scholarly journals Effect of Prenatal Protein Malnutrition on Long-Term Potentiation and BDNF Protein Expression in the Rat Entorhinal Cortex after Neocortical and Hippocampal Tetanization

2008 ◽  
Vol 2008 ◽  
pp. 1-9 ◽  
Author(s):  
Alejandro Hernández ◽  
Héctor Burgos ◽  
Mauricio Mondaca ◽  
Rafael Barra ◽  
Héctor Núñez ◽  
...  
Keyword(s):  
Entorhinal Cortex ◽  
Memory Performance ◽  
Occipital Cortex ◽  
Long Term Potentiation ◽  
Learning Performance ◽  
Pregnant Rats ◽  
Maternal Malnutrition ◽  
Term Potentiation ◽  
Stimulation Of

Reduction of the protein content from 25 to 8% casein in the diet of pregnant rats results in impaired neocortical long-term potentiation (LTP) of the offspring together with lower visuospatial memory performance. The present study was aimed to investigate whether this type of maternal malnutrition could result in modification of plastic capabilities of the entorhinal cortex (EC) in the adult progeny. Unlike normal eutrophic controls, 55–60-day-old prenatally malnourished rats were unable to develop LTP in the medial EC to tetanizing stimulation delivered to either the ipsilateral occipital cortex or the CA1 hippocampal region. Tetanizing stimulation of CA1 also failed to increase the concentration of brain-derived neurotrophic factor (BDNF) in the EC of malnourished rats. Impaired capacity of the EC of prenatally malnourished rats to develop LTP and to increase BDNF levels during adulthood may be an important factor contributing to deficits in learning performance having adult prenatally malnourished animals.

Evoked potentials and long-term potentiation in the mouse dentate gyrus after stimulation of the entorhinal cortex

1982 ◽  
Vol 75 (1) ◽  
pp. 134-148 ◽  
Author(s):  
Kathy Payne ◽  
Charles J. Wilson ◽  
Stephen Young ◽  
Eva Fifkova ◽  
Philip M. Groves
Keyword(s):  
Evoked Potentials ◽  
Dentate Gyrus ◽  
Entorhinal Cortex ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Stimulation Of

scholarly journals Long-term synaptic plasticity in hippocampal neurogliaform interneurons

2019 ◽  
Author(s):  
Marion S. Mercier ◽  
Vincent Magloire ◽  
Jonathan Cornford ◽  
Dimitri M. Kullmann
Keyword(s):  
Entorhinal Cortex ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Stratum Radiatum ◽  
Dependent Manner ◽  
Feed Forward ◽  
Term Potentiation ◽  
Feed Forward Inhibition ◽  
Stimulation Of

AbstractHippocampal interneurons located within stratum lacunosum-moleculare (SLM), which include neurogliaform (NGF) cells, mediate powerful feed-forward inhibition that can modulate spiking and plasticity in CA1 pyramidal cells. Despite evidence of long-term plasticity at excitatory inputs onto almost all other hippocampal interneuron subtypes, including stratum radiatum feed-forward interneurons, it is not known whether long-term potentiation (LTP) occurs in CA1 SLM interneurons. Here, we show that these interneurons exhibit Hebbian NMDA receptor-dependent LTP, and that Ca2+ influx through voltage-gated Ca2+ channels can also be sufficient for induction of plasticity. Furthermore, using an optogenetic dissection strategy, we find that selective stimulation of excitatory fibers from entorhinal cortex can induce LTP in SLM interneurons, whilst stimulation of thalamic afferents from the nucleus reuniens, also known to project to SLM, does not. Finally, we show that a mouse line selective for cortical NGF cells, where Cre recombinase is under the control of the neuron-derived neurotrophic factor (NDNF) promoter, can also be used to target these interneurons within the hippocampus, and that hippocampal NGF cells exhibit LTP. Recruitment of NGF cells can thus be persistently enhanced in an activity-dependent manner, implying that their role in gating dendritic signaling in pyramidal neurons is modifiable.Significance statementLong-term potentiation (LTP) of synaptic transmission within the hippocampus is involved in memory formation and spatial navigation. While LTP has been extensively studied in excitatory principal cells, less is known about plasticity mechanisms in inhibitory interneurons, which represent a diverse population of cells. Here we characterize LTP in interneurons that mediate powerful feed-forward inhibition of pyramidal neuron distal dendrites, and show that this plasticity can be induced by afferents originating in the entorhinal cortex. Importantly, we identify at least a subset of these LTP-expressing interneurons as neurogliaform cells. The results shed light on this relatively understudied sub-type of hippocampal interneurons and show that their recruitment by extrinsic afferents can be modified in a use-dependent manner.

