Subfield-specific immediate early gene expression associated with hippocampal long-term potentiation in vivo (original) (raw)
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Changes in hippocampal gene expression associated with the induction of long-term potentiation
Molecular Brain Research, 1996
The expression of four genes: zif/268. c-fob. tubulin and aCa"/calmodulin-dcpe~~dcnt protein kinase 11 (cxCAMK11) n'as studied following the induction of LTP in Schaffer collateral CA1 neurone synapses in rat hippocampal slices maintained in vitro. Leveis of c-fos mRNA and tubulin (T,,) mRNA in area CAI were unchanged after induction of LTP. howeve r. zifj268 ;ir,d aCAMKII mRNA levels showed a significant increase compared to non-potentiated controls. It is possible. therefore. to measure changes in gene expression using in situ hybridisation following induction of LTP in vitro and these results strengthen the theory that zif/268 and cvCAMKIl are in\4\~etl in some aspect of the induction or maintenance of hippocampal LTP.
Expression mechanisms of long-term potentiation in the hippocampus
Journal of Physiology-Paris, 1996
We have taken a number of different experimental approaches to address whether long-term potentiation (LIP) in hippocampal CA1 pyramidal cells is due primarily to presynaptic or postsynaptic modifications. Examination of miniature EPSCs or EPSCs evoked using minimal stimulation indicate that quanta1 size increasing during LIT The conversion of silent to functional synapses may contribute to the LTP-induced changes in mEPSC frequency and failure rate that previously have been attributed to an increase in the probability if transmitter release. long-term potentiation (LTF') / pairing-induced potentiation I probability of transmitter release I NMDA receptor I AMPA receptor I silent synapses I miniature synaptic current (mEPSC)
Nature Neuroscience, 2001
The induction of long-term potentiation (LTP) in the dentate gyrus of the hippocampus is associated with a rapid and robust transcription of the immediate early gene Zif268. We used a mutant mouse with a targeted disruption of Zif268 to ask whether this gene, which encodes a zinc finger transcription factor, is required for the maintenance of late LTP and for the expression of long-term memory. We show that whereas mutant mice exhibit early LTP in the dentate gyrus, late LTP is absent when measured 24 and 48 hours after tetanus in the freely moving animal. In both spatial and non-spatial learning tasks, short-term memory remained intact, whereas performance was impaired in tests requiring long-term memory. Thus, Zif268 is essential for the transition from short-to long-term synaptic plasticity and for the expression of long-term memories.
PLoS ONE, 2013
NMDA receptor subunits change during development and their synaptic expression is modified rapidly after synaptic plasticity induction in hippocampal slices. However, there is scarce information on subunits expression after synaptic plasticity induction or memory acquisition, particularly in adults. GluN1, GluN2A and GluN2B NMDA receptor subunits were assessed by western blot in 1) adult rats that had explored an open field (OF) for 5 minutes, a time sufficient to induce habituation, 2) mature rat hippocampal neuron cultures depolarized by KCl and 3) hippocampal slices from adult rats where long term potentiation (LTP) was induced by theta-burst stimulation (TBS). GluN1 and GluN2A, though not GluN2B, were significantly higher 70 minutes-but not 30 minutes-after a 5 minutes session in an OF. GluN1 and GluN2A total immunofluorescence and puncta in neurites increased in cultures, as evaluated 70 minutes after KCl stimulation. Similar changes were found in hippocampal slices 70 minutes after LTP induction. To start to explore underlying mechanisms, hippocampal slices were treated either with cycloheximide (a translation inhibitor) or actinomycin D (a transcription inhibitor) during electrophysiological assays. It was corroborated that translation was necessary for LTP induction and expression. The rise in GluN1 depends on transcription and translation, while the increase in GluN2A appears to mainly depend on translation, though a contribution of some remaining transcriptional activity during actinomycin D treatment could not be rouled out. LTP effective induction was required for the subunits to increase. Although in the three models same subunits suffered modifications in the same direction, within an apparently similar temporal course, further investigation is required to reveal if they are related processes and to find out whether they are causally related with synaptic plasticity, learning and memory.
