Evidence for a role for synaptophysin in expression of long-term potentiation in rat dentate gyrus

Mullany, Patricia M.; Lynch, Marina A.

doi:10.1097/00001756-199808030-00012

Cited by 47 publications

(29 citation statements)

References 12 publications

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“…Synaptophysin and other synaptic vesicle proteins have been implicated in mechanisms of cellular plasticity that are thought to underlie learning (Lynch et al, 1994;Mullany and Lynch, 1998;Janz et al, 1999). Viewed in the context of the overall circuit organization of the hippocampal formation (for review, see Amaral and Witter, 1995), this evidence provides a valuable framework for evaluating the functional implications of the present results.…”

Section: Discussionmentioning

confidence: 74%

Circuit-Specific Alterations in Hippocampal Synaptophysin Immunoreactivity Predict Spatial Learning Impairment in Aged Rats

Smith¹,

Adams²,

et al. 2000

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The present study examined the long-standing concept that changes in hippocampal circuitry contribute to age-related learning impairment. Individual differences in spatial learning were documented in young and aged Long-Evans rats by using a hippocampal-dependent version of the Morris water maze. Postmortem analysis used a confocal laser-scanning microscopy method to quantify changes in immunofluorescence staining for the presynaptic vesicle glycoprotein, synaptophysin (SYN), in the principal relays of hippocampal circuitry. Comparisons based on chronological age alone failed to reveal a reliable difference in the intensity of SYN staining in any region that was examined. In contrast, aged subjects with spatial learning deficits displayed significant reductions in SYN immunoreactivity in CA3 lacunosum-moleculare (LM) relative to either young controls or age-matched rats with preserved learning. SYN intensity values for the latter groups were indistinguishable. In addition, individual differences in spatial learning capacity among the aged rats correlated with levels of SYN staining selectively in three regions: outer and middle portions of the dentate gyrus molecular layer and CA3-LM. The cross-sectional area of SYN labeling, by comparison, was not reliably affected in relation cognitive status. These findings are the first to demonstrate that a circuit-specific pattern of variability in the connectional organization of the hippocampus is coupled to individual differences in the cognitive outcome of normal aging. The regional specificity of these effects suggests that a decline in the fidelity of input to the hippocampus from the entorhinal cortex may play a critical role. Key words: circuit organization; synaptophysin; hippocampus; entorhinal cortex; aging; spatial learning; Morris water mazeA substantial proportion of aged individuals exhibit learning and memory deficits that qualitatively resemble the effects of direct hippocampal damage (for review, see Gallagher and Rapp, 1997). Related alterations are observed in hippocampal neuronal activity in aged rats with spatial learning deficits, including a decline in the scope of information controlling location-specific firing, and modified place field stability Shen et al., 1997; Tanila et al., 1997a,b). Against this background recent stereological investigations indicate that the total number of dentate gyrus granule cells and pyramidal neurons in fields CA3/2 and CA1 remains stable in aged mice (Calhoun et al

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Section: Discussionmentioning

confidence: 74%

Circuit-Specific Alterations in Hippocampal Synaptophysin Immunoreactivity Predict Spatial Learning Impairment in Aged Rats

Smith¹,

Adams²,

et al. 2000

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“…The idea that activation of tyrosine kinases was important for expression of LTP was suggested by the finding that kinase inhibitors prevented expression of LTP in CA1 and dentate gyrus (436,465) and that mice, in which the nonreceptor tyrosine kinase fyn was knocked out, were unable to sustain LTP (205). These data were consolidated by the findings that tyrosine phosphorylation of several substrates was increased after induction of LTP; these included phospholipase C (PLC)-␥ (396), synaptophysin (436), the ␣-subunit of voltage-activated calcium channels (90), TrkA (366), TrkB (198), and the 2B subunit of the NMDA receptor (528,531). ERK is also a substrate for tyrosine kinase, but its activation requires dual phosphorylation on tyrosine and threonine residues.…”