Induction of long-term potentiation without participation of N-methyl-D-aspartate receptors in kitten visual cortex

1991 ◽  
Vol 65 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Y. Komatsu ◽  
S. Nakajima ◽  
K. Toyama
Keyword(s):  
Nmda Receptors ◽  
Stimulus Frequency ◽  
Low Frequency ◽  
Nmda Antagonist ◽  
Long Term Potentiation ◽  
Conditioning Stimulation ◽  
Postsynaptic Potential ◽  
Term Potentiation ◽  
Stimulation Of

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.

On the Respective Roles of Nitric Oxide and Carbon Monoxide in Long-Term Potentiation in the Hippocampus

1999 ◽  
Vol 6 (1) ◽  
pp. 63-76 ◽  
Author(s):  
Min Zhuo ◽  
Jarmo T. Laitinen ◽  
Xiao-Ching Li ◽  
Robert D. Hawkins
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Guanylyl Cyclase ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
No Synthase ◽  
Term Potentiation ◽  
Stimulation Of

Perfusion of hippocampal slices with an inhibitor nitric oxide (NO) synthase blocked induction of long-term potentiation (LTP) produced by a one-train tetanus and significantly reduced LTP by a two-train tetanus, but only slightly reduced LTP by a four-train tetanus. Inhibitors of heme oxygenase, the synthetic enzyme for carbon monoxide (CO), significantly reduced LTP by either a two-train or four-train tetanus. These results suggest that NO and CO are both involved in LTP but may play somewhat different roles. One possibility is that NO serves a phasic, signaling role, whereas CO provides tonic, background stimulation. Another possibility is that NO and CO are phasically activated under somewhat different circumstances, perhaps involving different receptors and second messengers. Because NO is known to be activated by stimulation of NMDA receptors during tetanus, we investigated the possibility that CO might be activated by stimulation of metabotropic glutamate receptors (mGluRs). Consistent with this idea, long-lasting potentiation by the mGluR agonist tACPD was blocked by inhibitors of heme oxygenase but not NO synthase. Potentiation by tACPD was also blocked by inhibitors of soluble guanylyl cyclase (a target of both NO and CO) or cGMP-dependent protein kinase, and guanylyl cyclase was activated by tACPD in hippocampal slices. However, biochemical assays indicate that whereas heme oxygenase is constitutively active in hippocampus, it does not appear to be stimulated by either tetanus or tACPD. These results are most consistent with the possibility that constitutive (tonic) rather than stimulated (phasic) heme oxygenase activity is necessary for potentiation by tetanus or tACPD, and suggest that mGluR activation stimulates guanylyl cyclase phasically through some other pathway.

Type I adenylyl cyclase functions as a coincidence detector for control of cyclic AMP response element-mediated transcription: synergistic regulation of transcription by Ca2+ and isoproterenol

1994 ◽  
Vol 14 (12) ◽  
pp. 8272-8281
Author(s):  
S Impey ◽  
G Wayman ◽  
Z Wu ◽  
D R Storm
Keyword(s):  
Cyclic Amp ◽  
Adenylyl Cyclase ◽  
Long Term Potentiation ◽  
Regulation Of Transcription ◽  
Type I ◽  
Hek 293 ◽  
293 Cells ◽  
Term Potentiation ◽  
Stimulation Of

Studies carried out with mammals and invertebrates suggest that Ca(2+)-sensitive adenylyl cyclases may be important for neuroplasticity. Long-term potentiation in the hippocampus requires increases in intracellular Ca2+ which are accompanied by elevated cyclic AMP (cAMP). Furthermore, activation of cAMP-dependent protein kinase is required for the late stage of long-term potentiation in the CA1 region of the hippocampus, which is also sensitive to inhibitors of transcription. Therefore, some forms of synaptic plasticity may require coordinate regulation of transcription by Ca2+ and cAMP. In this study, we demonstrate that the expression of type I adenylyl cyclase in HEK-293 cells allows Ca2+ to stimulate reporter gene activity mediated through the cAMP response element. Furthermore, simultaneous activation by Ca2+ and isoproterenol caused synergistic stimulation of transcription in HEK-293 cells and cultured neurons. We propose that Ca2+ and neurotransmitter stimulation of type I adenylyl cyclase may play a role in synaptic plasticity by generating optimal cAMP signals for regulation of transcription.

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