Mechanisms of Serotonergic Facilitation of a Command Neuron

2007 ◽  
Vol 98 (6) ◽  
pp. 3494-3504 ◽  
Author(s):  
Brian L. Antonsen ◽  
Donald H. Edwards

The lateral giant (LG) command neuron of crayfish responds to an attack directed at the abdomen by triggering a single highly stereotyped escape tail flip. Experimentally applied serotonin (5-hydroxytrptamine, 5-HT) can increase or decrease LG's excitability, depending on the concentration, rate, and duration of 5-HT application. Here we describe three physiological mechanisms that mediate serotonergic facilitation of LG. Two processes strengthen electrical coupling between the primary mechanosensory afferent neurons and LG: first, an early increase in the conductance of electrical synapses between primary afferent neurons and LG dendrites and second, an early increase in the membrane resistance of LG dendrites. The increased coupling facilitates LG's synaptic response and it promotes recruitment of weakly excited afferent neurons to contribute to the response. Third, a delayed increase in the membrane resistance of proximal regions of LG increases the cell's input resistance near the initial segment. Together these mechanisms contribute to serotonergic facilitation of LG's response.

2021 ◽  
Author(s):  
Julie Haas ◽  
Austin Mendoza

Electrical synapses couple inhibitory neurons across the brain, underlying a variety of functions that are modifiable by activity. Despite recent advances, many basic functions and contributions of electrical synapses within neural circuitry remain underappreciated. Among these is the source and impact of electrical synapse asymmetry. Using multi-compartmental models of neurons coupled through dendritic electrical synapses, we investigated intrinsic factors that contribute to synaptic asymmetry and that result in modulation of spike time between coupled cells. We show that electrical synapse location along a dendrite, input resistance, internal dendritic resistance, or directional conduction of the electrical synapse itself each alter asymmetry as measured by coupling between cell somas. Conversely, true synapse asymmetry can be masked by each of these properties. Furthermore, we show that asymmetry alters the spiking timing and latency of coupled cells by up to tens of milliseconds, depending on direction of conduction or dendritic location of the electrical synapse. These simulations illustrate that causes of asymmetry are multifactorial, may not be apparent in somatic measurements of electrical coupling, influence dendritic processing, and produce a variety of outcomes on spike timing of coupled cells. Our findings highlight aspects of electrical synapses that should be considered in experimental demonstrations of coupling, and when assembling networks containing electrical synapses.


2010 ◽  
Vol 103 (3) ◽  
pp. 1456-1466 ◽  
Author(s):  
Margaret Lin Veruki ◽  
Leif Oltedal ◽  
Espen Hartveit

AII amacrine cells in the mammalian retina are connected via electrical synapses to on-cone bipolar cells and to other AII amacrine cells. To understand synaptic integration in these interneurons, we need information about the junctional conductance ( gj), the membrane resistance ( rm), the membrane capacitance ( Cm), and the cytoplasmic resistivity ( Ri). Due to the extensive electrical coupling, it is difficult to obtain estimates of rm, as well as the relative contribution of the junctional and nonjunctional conductances to the total input resistance of an AII amacrine cell. Here we used dual voltage-clamp recording of pairs of electrically coupled AII amacrine cells in an in vitro slice preparation from rat retina and applied meclofenamic acid (MFA) to block the electrical coupling and isolate single AII amacrines electrically. In the control condition, the input resistance ( Rin) was ∼620 MΩ and the apparent rm was ∼760 MΩ. After block of electrical coupling, determined by estimating gj in the dual recordings, Rin and rm were ∼4,400 MΩ, suggesting that the nongap junctional conductance of an AII amacrine cell is ∼16% of the total input conductance. Control experiments with nucleated patches from AII amacrine cells suggested that MFA had no effect on the nongap junctional membrane of these cells. From morphological reconstructions of AII amacrine cells filled with biocytin, we obtained a surface area of ∼900 μm2 which, with a standard value for Cm of 0.01 pF/μm2, corresponds to an average capacitance of ∼9 pF and a specific membrane resistance of ∼41 kΩ cm2. Together with information concerning synaptic connectivity, these data will be important for developing realistic compartmental models of the network of AII amacrine cells.


1980 ◽  
Vol 84 (1) ◽  
pp. 187-199
Author(s):  
D. Mellon ◽  
G. Lnenicka

The morphologies and passive electrical parameters of fibres in two eye muscles of a surface- and a cave-dwelling crayfish were compared. In the cave-dwelling form the muscles contained fewer fibres, of less diameter, and hence had a smaller cross-sectional area. Current-voltage relationships were similar in both species. Input resistance was higher in the cave-dweller, but the difference was not as great as would be expected on the basis of geometry alone. Accordingly, the specific membrane resistance of muscle fibres in the cave-dweller is 50–60% smaller than that in the surface-dweller. This may account partially for the observation that identified excitatory junctional potentials in muscles of cave- and surface dwellers have similar amplitudes. We conclude that a functional oculomotor system is maintained in cave-dwelling crayfish, and that this system confers some positive selective advantage.


