scholarly journals Noise and Coupling Affect Signal Detection and Bursting in a Simulated Physiological Neural Network

2002 ◽  
Vol 88 (5) ◽  
pp. 2598-2611 ◽  
Author(s):  
William C. Stacey ◽  
Dominique M. Durand
Keyword(s):  
Signal Detection ◽  
Epileptiform Activity ◽  
Electrical Coupling ◽  
Periodic Signal ◽  
Physiological Noise ◽  
Ca1 Neurons ◽  
Ca1 Region ◽  
Noise Characteristics ◽  
Hippocampal Ca1

Signal detection in the CNS relies on a complex interaction between the numerous synaptic inputs to the detecting cells. Two effects, stochastic resonance (SR) and coherence resonance (CR) have been shown to affect signal detection in arrays of basic neuronal models. Here, an array of simulated hippocampal CA1 neurons was used to test the hypothesis that physiological noise and electrical coupling can interact to modulate signal detection in the CA1 region of the hippocampus. The array was tested using varying levels of coupling and noise with different input signals. Detection of a subthreshold signal in the network improved as the number of detecting cells increased and as coupling was increased as predicted by previous studies in SR; however, the response depended greatly on the noise characteristics present and varied from SR predictions at times. Careful evaluation of noise characteristics may be necessary to form conclusions about the role of SR in complex systems such as physiological neurons. The coupled array fired synchronous, periodic bursts when presented with noise alone. The synchrony of this firing changed as a function of noise and coupling as predicted by CR. The firing was very similar to certain models of epileptiform activity, leading to a discussion of CR as a possible simple model of epilepsy. A single neuron was unable to recruit its neighbors to a periodic signal unless the signal was very close to the synchronous bursting frequency. These findings, when viewed in comparison with physiological parameters in the hippocampus, suggest that both SR and CR can have significant effects on signal processing in vivo.

scholarly journals Reappearance of Hippocampal CA1 Neurons after Ischemia is Associated with Recovery of Learning and Memory

2005 ◽  
Vol 25 (12) ◽  
pp. 1586-1595 ◽  
Author(s):  
Olof Bendel ◽  
Tjerk Bueters ◽  
Mia von Euler ◽  
Sven Ove Ögren ◽  
Johan Sandin ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Cognitive Functions ◽  
Spatial Learning And Memory ◽  
Neuronal Marker ◽  
Ca1 Neurons ◽  
Ca1 Region ◽  
Hippocampal Ca1 ◽  
The Brain

The pyramidal neurons of the hippocampal CA1 region are essential for cognitive functions such as spatial learning and memory, and are selectively destroyed after cerebral ischemia. To analyze whether degenerated CA1 neurons are replaced by new neurons and whether such regeneration is associated with amelioration in learning and memory deficits, we have used a rat global ischemia model that provides an almost complete disappearance (to approximately 3% of control) of CA1 neurons associated with a robust impairment in spatial learning and memory at two weeks after ischemia. We found that transient cerebral ischemia can evoke a massive formation of new neurons in the CA1 region, reaching approximately 40% of the original number of neurons at 90 days after ischemia (DAI). Co-localization of the mature neuronal marker neuronal nuclei with 5-bromo-2'-deoxyuridine in CA1 confirmed that neurogenesis indeed had occurred after the ischemic insult. Furthermore, we found increased numbers of cells expressing the immature neuron marker polysialic acid neuronal cell adhesion molecule in the adjacent lateral periventricular region, suggesting that the newly formed neurons derive from this region. The reappearance of CA1 neurons was associated with a recovery of ischemia-induced impairments in spatial learning and memory at 90 DAI, suggesting that the newly formed CA1 neurons restore hippocampal CA1 function. In conclusion, these results show that the brain has an endogenous capacity to form new nerve cells after injury, which correlates with a restoration of cognitive functions of the brain.

scholarly journals A Possible Link Between HCN Channels and Depression

2018 ◽  
Vol 2 ◽  
pp. 247054701878778 ◽  
Author(s):  
Chung Sub Kim ◽  
Daniel Johnston
Keyword(s):  
Protein Expression ◽  
Neuronal Excitability ◽  
Acute Stress ◽  
Hcn Channels ◽  
Chronic Unpredictable Stress ◽  
Ca1 Neurons ◽  
Ca1 Region ◽  
Hcn1 Channels ◽  
The Brain

