPC disrupts fear extinction memory. Here we found in rats that immediate post-training HPC low-frequency stimulation (LFS) suppressed extinction-related LTP in the HPC-mPFC pathway and induced difficulties in extinction recall. HPC tetanus, applied several hours later, failed to re-establish mPFC LTP but facilitated recall of extinction. Delayed post-training HPC LFS also provoked mPFC depotentiation and difficulties with extinction recall. HPC tetanus abolished these two effects. We also found that damage to the mPFC induced fear return only in rats that received HPC LFS following extinction training. HPC tetanus also reversed this behavioral effect of HPC LFS in lesioned rats. These data suggest that the HPC interacts with the mPFC during fear extinction, but can modulate fear extinction independently of this interaction.