Long-term memory is formed immediately without the need for protein synthesis-dependent consolidation in Drosophila.

It is believed that long-term memory (LTM) cannot be formed immediately because it must go through a protein synthesis-dependent consolidation process. However, the current study uses Drosophila aversive olfactory conditioning to show that such processes are dispensable for context-dependent LTM (cLTM). Single-trial conditioning yields cLTM that is formed immediately in a protein-synthesis independent manner and is sustained over 14 days without decay.

Social Isolation Induces Rac1-Dependent Forgetting of Social Memory.

Social isolation (SI) has detrimental effects on human and animal cognitive functions. In particular, acute isolation in adult mice impairs social recognition memory (SRM). Previous accounts of this impairment have focused primarily on memory consolidation.

Fan-Shaped Body Neurons in the Drosophila Brain Regulate Both Innate and Conditioned Nociceptive Avoidance.

Multiple brain regions respond to harmful nociceptive stimuli. However, it remains unclear as to whether behavioral avoidance of such stimuli can be modulated within the same or distinct brain networks. Here, we found subgroups of neurons localized within a well-defined brain region capable of mediating both innate and conditioned nociceptive avoidance in Drosophila.

Active Protection: Learning-Activated Raf/MAPK Activity Protects Labile Memory from Rac1-Independent Forgetting.

Active forgetting explains the intrinsic instability of a labile memory lasting for hours. However, how such memory maintains stability against unwanted disruption is not completely understood. Here, we report a learning-activated active protection mechanism that enables labile memory to resist disruptive sensory experiences in Drosophila.

Altered resting-state regional homogeneity after 13 weeks of paliperidone injection treatment in schizophrenia patients.

This study aimed to explore the effects of the long-acting antipsychotic drug palmitate paliperidone in resting-state brain activity of schizophrenia patients. Seventeen schizophrenia outpatients were included and received palmitate paliperidone injection (PAL) treatment for 13 weeks. These patients were compared to seventeen matched healthy controls.

Hippocampal Activation of Rac1 Regulates the Forgetting of Object Recognition Memory.

Forgetting is a universal feature for most types of memories. The best-defined and extensively characterized behaviors that depict forgetting are natural memory decay and interference-based forgetting [1, 2]. Molecular mechanisms underlying the active forgetting remain to be determined for memories in vertebrates.

Cdc42-Dependent Forgetting Regulates Repetition Effect in Prolonging Memory Retention.

Repeated learning is used daily and is a powerful way to improve memory. A fundamental question is how multiple learning trials add up to improve memory. While the major studies so far of such a repetition effect have emphasized the strengthening of memory formation, the current study reveals a molecular mechanism through suppression of forgetting.

Inability to activate Rac1-dependent forgetting contributes to behavioral inflexibility in mutants of multiple autism-risk genes.

The etiology of autism is so complicated because it involves the effects of variants of several hundred risk genes along with the contribution of environmental factors. Therefore, it has been challenging to identify the causal paths that lead to the core autistic symptoms such as social deficit, repetitive behaviors, and behavioral inflexibility. As an alternative approach, extensive efforts have been devoted to identifying the convergence of the targets and functions of the autism-risk genes to facilitate mapping out causal paths.

Importin-7 mediates memory consolidation through regulation of nuclear translocation of training-activated MAPK in Drosophila.

Translocation of signaling molecules, MAPK in particular, from the cytosol to nucleus represents a universal key element in initiating the gene program that determines memory consolidation. Translocation mechanisms and their behavioral impact, however, remain to be determined. Here, we report that a highly conserved nuclear transporter, Drosophila importin-7 (DIM-7), regulates import of training-activated MAPK for consolidation of long-term memory (LTM).

Requirement of the combination of mushroom body γ lobe and α/β lobes for the retrieval of both aversive and appetitive early memories in Drosophila.

Extensive studies of Drosophila mushroom body in formation and retrieval of olfactory memories allow us to delineate the functional logic for memory storage and retrieval. Currently, there is a questionable disassociation of circuits for memory storage and retrieval during Drosophila olfactory memory processing. Formation of the initial aversive olfactory memory involves mushroom body γ lobe, whereas α/β lobes are reported to be necessary for the retrieval of such memory.

The differential requirement of mushroom body α/β subdivisions in long-term memory retrieval in Drosophila.

The mushroom body (MB), a bilateral brain structure possessing about 2000-2500 neurons per hemisphere, plays a central role in olfactory learning and memory in Drosophila melanogaster. Extensive studies have demonstrated that three major types of MB neurons (α/β, α'/β' and Γ) exhibit distinct functions in memory processing, including the critical role of approximately 1000 MB α/β neurons in retrieving long-term memory. Inspired by recent findings that MB α/β neurons can be further divided into three subdivisions (surface, posterior and core) and wherein the α/β core neurons play an permissive role in long-term memory consolidation, we examined the functional differences of all the three morphological subdivisions of MB α/β by temporally precise manipulation of their synaptic outputs during long-term memory retrieval.

Schizophrenia susceptibility gene dysbindin regulates glutamatergic and dopaminergic functions via distinctive mechanisms in Drosophila.

The dysfunction of multiple neurotransmitter systems is a striking pathophysiological feature of many mental disorders, schizophrenia in particular, but delineating the underlying mechanisms has been challenging. Here we show that manipulation of a single schizophrenia susceptibility gene, dysbindin, is capable of regulating both glutamatergic and dopaminergic functions through two independent mechanisms, consequently leading to two categories of clinically relevant behavioral phenotypes. Dysbindin has been reported to affect glutamatergic and dopaminergic functions as well as a range of clinically relevant behaviors in vertebrates and invertebrates but has been thought to have a mainly neuronal origin.

Forgetting is regulated through Rac activity in Drosophila.

Initially acquired memory dissipates rapidly if not consolidated. Such memory decay is thought to result either from the inherently labile nature of newly acquired memories or from interference by subsequently attained information. Here we report that a small G protein Rac-dependent forgetting mechanism contributes to both passive memory decay and interference-induced forgetting in Drosophila.

Suppressor of Hairless is required for long-term memory formation in Drosophila.

Suppressor of Hairless [Su(H)] is a DNA-binding protein of the Notch-signaling pathway, which is important for developmental processes and has been implicated in behavior plasticity. It acts as a transcriptional activator in the Notch pathway, but also as a repressor in the absence of Notch signaling. Our previous work has shown that Notch signaling contributes to long-term memory formation in the Drosophila adult brain.