Molecular mechanisms of memory formation

Ng, Kim T.; Gibbs, Marie E.; Crowe, Simon F.; Sedman, G.; Hua, Fuzhou; Zhao, Weiqin; O'Dowd, Brona S.; Rickard, Nikki; Gibbs, C. L.; Syková, Eva; Svoboda, J.; Jendelová, Pavla

doi:10.1007/bf02935556

Cited by 40 publications

(16 citation statements)

References 47 publications

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“…Detrimental effects of prolonged CY treatment on performance of control MRL +/+ mice in the "reversal" trial is consistent with its negative effects in paradigms that measure exploration and motivated behavior (Sakic et al, 1995(Sakic et al, , 1996. Although the principal mechanisms are unclear, one may hypothesize that by cross-linking strands of DNA/RNA and inhibiting protein synthesis, CY treatment impairs molecular mechanisms (e.g., phosphorylation) required for short-term memory formation and consolidation (Ng et al, 1991). Over the past 40 years, lesion studies demonstrating reduced SAB rate in rodents have implicated the role of the hippocampus in attention control and memory formation (Roberts et al, 1962).…”

Section: Discussionmentioning

confidence: 99%

Hippocampal damage in mouse and human forms of systemic autoimmune disease

Ballok¹,

Woulfe

Sur

et al. 2004

Hippocampus

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Systemic lupus erythematosus (SLE) is frequently accompanied by neuropsychiatric (NP) and cognitive deficits of unknown etiology. By using autoimmune MRL-lpr mice as an animal model of NP-SLE, we examine the relationship between autoimmunity, hippocampal damage, and behavioral dysfunction. Fluoro Jade B (FJB) staining and anti-ubiquitin (anti-Ub) immunocytochemistry were used to assess neuronal damage in young (asymptomatic) and aged (diseased) mice, while spontaneous alternation behavior (SAB) was used to estimate the severity of hippocampal dysfunction. The causal relationship between autoimmunity and neuropathology was tested by prolonged administration of the immunosuppressive drug cyclophosphamide (CY). In comparison to congenic MRL +/+ controls, SAB acquisition rates and performance in the "reversal" trial were impaired in diseased MRL-lpr mice, suggesting limited use of the spatial learning strategy. FJBpositive neurons and anti-Ub particles were frequent in the CA3 region. Conversely, CY treatment attenuated the SAB deficit and overall FJB staining. Similarly to mouse brain, the hippocampus from a patient who died from NP-SLE showed reduced neuronal density in the CA3 region and dentate gyrus, as well as increased FJB positivity in these regions. Gliosis and neuronal loss were observed in the gray matter, and T lymphocytes and stromal calcifications were common in the choroid plexus. Taken together, these results suggest that systemic autoimmunity induces significant hippocampal damage, which may underlie affective and cognitive deficits in NP-SLE.

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Section: Discussionmentioning

confidence: 99%

Hippocampal damage in mouse and human forms of systemic autoimmune disease

Ballok¹,

Woulfe

Sur

et al. 2004

Hippocampus

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“…Subsequently, the new memory is stored and it has been suggested that there are two stages of storing new information. This has been referred to as an early consolidation and a late consolidation phase [13,14]. Both phases are required to store new information in the long-term memory.…”

Section: Memory Systemsmentioning

confidence: 99%

Improving Memory: A Role for Phosphodiesterases

Blokland¹,

Schreiber

Prickaerts

2006

CPD

158

100

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During the last decennia, our understanding of the neurobiological processes underlying learning and memory has continuously improved, leading to the identification of targets for the development of memory-enhancing drugs. Here we review a class of drugs which has more recently been identified: the phosphodiesterase (PDE) inhibitors. An overview is given of the different PDEs that are known and we focus on three PDEs which have been identified as possible relevant targets for memory improvement: PDE2, PDE4 and PDE5. PDEs differ in the substrate, i.e. cyclic adenosine monophosphate (cAMP) and/or cyclic guanosine monophosphate (cGMP), being hydrolyzed. Since these cyclic nucleotides have been suggested to play distinct roles in processes of memory, selective PDE inhibitors preventing the breakdown of cAMP and/or cGMP could improve memory. The present data suggest that PDE4 (cAMP) is involved in acquisition processes, although a possible role in late consolidation processes cannot be excluded. PDE5 (cGMP) is involved in early consolidation processes. Since PDE2 inhibition affects both cAMP and cGMP, PDE2 inhibitors may improve both memory processes. The field of PDEs is highly dynamic and new isoforms of PDEs are still being described. This may lead to the discovery and development of new memory enhancing drugs that selectively inhibit such isoforms. Such drugs may exert their effects only in specific brain areas and hence possess an improved side effect profile.