Growing evidence suggests a possible link between hyperpolarization-activated cyclic nucleotide-gated nonselective cation (HCN) channels and depression. In a recent study published in Molecular Psychiatry, we first demonstrate that Ih (the membrane current mediated by HCN channels) and HCN1 protein expression were increased in dorsal, but not in ventral, CA1 region following chronic, but not acute stress. This upregulation of Ih was restricted to the perisomatic region of CA1 neurons and contributed to a reduction of neuronal excitability. A reduction of HCN1 protein expression in dorsal CA1 region before the onset of chronic unpredictable stress-induced depression was sufficient to provide resilient effects to chronic unpredictable stress. Furthermore, in vivo block of the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) pumps, a manipulation known to increase intracellular calcium levels and upregulate Ih, produced anxiogenic-like behavior and an increase in Ih, similar to that observed in chronic unpredictable stress model of depression. Here, we share our view on (1) how the function and expression of HCN1 channels are changed in the brain in a subcellular region-specific manner during the development of depression and (2) how a reduction of HCN1 protein expression provides resilience to chronic stress.

scholarly journals Different Effects of Monophasic Pulses and Biphasic Pulses Applied by a Bipolar Stimulation Electrode in the Rat Hippocampal CA1 Region

2020 ◽  
Author(s):  
Yue Yuan ◽  
Lvpiao Zheng ◽  
Zhouyan Feng ◽  
Gangsheng Yang
Keyword(s):  
Animal Experiments ◽  
Neuronal Firing ◽  
Brain Diseases ◽  
Neuron Activity ◽  
Neuronal Responses ◽  
Population Spikes ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1

Abstract Background: Deep brain stimulation (DBS) has been successfully used for treating certain brain diseases such as movement disorders. High-frequency stimulations (HFS) of charge-balanced biphasic pulses have been used in clinic DBS to minimize the risk of tissue damages caused by the electrical stimulations, while HFS sequences of monophasic pulses have been used in animal experiments to investigate DBS therapy. However, it is not clear whether HFS sequences of monophasic pulses could induce abnormal neuronal responses different from biphasic pulses. Thus, the present study investigates the differences of neuronal responses to HFS of monophasic pulses and biphasic pulses.Methods: Orthodromic-HFS (O-HFS) and antidromic-HFS (A-HFS) of the two types of pulses (with a 1-min duration) were delivered by bipolar electrodes to the Schaffer collaterals (i.e., afferent fibers) and the alveus fibers (i.e., efferent fibers) of the rat hippocampal CA1 region in-vivo, respectively. Responses of CA1 pyramidal neurons to the stimulations were recorded in the CA1 region. Single pulses of antidromic- and orthodromic-test stimuli were applied before and after HFS to evoke population spikes for evaluating the baseline and the recovery of neuronal activity. Results: Spreading depression (SD) appeared during sequences of 200 Hz monophasic O-HFS with a high incidence (4/5), but did not appear during corresponding 200 Hz biphasic O-HFS (0/6). The potential waveform of SD was accompanied by a preceding burst of population spikes, propagated slowly, silenced neuronal firing temporarily and resulted in a non-recovery of orthodromically-evoked population spikes (OPS) after the O-HFS. No SD events appeared during the O-HFS with a lower frequency of 100 Hz of monophasic and biphasic pulses (0/5 and 0/6, respectively) nor during the A-HFS of 200 Hz pulses (0/9). However, the antidromically-evoked population spikes (APS) only recovered partially after the 200 Hz A-HFS of monophasic pulses.Conclusions: The O-HFS with a high enough frequency of monophasic pulses may induce the abnormal neuron activity of SD instantaneously, which may be used as a biomarker to warn the damages caused by improper stimulations in brain tissues.