Section: Phosphatidyinositol 3-kinasementioning

confidence: 99%

Long-Term Potentiation and Memory

Lynch

2004

Physiological Reviews

1,684

1,098

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Lynch, MA. Long-Term Potentiation and Memory. Physiol Rev 84: 87–136, 2004; 10.1152/physrev.00014.2003.—One of the most significant challenges in neuroscience is to identify the cellular and molecular processes that underlie learning and memory formation. The past decade has seen remarkable progress in understanding changes that accompany certain forms of acquisition and recall, particularly those forms which require activation of afferent pathways in the hippocampus. This progress can be attributed to a number of factors including well-characterized animal models, well-defined probes for analysis of cell signaling events and changes in gene transcription, and technology which has allowed gene knockout and overexpression in cells and animals. Of the several animal models used in identifying the changes which accompany plasticity in synaptic connections, long-term potentiation (LTP) has received most attention, and although it is not yet clear whether the changes that underlie maintenance of LTP also underlie memory consolidation, significant advances have been made in understanding cell signaling events that contribute to this form of synaptic plasticity. In this review, emphasis is focused on analysis of changes that occur after learning, especially spatial learning, and LTP and the value of assessing these changes in parallel is discussed. The effect of different stressors on spatial learning/memory and LTP is emphasized, and the review concludes with a brief analysis of the contribution of studies, in which transgenic animals were used, to the literature on memory/learning and LTP.

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“…In addition, synaptophysin levels have been shown to correlate with resting-state brain glucose utilization (Rocher et al 2003). The function of this protein is still unknown but previous suggestions have included calcium binding (Rehm et al 1986), channel formation (Sudhof et al 1987;Thomas et al 1988), exocytosis Mullany and Lynch 1998), and synaptic vesicle recycling via endocytosis (Evans and Cousin 2005). Furthermore, synaptophysin has also been implicated in disorders of neurodevelopment such as schizophrenia.…”

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confidence: 99%

Synaptophysin and postsynaptic density protein 95 in the human prefrontal cortex from mid-gestation into early adulthood

Glantz¹,

Gilmore²,

Hamer³

et al. 2007

Neuroscience

235

162

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Previous studies of postnatal synaptic development in human frontal cortex have shown that synaptic density rises after birth, reaches a plateau in childhood and then decreases to adult levels by late adolescence. A similar pattern has been seen in nonhuman primate cortex. These earlier studies in human cortex are limited, however, by significant age gaps in study subjects at critical inflection points of the developmental curve. Additionally, it is unclear if synaptic development occurs in different patterns in different cortical layers in prefrontal cortex (PFC). The purpose of this study was to examine synaptic density in human PFC across development by measuring two synaptic marker proteins: synaptophysin (presynaptic), and postsynaptic density-95 (PSD-95; postsynaptic). Western blotting was used to assess the relative levels of synaptophysin and PSD-95 in dorsolateral PFC of 42 subjects, distributed in age from 18 weeks gestation to 25 years. In addition, synaptophysin immunoreactivity was examined in each layer of areas 9 and 46 of PFC in 24 subjects, ranging in age from 0.1 to 25 years. Synaptophysin levels slowly increased from birth until age 5 and then increased more rapidly to peak in late childhood around age 10. Synaptophysin subsequently decreased until the adult level was reached by mid-adolescence, around age 16. PSD-95 levels increased postnatally to reach a stable plateau by early childhood with a slight reduction in late adolescence and early adulthood. The pattern of synaptophysin immunoreactivity seen with immunohistochemistry was similar to the Western experiments but the changes across age were more subtle, with little change by layer within and across age. The developmental patterns exhibited by these synaptic marker proteins expand upon previous studies of developmental synaptic changes in human frontal cortex; synaptic density increases steadily from birth to late childhood, then decreases in early adolescence to reach adult levels by late adolescence. Keywordsadolescence; development; human; synapses; pruning; synaptogenesisThe human brain has the most protracted period of development of any species, with neurodevelopment continuing well into early adulthood. Imaging studies have shown that in the human, the overall volume of the brain increases during childhood and adolescence (Giedd Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 November 9. Sowell et al. 2002;Gilmore et al. 2007). Specifically, the cortical gray matter volume, particularly the f...

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Evidence for a role for synaptophysin in expression of long-term potentiation in rat dentate gyrus

Cited by 47 publications

References 12 publications

Circuit-Specific Alterations in Hippocampal Synaptophysin Immunoreactivity Predict Spatial Learning Impairment in Aged Rats

Circuit-Specific Alterations in Hippocampal Synaptophysin Immunoreactivity Predict Spatial Learning Impairment in Aged Rats

Long-Term Potentiation and Memory

Synaptophysin and postsynaptic density protein 95 in the human prefrontal cortex from mid-gestation into early adulthood

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