scholarly journals Simulations of Learning, Memory, and Forgetting Processes with Model of CA1 Region of the Hippocampus

Complexity ◽  
2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Dariusz Świetlik

The aim of this paper is to present a computational model of the CA1 region of the hippocampus, whose properties include (a) attenuation of receptors for external stimuli, (b) delay and decay of postsynaptic potentials, (c) modification of internal weights due to propagation of postsynaptic potentials through the dendrite, and (d) modification of weights for the analog memory of each input due to a pattern of long-term synaptic potentiation (LTP) with regard to its decay. The computer simulations showed that CA1 model performs efficient LTP induction and high rate of sub-millisecond coincidence detection. We also discuss a possibility of hardware implementation of pyramidal cells of CA1 region of the hippocampus.

1999 ◽  
Vol 202 (10) ◽  
pp. 1243-1253 ◽  
Author(s):  
N.J. Berman ◽  
L. Maler

The electrosensory lateral line lobe (ELL) of weakly electric fish is the only nucleus that receives direct input from peripheral electroreceptor afferents. This review summarises the neurotransmitters, receptors and second messengers identified in the intrinsic circuitry of the ELL and the extrinsic descending direct and indirect feedback pathways, as revealed by recent in vitro and in vivo studies. Several hypotheses of circuitry function are examined on this basis and on the basis of recent functional evidence: (1) fast primary afferent excitatory postsynaptic potentials (EPSPs) and fast granule cell 2 GABAA inhibitory postsynaptic potentials (IPSPs) suggest the involvement of basilar pyramidal cells in coincidence detection; (2) voltage-dependent EPSPs and IPSPs, dendritic spike bursts and frequency-dependent synaptic facilitation support a sensory searchlight role for the direct feedback pathway; and (3) the contributions of distal and proximal inhibition, anti-Hebbian plasticity and beam versus isolated fiber activity patterns are discussed with reference to an adaptive spatio-temporal filtering role for the indirect descending pathway.


Behaviour ◽  
1970 ◽  
Vol 37 (1-2) ◽  
pp. 24-39 ◽  
Author(s):  
Peter J.B. Slater

AbstractAttempts to induce carrying of nest material in isolated male Bengalese finches by injecting testosterone, oestrogen, progesterone or prolactin were ineffective. Neither prolactin nor progesterone in the doses used appeared to affect incubation behaviour. There was a suggestion that prolactin depressed song numbers. Inexperienced birds are in general slower than experienced ones in settling down and starting to build. Monosexual male pairs start to carry more quickly when both partners have been kept in the same small group before pairing, than when they are from different groups. Most birds with previous breeding experience and which had been in the same group as their partners before pairing began to carry at a high rate immediately after pairing. The slight increase in carrying in the few days thereafter is probably attributable to the need to settle down in the new situation and to practice making a higher rate of carrying possible. It is probable that the hormonal state is appropriate for carrying at the time of pairing but that the 75% of males which do not carry in isolation are only stimulated to do so by the presence of a known mate, a nest site and an uncompleted nest. The main control of carrying thus appears to lie with external stimuli acting directly on the nervous system rather than through the meditation of endocrine changes. In the discussion it is suggested that direct effects of external stimuli may be more important in inducing long term behaviour changes during reproduction than has previously been supposed.


2001 ◽  
Vol 86 (2) ◽  
pp. 881-899 ◽  
Author(s):  
Pavel A. Gusev ◽  
Daniel L. Alkon