Low, but Not High, Doses of Copper Sulfate Impair Synaptic Plasticity in the Hippocampal CA1 Region In Vivo

2018 ◽  
Vol 185 (1) ◽  
pp. 143-147 ◽  
Author(s):  
Abolfazl Jand ◽  
Mohammad Reza Taheri-nejad ◽  
Masoumeh Mosleh ◽  
Mohammad Reza Palizvan
Keyword(s):  
Synaptic Plasticity ◽  
Copper Sulfate ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hippocampal Ca1 ◽  
High Doses

Decrease in Synaptic Transmission Can Reverse the Propagation Direction of Epileptiform Activity in Hippocampus In Vivo

2005 ◽  
Vol 93 (3) ◽  
pp. 1158-1164 ◽  
Author(s):  
Zhouyan Feng ◽  
Dominique M. Durand
Keyword(s):  
Synaptic Transmission ◽  
Epileptiform Activity ◽  
Epileptic Activity ◽  
Propagation Direction ◽  
Synaptic Activity ◽  
Multiple Channel ◽  
Ca1 Region ◽  
Partial Suppression

Most types of epileptiform activity with synaptic transmission have been shown to propagate from the CA3 to CA1 region in hippocampus. However, nonsynaptic epileptiform activity induced in vitro is known to propagate slowly from the caudal end of CA1 toward CA2/CA3. Understanding the propagation modes of epileptiform activity, and their causality is important to revealing the underlying mechanisms of epilepsy and developing new treatments. In this paper, the effect of the synaptic transmission suppression on the propagation of epilepsy in vivo was investigated by using multiple-channel recording probes in CA1. Nonsynaptic epileptiform activity was induced by calcium chelator EGTA with varied concentrations of potassium. For comparison, disinhibition synaptic epileptiform activity was induced by picrotoxin (PTX) with or without partial suppression of excitatory synaptic transmission. The propagation velocity was calculated by measuring the time delay between two electrodes separated by a known distance. The results show that in vivo nonsynaptic epileptiform activity propagates with a direction and velocity comparable to those observed in in vitro preparations. The direction of propagation for nonsynaptic activity is reversed from the PTX-induced synaptic activity. A reversal in propagation direction and change in velocity were also observed dynamically during the process of synaptic transmission suppression. Even a partial suppression of synaptic transmission was sufficient to significantly change the propagation direction and velocity of epileptiform activity. These results suggest the possibility that the measurement of propagation can provide important information about the synaptic mechanism underlying epileptic activity.

scholarly journals Selective Neuronal Vulnerability of Human Hippocampal CA1 Neurons: Lesion Evolution, Temporal Course, and Pattern of Hippocampal Damage in Diffusion-Weighted MR Imaging

2015 ◽  
Vol 35 (11) ◽  
pp. 1836-1845 ◽  
Author(s):  
Thorsten Bartsch ◽  
Juliane Döhring ◽  
Sigrid Reuter ◽  
Carsten Finke ◽  
Axel Rohr ◽  
...  
Keyword(s):  
Time Course ◽  
Transient Global Amnesia ◽  
Hippocampal Damage ◽  
Valuable Insight ◽  
Ca1 Neurons ◽  
Ca1 Region ◽  
Hippocampal Ca1 ◽  
Temporal Course ◽  
Cornu Ammonis ◽  
Global Amnesia

The CA1 (cornu ammonis) region of hippocampus is selectively vulnerable to a variety of metabolic and cytotoxic insults, which is mirrored in a delayed neuronal death of CA1 neurons. The basis and mechanisms of this regional susceptibility of CA1 neurons are poorly understood, and the correlates in human diseases affecting the hippocampus are not clear. Adopting a translational approach, the lesion evolution, temporal course, pattern of diffusion changes, and damage in hippocampal CA1 in acute neurologic disorders were studied using high-resolution magnetic resonance imaging. In patients with hippocampal ischemia ( n = 50), limbic encephalitis ( n = 30), after status epilepticus ( n = 17), and transient global amnesia ( n = 53), the CA1 region was selectively affected compared with other CA regions of the hippocampus. CA1 neurons exhibited a maximum decrease of apparent diffusion coefficient (ADC) 48 to 72 hours after the insult, irrespective of the nature of the insult. Hypoxic-ischemic insults led to a significant lower ADC suggesting that the ischemic insult results in a stronger impairment of cellular metabolism. The evolution of diffusion changes show that CA1 diffusion lesions mirror the delayed time course of the pathophysiologic cascade typically observed in animal models. Studying the imaging correlates of hippocampal damage in humans provides valuable insight into the pathophysiology and neurobiology of the hippocampus.

Sign in / Sign up

Export Citation Format

Share Document