Nonsynaptic modulation of neuronal activity in the brain: electric currents and extracellular ions

1995 ◽  
Vol 75 (4) ◽  
pp. 689-723 ◽  
Author(s):  
J. G. Jefferys
Keyword(s):  
Electric Fields ◽  
Neuronal Activity ◽  
Neuronal Excitability ◽  
Physiological Activity ◽  
Electrical Coupling ◽  
Epileptic Seizures ◽  
Mammalian Brain ◽  
Chemical Coupling ◽  
Extracellular Ions ◽  
Chemical Synapses

Nonsynaptic interactions between neurons have been eclipsed by our increasingly detailed understanding of chemical synapses, but they do play significant roles in the nervous system. This review considers four classes of nonsynaptic interaction, mainly in mammalian brain. 1) Electrotonic (and chemical) coupling through gap junctions has effects during development and under some, often pathological, conditions in the mature brain. 2) Ephaptic transmission is mediated by electrical coupling between specific neuronal elements in the absence of specialized contacts, notably in the cerebellum, and in axon tracts affected by demyelination. 3) Field effect interactions are mediated by large extracellular currents and potential fields generated by the hippocampus and other cortical structures. Both endogenous and applied electric fields alter neuronal excitability at field strengths over a few millivolts per millimeter. Weaker fields have more subtle effects, for instance, on axonal growth during development and repair and, more controversially, in behavioral responses to environmental fields. 4) There are fluctuations in extracellular ions such as K+, which are released during neuronal activity and which alter neuronal excitability. Field effects and ion fluctuations probably have modest effects during physiological activity but have a significant impact on epileptic seizures, and can sustain them in the absence of synaptic transmission.

scholarly journals Response to coincident inputs in electrically coupled primary afferents is heterogeneous and is enhanced by H-current (IH) modulation

2019 ◽  
Vol 122 (1) ◽  
pp. 151-175
Author(s):  
Federico Davoine ◽  
Sebastian Curti
Keyword(s):  
Neuronal Excitability ◽  
Signal To Noise Ratio ◽  
Electrical Coupling ◽  
Primary Afferents ◽  
Coincidence Detection ◽  
Mammalian Brain ◽  
Electrical Transmission ◽  
Electrical Synapses ◽  
Electrophysiological Properties ◽  
Cationic Current

Electrical synapses represent a widespread modality of interneuronal communication in the mammalian brain. These contacts, by lowering the effectiveness of random or temporally uncorrelated inputs, endow circuits of coupled neurons with the ability to selectively respond to simultaneous depolarizations. This mechanism may support coincidence detection, a property involved in sensory perception, organization of motor outputs, and improvement signal-to-noise ratio. While the role of electrical coupling is well established, little is known about the contribution of the cellular excitability and its modulations to the susceptibility of groups of neurons to coincident inputs. Here, we obtained dual whole cell patch-clamp recordings of pairs of mesencephalic trigeminal (MesV) neurons in brainstem slices from rats to evaluate coincidence detection and its determinants. MesV neurons are primary afferents involved in the organization of orofacial behaviors whose cell bodies are electrically coupled mainly in pairs through soma-somatic gap junctions. We found that coincidence detection is highly heterogeneous across the population of coupled neurons. Furthermore, combined electrophysiological and modeling approaches reveal that this heterogeneity arises from the diversity of MesV neuron intrinsic excitability. Consistently, increasing these cells’ excitability by upregulating the hyperpolarization-activated cationic current ( IH) triggered by cGMP results in a dramatic enhancement of the susceptibility of coupled neurons to coincident inputs. In conclusion, the ability of coupled neurons to detect coincident inputs is critically shaped by their intrinsic electrophysiological properties, emphasizing the relevance of neuronal excitability for the many functional operations supported by electrical transmission in mammals. NEW & NOTEWORTHY We show that the susceptibility of pairs of coupled mesencephalic trigeminal (MesV) neurons to coincident inputs is highly heterogenous and depends on the interaction between electrical coupling and neuronal excitability. Additionally, upregulating the hyperpolarization-activated cationic current ( IH) by cGMP results in a dramatic increase of this susceptibility. The IH and electrical synapses have been shown to coexist in many neuronal populations, suggesting that modulation of this conductance could represent a common strategy to regulate circuit operation supported by electrical coupling.

scholarly journals Synchronization and chimera states in the network of electrochemically coupled memristive Rulkov neuron maps