Despite many advances in our understanding of synaptic models of memory such as long-term potentiation and depression, cellular mechanisms that correlate with and may underlie behavioral learning and memory have not yet been conclusively determined. We used multiple intracellular recordings to study learning-specific modifications of intrinsic membrane and synaptic responses of the CA1 pyramidal cells (PCs) in slices of the rat dorsal hippocampus prepared at different stages of the Morris water maze (WM) task acquisition. Schaffer collateral stimulation evoked complex postsynaptic potentials (PSP) consisting of the excitatory and inhibitory postsynaptic potentials (EPSP and IPSP, respectively). After rats had learned the WM task, our major learning-specific findings included reduction of the mean peak amplitude of the IPSPs, delays in the mean peak latencies of the EPSPs and IPSPs, and correlation of the depolarizing-shifted IPSP reversal potentials and reduced IPSP-evoked membrane conductance. In addition, detailed isochronal analyses revealed that amplitudes of both early and late IPSP phases were reduced in a subset of the CA1 PCs after WM training was completed. These reduced IPSPs were significantly correlated with decreased IPSP conductance and with depolarizing-shifted IPSP reversal potentials. Input-output relations and initial rising slopes of the EPSP phase did not indicate learning-related facilitation as compared with the swim and naı̈ve controls. Another subset of WM-trained CA1 PCs had enhanced amplitudes of action potentials but no learning-specific synaptic changes. There were no WM training-specific modifications of other intrinsic membrane properties. These data suggest that long-term disinhibition in a subset of CA1 PCs may facilitate cell discharges that represent and record the spatial location of a hidden platform in a Morris WM.


1995 ◽  
Vol 74 (2) ◽  
pp. 841-848 ◽  
Author(s):  
E. W. Lothman ◽  
D. A. Rempe ◽  
P. S. Mangan

1. In this report we compare changes of excitatory neurotransmission within the CA1 region and the dentate gyrus (DG) in a model of chronic temporal lobe epilepsy (TLE). Extracellular and intracellular recordings were obtained from in vitro hippocampal-parahippocampal slices > or = 1 mo after a period of self-sustaining limbic status epilepticus (SSLSE) induced by continuous hippocampal stimulation. Pyramidal cells in CA1 were activated by electrodes in the stratum lacunosum/moleculare or stratum radiatum. Granule cells in DG were similarly activated by electrodes positioned in the perforant path. 2. Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked in CA1 pyramidal cells in post-SSLSE tissue were always longer than those evoked in control tissue, irrespective of whether hyperresponsiveness was present or not. EPSPs elicited by stimulus subthreshold for action potentials (APs) in post-SSLSE and in control slices and matched in amplitude had a statistically greater duration in the post-SSLSE slices. Durations of monosynaptic EPSPs elicited by stimuli subthreshold for APs in DG granule cells in post-SSLSE slices were not longer than EPSPs of equal amplitude elicited in control slices. 3. Higher-intensity stimuli produced EPSPs with associated APs and, in certain cases in the post-SSLSE tissue, hyperresponsive events with multiple (> or = 3) APs. Durations of depolarizing profiles with stimuli producing APs were overall longer in both CA1 pyramidal cells and DG granule cells and correlated with the degree of hyperresponsiveness. 4. Neither the amplitudes nor the durations of monosynaptic EPSPs evoked in CA1 pyramidal cells in slices from control animals were affected by the addition of D(-)-2-amino-5-phosphonovaleric acid (APV), a blocker of the N-methyl-D-aspartate (NMDA) receptor, to the artificial cerebrospinal fluid (ACSF) bathing the slices. In contrast to the situation in control tissue, in post-SSLSE tissue APV shortened EPSPs evoked in CA1 pyramidal cells while not changing their amplitudes. After APV, inhibitory postsynaptic potentials (IPSPs) remained greatly diminished or absent in CA1 pyramidal cells. APV did not statistically decrease amplitudes of monosynaptic EPSPs evoked in DG granule cells in either control slices or post-SSLSE slices. APV decreased EPSP durations in both types of slices, more so in the post-SSLSE tissue. 5. In control slices, APV did not change the amplitudes or durations of depolarizing profiles of responses evoked by stimuli producing APs in CA1. Similarly, APV did not change the amplitudes of such responses in DG. However, APV did reduce the durations of such responses in DG in control slices.(ABSTRACT TRUNCATED AT 400 WORDS)


2000 ◽  
Vol 149 (7) ◽  
pp. 1325-1334 ◽  
Author(s):  
Feng Wei ◽  
Zao C. Xu ◽  
Zhican Qu ◽  
Jeffrey Milbrandt ◽  
Min Zhuo

