Sustained excitatory synaptic input to motor cortex neurons in awake animals revealed by intracellular recording of membrane potentials

1988 ◽  
Vol 70 (3) ◽  
Author(s):  
M. Matsumura ◽  
T. Cope ◽  
E.E. Fetz
Keyword(s):  
Motor Cortex ◽  
Synaptic Input ◽  
Intracellular Recording ◽  
Membrane Potentials ◽  
Excitatory Synaptic Input

Tachykinins mediate slow excitatory postsynaptic transmission in guinea pig sphincter of Oddi ganglia

2001 ◽  
Vol 281 (2) ◽  
pp. G357-G364 ◽  
Author(s):  
Brian P. Manning ◽  
Gary M. Mawe
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Receptor Antagonist ◽  
Synaptic Input ◽  
Intracellular Recording ◽  
Small Diameter ◽  
Sphincter Of Oddi ◽  
Receptor Desensitization ◽  
Afferent Fibers ◽  
Excitatory Synaptic Input

Intracellular recording techniques were used to test whether tachykinins could be mediators of slow excitatory postsynaptic potentials (EPSPs) in guinea pig sphincter of Oddi (SO) ganglia. Application of the tachykinin substance P (SP) onto SO neurons caused a prolonged membrane depolarization that was reminiscent of the slow EPSP in these cells. Pressure ejection of the neurokinin 3 (NK3) receptor-specific agonist senktide caused a similar depolarization; however, no responses were detected on application of NK1 or NK2 receptor agonists. The NK3 receptor antagonist SR-142801 (100 nM) significantly inhibited both SP-induced depolarization and the stimulation-evoked slow EPSP, as did NK3 receptor desensitization with senktide. Capsaicin, which causes the release of SP from small-diameter afferent fibers, induced a depolarization that was similar to the evoked slow EPSP in both amplitude and duration. The capsaicin-induced depolarization was significantly attenuated in the presence of SR-142801. These data indicate that tachykinins, released from extrinsic afferent fibers, act via NK3 receptors to provide slow excitatory synaptic input to SO neurons.

Inhibition of Glutamatergic Synaptic Input to Spinal Lamina IIo Neurons by Presynaptic α2-Adrenergic Receptors

2002 ◽  
Vol 87 (4) ◽  
pp. 1938-1947 ◽  
Author(s):  
Yu-Zhen Pan ◽  
De-Pei Li ◽  
Hui-Lin Pan
Keyword(s):  
Receptor Antagonist ◽  
Synaptic Input ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Dorsal Root ◽  
Primary Afferents ◽  
Noradrenergic System ◽  
Analgesic Action ◽  
Adrenergic Agonists ◽  
Excitatory Synaptic Input

Activation of spinal α2-adrenergic receptors by the descending noradrenergic system and α2-adrenergic agonists produces analgesia. However, the sites and mechanisms of the analgesic action of spinally administered α2-adrenergic receptor agonists such as clonidine are not fully known. The dorsal horn neurons in the outer zone of lamina II (lamina IIo) are important for processing nociceptive information from C-fiber primary afferents. In the present study, we tested a hypothesis that activation of presynaptic α2-adrenergic receptors by clonidine inhibits the excitatory synaptic input to lamina IIo neurons. Whole cell voltage-clamp recordings were performed on visualized lamina IIo neurons in the spinal cord slice of rats. The miniature excitatory postsynaptic currents (mEPSCs) were recorded in the presence of tetrodotoxin, bicuculline, and strychnine. The evoked EPSCs were obtained by electrical stimulation of the dorsal root entry zone or the attached dorsal root. Both mEPSCs and evoked EPSCs were abolished by application of 6-cyano-7-nitroquinoxaline-2,3-dione. Clonidine (10 μM) significantly decreased the frequency of mEPSCs from 5.8 ± 0.9 to 2.7 ± 0.6 Hz (means ± SE) without altering the amplitude and the decay time constant of mEPSCs in 25 of 27 lamina IIo neurons. Yohimbine (2 μM, an α2-adrenergic receptor antagonist), but not prazosin (2 μM, an α1-adrenergic receptor antagonist), blocked the inhibitory effect of clonidine on the mEPSCs. Clonidine (1–20 μM, n = 8) also significantly attenuated the peak amplitude of evoked EPSCs in a concentration-dependent manner. The effect of clonidine on evoked EPSCs was abolished in the presence of yohimbine ( n = 5). These data suggest that clonidine inhibits the excitatory synaptic input to lamina IIo neurons through activation of α2-adrenergic receptors located on the glutamatergic afferent terminals. Presynaptic inhibition of glutamate release from primary afferents onto lamina IIoneurons likely plays an important role in the analgesic action produced by activation of the descending noradrenergic system and α2-adrenergic agonists.