2021 ◽  
Vol 18 (6) ◽  
pp. 9394-9409
Author(s):  
Mahtab Mehrabbeik ◽  
◽  
Fatemeh Parastesh ◽  
Janarthanan Ramadoss ◽  
Karthikeyan Rajagopal ◽  
...  
Keyword(s):  
High Speed ◽  
Phase Synchronization ◽  
Electrical Coupling ◽  
Amplitude Death ◽  
Collective Behaviors ◽  
Chimera State ◽  
Dynamical Behaviors ◽  
Chemical Coupling ◽  
Coupling Strengths ◽  
Chemical Synapses

<abstract> <p>Map-based neuronal models have received much attention due to their high speed, efficiency, flexibility, and simplicity. Therefore, they are suitable for investigating different dynamical behaviors in neuronal networks, which is one of the recent hottest topics. Recently, the memristive version of the Rulkov model, known as the m-Rulkov model, has been introduced. This paper investigates the network of the memristive version of the Rulkov neuron map to study the effect of the memristor on collective behaviors. Firstly, two m-Rulkov neuronal models are coupled in different cases, through electrical synapses, chemical synapses, and both electrical and chemical synapses. The results show that two electrically coupled memristive neurons can become synchronous, while the previous studies have shown that two non-memristive Rulkov neurons do not synchronize when they are coupled electrically. In contrast, chemical coupling does not lead to synchronization; instead, two neurons reach the same resting state. However, the presence of both types of couplings results in synchronization. The same investigations are carried out for a network of 100 m-Rulkov models locating in a ring topology. Different firing patterns, such as synchronization, lagged-phase synchronization, amplitude death, non-stationary chimera state, and traveling chimera state, are observed for various electrical and chemical coupling strengths. Furthermore, the synchronization of neurons in the electrical coupling relies on the network's size and disappears with increasing the nodes number.</p> </abstract>

scholarly journals Modeling temperature- and Cav3 subtype-dependent alterations in T-type calcium channel mediated burst firing

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Fernando R. Fernandez ◽  
Mircea C. Iftinca ◽  
Gerald W. Zamponi ◽  
Ray W. Turner
Keyword(s):  
Calcium Channel ◽  
Neuronal Excitability ◽  
Neuronal Firing ◽  
Mammalian Brain ◽  
Peripheral Tissues ◽  
Window Current ◽  
Modeling Data ◽  
The Brain ◽  
Firing Neuron ◽  
Cav3 Channel

AbstractT-type calcium channels are important regulators of neuronal excitability. The mammalian brain expresses three T-type channel isoforms (Cav3.1, Cav3.2 and Cav3.3) with distinct biophysical properties that are critically regulated by temperature. Here, we test the effects of how temperature affects spike output in a reduced firing neuron model expressing specific Cav3 channel isoforms. The modeling data revealed only a minimal effect on baseline spontaneous firing near rest, but a dramatic increase in rebound burst discharge frequency for Cav3.1 compared to Cav3.2 or Cav3.3 due to differences in window current or activation/recovery time constants. The reduced response by Cav3.2 could optimize its activity where it is expressed in peripheral tissues more subject to temperature variations than Cav3.1 or Cav3.3 channels expressed prominently in the brain. These tests thus reveal that aspects of neuronal firing behavior are critically dependent on both temperature and T-type calcium channel subtype.

scholarly journals Evaluation of Serum Calcium Levels in Patients with Epileptic Seizure

2020 ◽  
Vol 5 (2) ◽  
pp. 35-37
Author(s):  
Bushra Fiza ◽  
Maheep Sinha ◽  
Shalu Sharma ◽  
Sumit Kumar Tiwari
Keyword(s):  
Bone Metabolism ◽  
Serum Calcium ◽  
Epileptic Seizure ◽  
Neuronal Excitability ◽  
Epileptic Seizures ◽  
Bone Metabolism Markers ◽  
Mahatma Gandhi ◽  
Medical College ◽  
The Central Nervous System ◽  
Gandhi Medical College