1990 ◽  
Vol 258 (1) ◽  
pp. H145-H152 ◽  
Author(s):  
O. F. Schanne ◽  
M. Lefloch ◽  
B. Fermini ◽  
E. Ruiz-Petrich

We compared the passive electrical properties of isolated ventricular myocytes (resting potential -65 mV, fast action potentials, and no spontaneous activity) with those of 2- to 7-day-old cultured ventricle cells from neonatal rats (resting potential -50 mV, slow action potentials, and presence of spontaneous activity). In myocytes the specific membrane capacity was 0.99 microF/cm2, and the specific membrane resistance increased from 2.46 k omega.cm2 at -65 mV to 7.30 k omega.cm2 at -30 mV. In clusters, the current-voltage relationships measured under current-clamp conditions showed anomalous rectification and the input resistance decreased from 1.05 to 0.48 M omega when external K+ concentration was increased from 6 to 100 mM. Using the model of a finite disk we determined the specific membrane resistance (12.9 k omega.cm2), the effective membrane capacity (17.8 microF/cm2), and the lumped resistivity of the disk interior (1,964 omega.cm). We conclude that 1) the voltage dependence of the specific membrane resistance cannot completely explain the membrane resistance increase that accompanies the appearance of spontaneous activity; 2) a decrease of the inwardly rectifying conductance (gk1) is mainly responsible for the increase in the specific membrane resistance and depolarization; and 3) approximately 41% of the inward-rectifying channels are electrically silent when spontaneous activity develops in explanted ventricle cells.


1991 ◽  
Vol 65 (3) ◽  
pp. 736-746 ◽  
Author(s):  
W. R. Schlue

1. The intracellular K+, Na+, and Ca2+ of mechanosensory neurons in the central nervous system of the leech Hirudo medicinalis was measured using double-barreled ion-sensitive microelectrodes. 2. After inhibition of the Na(+)-K+ pump with 5 x 10(-4) M ouabain, the intracellular K+ activity (aKi) decreased, while the intracellular Na+ activity (aNai) increased. The input resistance decreased in the presence of ouabain. The intracellular Ca2+ increased more than one order of magnitude after ouabain addition. All changes in intracellular ion activities and membrane resistance were fully reversible. 3. When extracellular Na+ concentration ([Na+]o) was removed [replaced by tris(hydroxymethyl)aminomethane (Tris)], aNai decreased. In the absence of [Na+]o, aKi and aNai remained unchanged after inhibition of the Na(+)-K+ pump by reducing the extracellular K+ concentration ([K+]o) to 0.2 mM. The membrane resistance increased under these conditions. 4. The intracellular Ca2+ decreased or remained constant after removal of [Na+]o. Addition of ouabain in the absence of [Na+]o did not change intracellular Ca2+, which only increased after readdition of [Na+]o. 5. The relative K+ permeability (PK) measured as membrane potential change during a brief increase of the [K+]o from 4 to 10 mM, increased manyfold after addition of ouabain but only little if [Na+]o had been removed before adding ouabain. 6. The results suggest that the intracellular Na+ increase after inhibition of the Na(+)-K+ pump affects the intracellular Ca2+ level by stimulating a Nai(+)-Ca2+ exchange mechanism. The subsequent intracellular Ca2+ activity (aCai) rise may result in an increase of the membrane permeability to K+ ions.


2000 ◽  
Vol 279 (1) ◽  
pp. H250-H259 ◽  
Author(s):  
Delilah J. Huelsing ◽  
Kenneth W. Spitzer ◽  
Andrew E. Pollard

Many studies suggest that early afterdepolarizations (EADs) arising from Purkinje fibers initiate triggered arrhythmias under pathological conditions. However, electrotonic interactions between Purkinje and ventricular myocytes may either facilitate or suppress EAD formation at the Purkinje-ventricular interface. To determine conditions that facilitated or suppressed EADs during Purkinje-ventricular interactions, we coupled single Purkinje myocytes and aggregates isolated from rabbit hearts to a passive model cell via an electronic circuit with junctional resistance ( R j). The model cell had input resistance ( R m,v) of 50 MΩ, capacitance of 39 pF, and a variable rest potential ( V rest,v). EADs were induced in Purkinje myocytes during superfusion with 1 μM isoproterenol. Coupling at high R j to normally polarized V rest,v established a repolarizing coupling current during all phases of the Purkinje action potential. This coupling current preferentially suppressed EADs in single cells with mean membrane resistance ( R m,p) of 297 MΩ, whereas EAD suppression in larger aggregates with mean R m,p of 80 MΩ required larger coupling currents. In contrast, coupling to elevated V rest,v established a depolarizing coupling current during late phase 2, phase 3, and phase 4 that facilitated EAD formation and induced spontaneous activity in single Purkinje myocytes and aggregates. These results have important implications for arrhythmogenesis in the infarcted heart when reduction of the ventricular mass due to scarring alters the R m,p-to- R m,v ratio and in the ischemic heart when injury currents are established during coupling between polarized Purkinje myocytes and depolarized ventricular myocytes.