Mapping Gene Expression in Excitatory Neurons during Hippocampal Late-Phase Long-Term Potentiation
Frontiers in molecular neuroscience, 2017
The persistence of long-lasting changes in synaptic connectivity that underlie long-term memory require new RNA and protein synthesis. To elucidate the temporal pattern of gene expression that gives rise to long-lasting neuronal plasticity, we analyzed differentially-expressed (DE) RNAs in mouse hippocampal slices following induction of late phase long-term potentiation (L-LTP) specifically within pyramidal excitatory neurons using Translating Ribosome Affinity Purification RNA sequencing (TRAP-seq). We detected time-dependent changes in up- and down-regulated ribosome-associated mRNAs over 2 h following L-LTP induction, with minimal overlap of DE transcripts between time points. TRAP-seq revealed greater numbers of DE transcripts and magnitudes of LTP-induced changes than RNA-seq of all cell types in the hippocampus. Neuron-enriched transcripts had greater changes at the ribosome-loading level than the total RNA level, while RNA-seq identified many non-neuronal DE mRNAs. Our result...
Seizure-induced gene expression in area CA1 of the mouse hippocampus
European Journal of Neuroscience, 2001
Synaptic plasticity in the hippocampus requires activity-dependent gene expression. We have therefore pro®led gene expression in area CA1 following the induction of an electroshock-evoked maximal seizure. Using cDNA microarrays, the differential expression of » 9000 cDNAs was examined. In situ hybridization on 14 transcripts that showed strongest modulation in the microarray screen (1.8±2-fold) con®rmed the differential expression of a single gene that encodes for the nuclear hormone receptor NGFI-B (Nur77, N10). Although this gene is only modestly up-regulated (» 2-fold) in area CA1, in situ hybridization revealed that maximal seizures induce a marked (» 12-fold) up-regulation of NGFI-B in the dentate gyrus. These data support the notion Eur. J. Neurosci., 13, 968±976] that CA1 pyramidal neurons are more refractory than granule cells of the dentate gyrus with respect to activity-dependent gene transcription. Furthermore, our results argue against a large cohort of activity-dependent genes in area CA1.
Long-term potentiation in vivo in the intact mouse hippocampus
Brain Research, 1995
We describe the characteristics of long-term potentiation (LTP) in the intact mouse. Perforant path stimulation evokes both a population excitatory postsynaptic potential (pop-EPSP) and a population spike potential (pop-spike) from the hippocampal dentate gyrus in urethane anesthetized animals. LTP, as measured by increased pop-spike amplitude and pop-EPSP slope, was successfully induced and reliably maintained at a stable level for at least 12 h, the longest time tested. The LTP-inducing stimulus (3 trains of 400 Hz, 8 0.4 ms pulses/train) used in two strains of mice was less by half than that used in rat. These parameters for inducing LTP were also successfully applied to obtain LTP in two different transgenic mouse strains: one bearing a F1/GAP-43 promoter-lacZ fusion gene and another which overexpresses the S100fl gene. We also examined the effects of protein synthesis inhibitors, cycloheximide (CXM) and anisomycin (AND. When CXM or ANI was given 30 min before LTP induction, there was no persistent loss of LTP at the 4 h time point. However, if CXM was given 4 h before LTP induction, significant decay of the potentiated responses occurred 90 min after induction. Half of the animals receiving CXM but not ANI showed a complete and sudden elimination of the entire response after the LTP-inducing stimulus. It was speculated that loss of a constitutively-expressed housekeeping protein, for example a calcium buffering protein, with an estimated half-life of 2 h would lead to an inability to buffer LTP-induced alterations, such as intracellular calcium elevation, increasing intracellular calcium to toxic levels. LTP can be reliably studied in the intact mouse hippocampus and can be usefully applied in both wild-type and transgenic preparations. It will afford the opportunity to study LTP in mouse mutants in their in vivo state rather than in vitro in the slice preparation permitting characterization of biochemical and molecular events after LTP and then to determine the explicit relation of these events with the physiology of synaptic enhancement.