ABSTRACT Introduction Epilepsy is a disorder of the central nervous system, characterized by an epileptic seizure. Epileptic seizures occur due to abnormal synchronous activity in the brain. Calcium is an essential component of bone. Hypocalcemia enhances neuronal excitability, and there are many causes of which include hypocalcemia, vitamin D deficiency, and PTH resistance. Materials and methods The study was conducted in Department of Biochemistry in association with the Department of Neurology of Mahatma Gandhi Medical College and Hospital, Jaipur. Fifty patients diagnosed for epileptic seizure and 50 controls, visiting the inpatient department (IPD) and outpatient department (OPD) of Neurology fulfilling the inclusion criteria, were enrolled for the study. Result The present study showed significantly lower level of serum calcium in patients with epileptic seizure when compared to controls. Conclusion The serum calcium was measured between epileptic seizure and controls. Our present study showed significantly lower value of calcium. It is therefore suggested that there should be regular screening for calcium in patients with epileptic seizure. The serum calcium is biomarker of bone metabolism; so, the correlation can be further studied with some more bone metabolism markers in epileptic seizure patients. How to cite this article Sharma S, Fiza B, Tiwari SK, et al. Evaluation of Serum Calcium Levels in Patients with Epileptic Seizure. J Mahatma Gandhi Univ Med Sci Tech 2020;5(2):35–37.

scholarly journals The role of thickness inhomogeneities in hierarchical cortical folding

2020 ◽  
Author(s):  
Lucas da Costa Campos ◽  
Raphael Hornung ◽  
Gerhard Gompper ◽  
Jens Elgeti ◽  
Svenja Caspers
Keyword(s):  
Fetal Brain ◽  
Epileptic Seizures ◽  
Quantitative Model ◽  
Higher Order ◽  
Mammalian Brain ◽  
Cortical Folding ◽  
Differential Growth ◽  
The Brain ◽  
Short Life Expectancy

AbstractThe morphology of the mammalian brain cortex is highly folded. For long it has been known that specific patterns of folding are necessary for an optimally functioning brain. On the extremes, lissencephaly, a lack of folds in humans, and polymicrogyria, an overly folded brain, can lead to severe mental retardation, short life expectancy, epileptic seizures, and tetraplegia. The construction of a quantitative model on how and why these folds appear during the development of the brain is the first step in understanding the cause of these conditions. In recent years, there have been various attempts to understand and model the mechanisms of brain folding. Previous works have shown that mechanical instabilities play a crucial role in the formation of brain folds, and that the geometry of the fetal brain is one of the main factors in dictating the folding characteristics. However, modeling higher-order folding, one of the main characteristics of the highly gyrencephalic brain, has not been fully tackled. The effects of thickness inhomogeneity in the gyrogenesis of the mammalian brain are studied in silico. Finite-element simulations of rectangular slabs are performed. The slabs are divided into two distinct regions, where the outer layer mimics the gray matter, and the inner layer the underlying white matter. Differential growth is introduced by growing the top layer tangentially, while keeping the underlying layer untouched. The brain tissue is modeled as a neo-Hookean hyperelastic material. Simulations are performed with both, homogeneous and inhomogeneous cortical thickness. The homogeneous cortex is shown to fold into a single wavelength, as is common for bilayered materials, while the inhomogeneous cortex folds into more complex conformations. In the early stages of development of the inhomogeneous cortex, structures reminiscent of the deep sulci in the brain are obtained. As the cortex continues to develop, secondary undulations, which are shallower and more variable than the structures obtained in earlier gyrification stage emerge, reproducing well-known characteristics of higher-order folding in the mammalian, and particularly the human, brain.

scholarly journals The Good, the Bad, and the Deadly: Adenosinergic Mechanisms Underlying Sudden Unexpected Death in Epilepsy

2021 ◽  
Vol 15 ◽  
Author(s):  
Benton Purnell ◽  
Madhuvika Murugan ◽  
Raja Jani ◽  
Detlev Boison
Keyword(s):  
Neuronal Activity ◽  
Neuronal Excitability ◽  
Receptor Activation ◽  
Sudden Unexpected Death ◽  
Unexpected Death ◽  
Neuroprotective Effects ◽  
Respiratory Dysfunction ◽  
Extracellular Adenosine ◽  
Hypoxic Conditions ◽  
Adenosine Signaling