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“…Indeed, the anatomical proximity of astrocytes to neuronal synapses and the blood brain barrier ( Fig. 3) makes these cells ideally suited for taking an active role in the ion, water and neurotransmitter metabolism of the CNS during both normal and abnormal neuronal function (13,(24)(25)(26)(27)(28)(29)(30).…”

Section: Introductionmentioning

confidence: 99%

Cross-talk signals in the CNS Role of neurotrophic and hormonal factors adhesion molecules and intercellular signaling agents in luteinizing hormone-releasing hormone LHRH -astroglial interactive network

Marchetti

1997

Front Biosci

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Neuron-astrocyte interactions play a crucial role during development and in the adult brain. During development, glial cells are involved in the guidance of neuronal precursors and in extending neuronal fiber projections. Astrocytes can promote neurite outgrowth, both "in vitro" and "in vivo". In the central nervous system (CNS), they express receptors for a variety of growth factors (GFs), neurotransmitters and/or neuromodulators. In turn, neuronal cells can respond to astrocyte-derived growth factors and control astrocyte function via a common set of signaling molecules and intracellular transducing pathways. It is also well established that astrocytes are involved with regenerative failure within the CNS following injury. Increasing evidence support the viewpoint that soluble factors from lymphoid/mononuclear cells modulate the growth and function of cells found in the CNS, specifically macroglia and microglia cells. Furthermore, glial cells can secrete immunoregulatory molecules that influence immune cells, as well as the glial cells themselves. In recent years, a bi-directional flow of informational molecules between LHRH neurons, subserving the neuroendocrine control of reproductive function, and astroglia cells has been disclosed. During their maturation and differentiation in vitro, astroglial cells release peptide growth factors that markedly accelerate LHRH neuronal phenotypic differentiation . In addition, these peptides induce the acquisition of mature LHRH secretory potential, with a potency depending on both the "age" and the specific brain localization of the astroglia, as well as the degree of LHRH neuronal differentiation "in vitro". Different experimental paradigms such as co-culture and mixed culture models between the GT1-1 neurons and astroglial cells in primary culture, disclosed the presence of a bi-directional flow of informational molecules regulating both proliferative and secretory capacities of each cell type. Growth factors are key players in LHRH neuron-astroglia crosstalk. In particular, basic fibroblast growth factor (bFGF) was identified as a major differentiation factor for the immortalized hypothalamic LHRH neuronal cell line. A specific synergy/cooperation between bFGF and other growth factors was also revealed at specific stages of LHRH neuron differentiation, indicating that the sequential expression of specific growth factors may participate in the processes of LHRH neuron migration, differentiation and functional regulation. Since bFGF is expressed in GT1-1 neurons and glial cells a possible paracrine/autocrine regulatory loop is suggested. Indeed, neutralization experiments aimed at counteracting endogenous bFGF during neuron-glia interactions dramatically inhibited astroglia neurotrophic effects. On the other hand, the importance of adhesion molecules in cell-to-cell communication was underscored by the significant inhibition of GT1-1 LHRH production and cell proliferation following the counteraction of neuron-neuron/neuron-glia interactions through addition of neuronal c...

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Molecular mechanisms of memory formation

Cited by 40 publications

References 47 publications

Hippocampal damage in mouse and human forms of systemic autoimmune disease

Hippocampal damage in mouse and human forms of systemic autoimmune disease

Improving Memory: A Role for Phosphodiesterases

Cross-talk signals in the CNS Role of neurotrophic and hormonal factors adhesion molecules and intercellular signaling agents in luteinizing hormone-releasing hormone LHRH -astroglial interactive network

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