Recent research in a variety of systems indicates that memory formation can involve the activation of a wide range of molecular cascades. In assessing this recent work it is clear that no single cascade is uniquely important for all forms of memory, nor is a single form of memory uniquely dependent on a single cascade. Rather, it appears that molecular networks are differentially engaged in the induction of various forms of memory. Despite this highly interactive array of possible cascades, specific 'molecular nodes' have emerged as critical regulatory points in memory formation. Functionally, these nodes can operate in two sequential steps, beginning with a convergence of inputs which coordinately influence the activation state of the node, in which the nature of stimulation determines the dynamics of nodal activity, followed by a divergence of substrate selection, in which the node serves as a gateway that activates specific downstream effectors. Finally, specific nodes can be differentially engaged (i.e. have different 'weights') depending upon the nature and pattern of the activating stimulus. The marine mollusk Aplysia has proven useful for a molecular analysis of memory formation. We will use this system to highlight some of the molecular strategies employed by the nervous system in the formation of memory for sensitization, and we will focus on extracellular signal-related kinase as a candidate node integral to these processes.
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http://dx.doi.org/10.1007/s00018-006-6022-x | DOI Listing |
Commun Psychol
January 2025
Institute of Psychology, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany.
Learning an association does not always succeed on the first attempt. Previous studies associated increased error signals in posterior medial frontal cortex with improved memory formation. However, the neurophysiological mechanisms that facilitate post-error learning remain poorly understood.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Neurosurgery, University of Alabama at Birmingham, Birmingham, AL, USA.
Oncolytic viruses (OVs) emerge as a promising cancer immunotherapy. However, the temporal impact on tumor cells and the tumor microenvironment, and the nature of anti-tumor immunity post-therapy remain largely unclear. Here we report that CD4 T cells are required for durable tumor control in syngeneic murine models of glioblastoma multiforme after treatment with an oncolytic herpes simplex virus (oHSV) engineered to express IL-12.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Heidelberg University Hospital Department of Hematology Oncology and Rheumatology, Heidelberg, Germany
Bispecific antibodies (BsAb) have emerged as a leading treatment modality in patients suffering from B-cell non-Hodgkin's lymphoma (B-NHL). However, treatment failure is common and may potentially be attributed to pre-existing or emerging T-cell exhaustion. CD39 catalyzes-together with CD73-the hydrolysis of immunogenic ATP into immunosuppressive adenosine and thus actively promotes an immunosuppressive micromilieu.
View Article and Find Full Text PDFJ Nutr
January 2025
Jean Mayer USDA HNRCA, Tufts University, Boston, MA 02111.
Background: In addition to its important roles in blood coagulation and bone formation, vitamin K (VK) contributes to brain function. Low dietary VK intake, which is common among older adults, is associated with age-related cognitive impairment.
Objective: To elucidate the biological mechanisms underlying VK's effects on cognition, we investigated the effects of low VK (LVK) intake on cognition in C57BL/6 mice.
Biomaterials
January 2025
Department of Urology, The Fourth Affiliated Hospital of Soochow University, Suzhou Dushu Lake Hospital, Medical Center of Soochow University, Suzhou, 215000, China; Department of Urology, First Affiliated Hospital of Soochow University, Suzhou, 215006, China. Electronic address:
Activating the cGAS-STING pathway presents a promising strategy to enhance the innate immunity and combat the immunosuppressive tumor microenvironment. One key mechanism for triggering this pathway involves the release of damaged DNA fragments caused by nuclear DNA damage. However, conventional cGAS-STING agonists often suffer from limited nucleus-targeting efficiency and potential biotoxicity.
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