A review paper on memory fault models and test algorithms

Testing embedded memories in a chip can be very challenging due to their high-density nature and manufactured using very deep submicron (VDSM) technologies. In this review paper, functional fault models which may exist in the memory are described, in terms of their definition and detection requirement. Several memory testing algorithms that are used in memory built-in self-test (BIST) are discussed, in terms of test operation sequences, fault detection ability, and also test complexity. From the studies, it shows that tests with 22 N of complexity such as March SS and March AB are needed to detect all static unlinked or simple faults within the memory cells. The N in the algorithm complexity refers to Nx*Ny*Nz whereby Nx represents the number of rows, Ny represents the number of columns and Nz represents the number of banks. This paper also looks into optimization and further improvement that can be achieved on existing March test algorithms to increase the fault coverage or to reduce the test complexity.

Transparent memory testing based on dual address sequences

An effectiveness of the application of classical non-destructive tests for testing storage devices and their main disadvantages, among which there are great time complexity and low diagnostic ability, are analysed. The concept of double address sequence 2A is defined and the examples of their formation based on counter address sequences and Gray code are provided. The basic element of non-destructive tests with the use of double address sequences is synthesized and its detecting and diagnostic abilities for different storage devices defects are explored. There are two new non-destructive tests of memory devices March_2A_1 and March_2A_2 and an estimation of their time complexity and efficiency of failure detection are given. A significantly lower time complexity of the proposed tests and their high diagnostic ability in comparison with classical non-destructive tests are shown.

Photobiomodulation prevents PTSD-like memory impairments in rats

A precise fear memory encoding a traumatic event enables an individual to avoid danger and identify safety. An impaired fear memory (contextual amnesia), however, puts the individual at risk of developing posttraumatic stress disorder (PTSD) due to the inability to identify a safe context when encountering trauma-associated cues later in life. Although it is gaining attention that contextual amnesia is a critical etiologic factor for PTSD, there is no treatment currently available that can reverse contextual amnesia, and whether such treatment can prevent the development of PTSD is unknown. Here, we report that (I) a single dose of transcranial photobiomodulation (PBM) applied immediately after tone fear conditioning can reverse contextual amnesia. PBM treatment preserved an appropriately high level of contextual fear memory in rats revisiting the “dangerous” context, while control rats displayed memory impairment. (II) A single dose of PBM applied after memory recall can reduce contextual fear during both contextual and cued memory testing. (III) In a model of complex PTSD with repeated trauma, rats given early PBM interventions efficiently discriminated safety from danger during cued memory testing and, importantly, these rats did not develop PTSD-like symptoms and comorbidities. (IV) Finally, we report that fear extinction was facilitated when PBM was applied in the early intervention window of memory consolidation. Our results demonstrate that PBM treatment applied immediately after a traumatic event or its memory recall can protect contextual fear memory and prevent the development of PTSD-like psychopathological fear in rats.

An opposing self-reinforced odor pre-exposure memory produces latent inhibition in Drosophila

Prior experience of a stimulus can inhibit subsequent acquisition or expression of a learned association of that stimulus. However, the neuronal manifestations of this learning effect, named latent inhibition (LI), are poorly understood. Here we show that odor pre-exposure produces LI of appetitive olfactory memory performance in Drosophila. Behavioral expression of LI requires that the context during memory testing resembles that during the odor pre-exposures. Odor pre-exposure forms an aversive memory that requires dopaminergic neurons that innervate the γ2α′1 and α3 mushroom body compartments - those to α3 exhibit increasing odor-driven activity with successive pre-exposures. In contrast, odor-specific responses of the corresponding mushroom body output neurons are suppressed. Odor pre-exposure therefore recruits specific dopaminergic neurons that provide teaching signals that attach negative valence to the odor itself. LI of Drosophila appetitive memory consequently results from a temporary and context-dependent retrieval deficit imposed by competition with this short-lived aversive memory.