Adenosine is an inhibitory modulator of neuronal excitability. Neuronal activity results in increased adenosine release, thereby constraining excessive excitation. The exceptionally high neuronal activity of a seizure results in a surge in extracellular adenosine to concentrations many-fold higher than would be observed under normal conditions. In this review, we discuss the multifarious effects of adenosine signaling in the context of epilepsy, with emphasis on sudden unexpected death in epilepsy (SUDEP). We describe and categorize the beneficial, detrimental, and potentially deadly aspects of adenosine signaling. The good or beneficial characteristics of adenosine signaling in the context of seizures include: (1) its direct effect on seizure termination and the prevention of status epilepticus; (2) the vasodilatory effect of adenosine, potentially counteracting postictal vasoconstriction; (3) its neuroprotective effects under hypoxic conditions; and (4) its disease modifying antiepileptogenic effect. The bad or detrimental effects of adenosine signaling include: (1) its capacity to suppress breathing and contribute to peri-ictal respiratory dysfunction; (2) its contribution to postictal generalized EEG suppression (PGES); (3) the prolonged increase in extracellular adenosine following spreading depolarization waves may contribute to postictal neuronal dysfunction; (4) the excitatory effects of A2A receptor activation is thought to exacerbate seizures in some instances; and (5) its potential contributions to sleep alterations in epilepsy. Finally, the adverse effects of adenosine signaling may potentiate a deadly outcome in the form of SUDEP by suppressing breathing and arousal in the postictal period. Evidence from animal models suggests that excessive postictal adenosine signaling contributes to the pathophysiology of SUDEP. The goal of this review is to discuss the beneficial, harmful, and potentially deadly roles that adenosine plays in the context of epilepsy and to identify crucial gaps in knowledge where further investigation is necessary. By better understanding adenosine dynamics, we may gain insights into the treatment of epilepsy and the prevention of SUDEP.

Epilepsy in later childhood and adulthood

2010 ◽  
pp. 4810-4826
Author(s):  
G.D. Perkin ◽  
M.R. Johnson
Keyword(s):  
Brain Imaging ◽  
Neuronal Activity ◽  
Case History ◽  
Epileptic Seizure ◽  
Neurological Disease ◽  
Epileptic Seizures ◽  
Social Consequences ◽  
Definition Of ◽  
The Brain ◽  
Structural Brain

Case History—A 33 yr old woman, known to have epilepsy, now presenting with odd behaviour. An epileptic seizure is a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. Epilepsy is defined as a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiological, cognitive, psychological, and social consequences of this condition. The definition of epilepsy requires the occurrence of at least one epileptic seizure and evidence for an enduring alteration in the brain that increases the likelihood of future seizures such as an ‘epileptiform’ EEG abnormality, an appropriate lesion on structural brain imaging (CT or MRI), or the presence of recurrent (two or more) seizures. Epilepsy is a common, serious neurological disease, with prevalence 1% and a cumulative lifetime risk of 5%....

scholarly journals Neuronal Hyperexcitability and Reduction of GABAA-Receptor Expression in the Surround of Cerebral Photothrombosis

1996 ◽  
Vol 16 (5) ◽  
pp. 906-914 ◽  
Author(s):  
Klaus Schiene ◽  
Claus Bruehl ◽  
Karl Zilles ◽  
Meishu Qu ◽  
Georg Hagemann ◽  
...  
Keyword(s):  
Gabaa Receptor ◽  
Rose Bengal ◽  
Sensorimotor Cortex ◽  
Neuronal Excitability ◽  
Epileptic Seizures ◽  
Receptor Expression ◽  
Aminobutyric Acid ◽  
Brain Areas ◽  
Series Of Experiments ◽  
The Rose

Changes of neuronal excitability and γ-aminobutyric acid (GABAA)-receptor expression were studied in the surround of photothrombotic infarcts, which were produced in the sensorimotor cortex of the rat by using the rose bengal technique. In a first series of experiments, multiunit recordings were performed on anesthetized animals 2–3 mm lateral from the lesion. Mean discharge frequency was considerably higher in recordings from lesioned animals (>100 Hz in the first postlesional week) compared with control animals (mean, 15 Hz). These alterations were already present after 1 day but were most pronounced 3 to 7 days after lesion induction. Thereafter the hyperexcitability declined again, although it remained visible up to 4 months. In a second series of experiments, the GABAA-receptor expression was studied autoradiographically. This revealed a reduction of GABAA receptors in widespread brain areas ipsilateral to the lesion. The reduction was most pronounced in the first days after lesion induction and declined with longer intervals. It is concluded that cortical infarction due to photothrombosis leads to a long-lasting and widespread reduction of GABAA-receptor expression in the surround of the lesion, which is associated with an increased neuronal excitability. Such alterations may be responsible for epileptic seizures that can be observed in some patients after stroke and may contribute to neurologic deficits after stroke.

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