Model of spatio-temporal propagation of action potentials in the Schaffer collateral pathway of the CA1 area of the rat hippocampus

Hippocampus ◽  
1997 ◽  
Vol 7 (1) ◽  
pp. 58-72 ◽  
Author(s):  
C. Bernard ◽  
R.C. Cannon ◽  
Y. Ben Ari ◽  
H.V. Wheal
Neuroscience ◽  
2002 ◽  
Vol 109 (1) ◽  
pp. 63-80 ◽  
Author(s):  
D.W Cope ◽  
G Maccaferri ◽  
L.F Márton ◽  
J.D.B Roberts ◽  
P.M Cobden ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hieu Hoang Trung ◽  
Toru Yoshihara ◽  
Akito Nakao ◽  
Katsumi Hayashida ◽  
Yoshiki Hirata ◽  
...  

AbstractThe RIβ subunit of cAMP-dependent protein kinase (PKA), encoded by Prkar1b, is a neuronal isoform of the type I regulatory subunit of PKA. Mice lacking the RIβ subunit exhibit normal long-term potentiation (LTP) in the Schaffer collateral pathway of the hippocampus and normal behavior in the open-field and fear conditioning tests. Here, we combined genetic, electrophysiological, and behavioral approaches to demonstrate that the RIβ subunit was involved in body tremor, LTP in the Schaffer collateral pathway, and fear conditioning memory in rats. Genetic analysis of WTC-furue, a mutant strain with spontaneous tremors, revealed a deletion in the Prkar1b gene of the WTC-furue genome. Prkar1b-deficient rats created by the CRISPR/Cas9 system exhibited body tremor. Hippocampal slices from mutant rats showed deficient LTP in the Schaffer collateral–CA1 synapse. Mutant rats also exhibited decreased freezing time following contextual and cued fear conditioning, as well as increased exploratory behavior in the open field. These findings indicate the roles of the RIβ subunit in tremor pathogenesis and contextual and cued fear memory, and suggest that the hippocampal and amygdala roles of this subunit differ between mice and rats and that rats are therefore beneficial for exploring RIβ function.


2021 ◽  
Vol 3 (5) ◽  
Author(s):  
Sumedha Gandharava Dahl ◽  
Robert C. Ivans ◽  
Kurtis D. Cantley

AbstractThis study uses advanced modeling and simulation to explore the effects of external events such as radiation interactions on the synaptic devices in an electronic spiking neural network. Specifically, the networks are trained using the spike-timing-dependent plasticity (STDP) learning rule to recognize spatio-temporal patterns (STPs) representing 25 and 100-pixel characters. Memristive synapses based on a TiO2 non-linear drift model designed in Verilog-A are utilized, with STDP learning behavior achieved through bi-phasic pre- and post-synaptic action potentials. The models are modified to include experimentally observed state-altering and ionizing radiation effects on the device. It is found that radiation interactions tend to make the connection between afferents stronger by increasing the conductance of synapses overall, subsequently distorting the STDP learning curve. In the absence of consistent STPs, these effects accumulate over time and make the synaptic weight evolutions unstable. With STPs at lower flux intensities, the network can recover and relearn with constant training. However, higher flux can overwhelm the leaky integrate-and-fire post-synaptic neuron circuits and reduce stability of the network.


2002 ◽  
Vol 87 (3) ◽  
pp. 1655-1658 ◽  
Author(s):  
Bret N. Smith ◽  
F. Edward Dudek

Axon sprouting and synaptic reorganization in the hippocampus are associated with the development of seizures in temporal lobe epilepsy. Synaptic interactions among CA1 pyramidal cells were examined in fragments of hippocampal slices containing only the CA1 area from saline- and kainate-treated rats. Glutamate microapplication to the pyramidal cell layer increased excitatory postsynaptic current (EPSC) frequency, but only in rats with kainate-induced epilepsy. In bicuculline, action potentials evoked in single pyramidal cells increased the frequency of network bursts only in slices from rats with kainate-induced epilepsy. These data further support the hypothesis that excitatory connections between CA1 pyramidal cells increase after kainate-induced status epilepticus.


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