2000 ◽  
Vol 279 (4) ◽  
pp. F747-F754 ◽  
Author(s):  
R. Masia ◽  
D. Aneshansley ◽  
W. Nagel ◽  
R. J. Nachman ◽  
K. W. Beyenbach

Principal cells of the Malpighian tubule of the yellow fever mosquito were studied with the methods of two-electrode voltage clamp (TEVC). Intracellular voltage ( V pc) was −86.7 mV, and input resistance ( R pc) was 388.5 kΩ ( n = 49 cells). In six cells, Ba2+ (15 mM) had negligible effects on V pc, but it increased R pc from 325.3 to 684.5 kΩ ( P< 0.001). In the presence of Ba2+, leucokinin-VIII (1 μM) increased V pc to −101.8 mV ( P < 0.001) and reduced R pc to 340.2 kΩ ( P < 0.002). Circuit analysis yields the following: basolateral membrane resistance, 652.0 kΩ; apical membrane resistance, 340.2 kΩ; shunt resistance ( R sh), 344.3 kΩ; transcellular resistance, 992.2 kΩ. The fractional resistance of the apical membrane (0.35) and the ratio of transcellular resistance and R sh (3.53) agree closely with values obtained by cable analysis in isolated perfused tubules and confirm the usefulness of TEVC methods in single principal cells of the intact Malpighian tubule. Dinitrophenol (0.1 mM) reversibly depolarized V pc from −94.3 to −10.7 mV ( P< 0.001) and reversibly increased R pc from 412 to 2,879 kΩ ( P < 0.001), effects that were duplicated by cyanide (0.3 mM). Significant effects of metabolic inhibition on voltage and resistance suggest a role of ATP in electrogenesis and the maintenance of conductive transport pathways.


2019 ◽  
Vol 122 (1) ◽  
pp. 151-175
Author(s):  
Federico Davoine ◽  
Sebastian Curti

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.


1978 ◽  
Vol 234 (3) ◽  
pp. C90-C95 ◽  
Author(s):  
J. Grossie

Basic mechanical and electrical properties of rat extensor muscle were analyzed 4--6 wk after thyroid removal. Isometric twitch tensions in thyroidectomized (Tx) rat muscle varied considerably, with over 60% of the muscles showing abnormally low values and the remainder showing a high twitch force. The duration of the twitch was significantly increased from 137 to 245 ms but contraction and half-relaxation times were not significantly changed. Tetanic force was not effected by thyroidectomy. Electrical properties of the muscle fiber membranes were made exclusively via intracellular techniques. The resting membrane potential was slightly higher in thyroidectomized rats (-79 mV) as compared to sham controls (-78 mV). Both direct and indirect action potentials showed higher overshoots, amplitudes, and rates of depolarization in thyroidectomized rats. The threshold of the indirect action potential appeared at a higher transmembrane potential as compared to sham-operated controls. The input resistance, space constant, time constant, and specific membrane resistance were all significantly increased in thyroidectomized rat extensor muscle, whereas fiber diameter and capacitance were significantly decreased. Estimates of specific ionic conductance show that both potassium and chloride conductance are decreased in thyroidectomized rat muscle.


1969 ◽  
Vol 53 (5) ◽  
pp. 530-540 ◽  
Author(s):  
H. A. Fozzard ◽  
G. Dominguez

The effects of formaldehyde, glutaraldehyde, 1-fluoro-2,4-dinitrobenzene, and 1,5-difluoro-2,4-dinitrobenzene on the electrophysiological properties of cardiac Purkinje fibers were studied. At concentrations of 2.5 mM the aldehydes produced a transient hyperpolarization, lengthening of the plateau of the action potential, and an increase in action potential overshoot and upstroke velocity. If exposure to aldehyde was continued, the fiber failed to repolarize after an action potential and the membrane potential stabilized at about -30 mv. If exposure was terminated before this, recovery was usually complete. At the time the fibers were hyperpolarized the input resistance was increased without much change in length constant, leading to an increase in both calculated membrane resistance and calculated core resistance. Although it was anticipated that an effect of the aldehydes on the membrane was to increase fixed negative charge, it was difficult to explain all the electrophysiological changes on this basis. The major effects of the fluorobenzene compounds were not the same; they produced a shortening of the action potential and a rapid loss of excitability.


Sign in / Sign up

Export Citation Format

Share Document