Hippocampal neurons fire spikes when an animal is at a particular location or performs certain behaviors in a particular place, providing a cellular basis for hippocampal involvement in spatial learning and memory. In a natural environment, spatial memory is often associated with potentially dangerous sensory experiences such as noxious or painful stimuli. The central sites for such pain-associated memory or plasticity have not been identified. Here we present evidence that excitatory glutamatergic synapses within the CA1 region of the hippocampus may play a role in storing pain-related information. Peripheral noxious stimulation induced excitatory postsynaptic potentials (EPSPs) in CA1 pyramidal cells in anesthetized animals. Tissue/nerve injury caused a rapid increase in the level of the immediate-early gene product Egr1 (also called NGFI-A, Krox24, or zif/268) in hippocampal CA1 neurons. In parallel, synaptic potentiation induced by a single tetanic stimulation (100 Hz for 1 s) was enhanced after the injury. This enhancement of synaptic potentiation was absent in mice lacking Egr1. Our data suggest that Egr1 may act as an important regulator of pain-related synaptic plasticity within the hippocampus.


1979 ◽  
Vol 42 (6) ◽  
pp. 1557-1570 ◽  
Author(s):  
L. W. Leung

1. The field potentials and unit activities evoked by the alvear tract (AT) in CA1 region of the dorsal hippocampus of rats were studied under sodium pentobarbital anesthesia. 2. The localized activity evoked anterior to an AT stimulus began as a compound action potential, followed by a slower negative wave, and ended in a long-lasting, slow positive wave. Observed with a 64-electrode recording array, topographical projections of the AT in CA1 were seen as parallel strips inclined at an angle of 5-30 degrees medially from the sagittal plane. 3. Three overlapping components in the averaged evoked potentials (AEPs) were distinguished. The first event (component I) was a brief compound antidromic action potential of pyramidal cells. The second field event (component II) reversed from surface negative to deep positive at 200 micrometer from the ventricular surface, increased rapidly with stimulus intensity, potentiated with double shocks, and followed stimulus frequency up to 50/s. The third component was long lasting (up to 200 ms), surface positive and ventral negative (turnover at 150 micron below the pyramidal layer), followed stimulus frequency up to about 10/s, and saturated at a low stimulus intensity (about 3 x threshold). 4. In some preparations, another fast negative peak of about 2 ms duration was found to follow the axon compound action potential on the hippocampal surface and appeared to propagate from the pyramidal layer to the ventricular surface. It was probably of nonsynaptic origin, perhaps due to the centrifugal basal dendritic spikes of the pyramidal cells. 5. Single units were recorded in CA1. Antidromic units were identified by their firing at a fixed latency (1.5 ms) and ability to follow high stimulus frequencies. Units firing at about 2.7 ms latency possessed characteristics of monosynaptic excitation. Under light anesthesia, many of the latter units also showed a late, prolonged suppression of background firing. Tentative interneuronal types fired with peak latencies of 4-5 ms or showed prolonged increase in firing rate. 6. From the correlation with unit post-stimulus time histograms, AEP component II was inferred to be the extracellular, monosynaptic, excitatory postsynaptic potentials, and component III the di- or polysynaptic inhibitory postsynaptic potentials. These postsynaptic potentials were generated by the pyramidal cells and interneurons.


2020 ◽  
Vol 118 (2) ◽  
pp. e2014157118
Author(s):  
Stephanie Rogers ◽  
Peter A. Rozman ◽  
Manuel Valero ◽  
Werner K. Doyle ◽  
György Buzsáki

How do firing patterns in a cortical circuit change when inhibitory neurons are excited? We virally expressed an excitatory designer receptor exclusively activated by a designer drug (Gq-DREADD) in all inhibitory interneuron types of the CA1 region of the hippocampus in the rat. While clozapine N-oxide (CNO) activation of interneurons suppressed firing of pyramidal cells, unexpectedly the majority of interneurons also decreased their activity. CNO-induced inhibition decreased over repeated sessions, which we attribute to long-term synaptic plasticity between interneurons and pyramidal cells. Individual interneurons did not display sustained firing but instead transiently enhanced their activity, interleaved with suppression of others. The power of the local fields in the theta band was unaffected, while power at higher frequencies was attenuated, likely reflecting reduced pyramidal neuron spiking. The incidence of sharp wave ripples decreased but the surviving ripples were associated with stronger population firing compared with the control condition. These findings demonstrate that DREADD activation of interneurons brings about both short-term and long-term circuit reorganization, which should be taken into account in the interpretation of chemogenic effects on behavior.


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