PHASE DEPENDENT TRANSITION BETWEEN MULTISTABLE STATES IN A NEURAL NETWORK WITH RECIPROCAL INHIBITION

2004 ◽  
Vol 14 (05) ◽  
pp. 1559-1575 ◽  
Author(s):  
KATSUMI TATENO ◽  
HIDEYUKI TOMONARI ◽  
HATSUO HAYASHI ◽  
SATORU ISHIZUKA
Keyword(s):  
Neural Network ◽  
Network Model ◽  
Neural Network Model ◽  
Synaptic Input ◽  
Reciprocal Inhibition ◽  
Conduction Delay ◽  
Inhibitory Connection ◽  
Pacemaker Neurons ◽  
Excitatory Synaptic Input ◽  
Multistable State

We studied multistable oscillatory states of a small neural network model and switching of an oscillatory mode. In the present neural network model, two pacemaker neurons are reciprocally inhibited with conduction delay; one pacemaker neuron inhibits the other via an inhibitory nonpacemaker interneuron, and vice versa. The small network model shows bifurcations from quasi-periodic oscillation to chaos via period 3 with increase in the synaptic weight of the reciprocal inhibition. The route to chaos in the network model is different from that in the single pacemaker neuron. The network model exhibits several multistable states. In a regime of a weak inhibitory connection, in-phase beat, out-of-phase beat (period 3), and chaotic oscillation coexist at the multistable state. We can switch an oscillatory mode by an excitatory synaptic input to one of the pacemaker neurons through an afferent path. In a strong inhibitory connection regime, in-phase beat and out-of-phase beat (period 4) coexist at the multistable state. An excitatory synaptic input through the afferent path leads to the transition from the in-phase beat to the out-of-phase beat. The transition from the out-of-phase beat to the in-phase beat is induced by an inhibitory synaptic input via interneurons. A conduction delay, furthermore, causes the spontaneous transition from the in-phase beat to the out-of-phase beat. These transitions can be explained by phase response curves.

scholarly journals The principal neurons of the medial nucleus of the trapezoid body and NG2+ glial cells receive coordinated excitatory synaptic input

2009 ◽  
Vol 134 (2) ◽  
pp. 115-127 ◽  
Author(s):  
Jochen Müller ◽  
Daniel Reyes-Haro ◽  
Tatjyana Pivneva ◽  
Christiane Nolte ◽  
Roland Schaette ◽  
...  
Keyword(s):  
Glial Cell ◽  
Glial Cells ◽  
Synaptic Input ◽  
Medial Nucleus ◽  
Synaptic Structure ◽  
Excitatory Synaptic Input ◽  
Cell Processes ◽  
To Receive ◽  
Trapezoid Body ◽  
Axosomatic Synapse

Glial cell processes are part of the synaptic structure and sense spillover of transmitter, while some glial cells can even receive direct synaptic input. Here, we report that a defined type of glial cell in the medial nucleus of the trapezoid body (MNTB) receives excitatory glutamatergic synaptic input from the calyx of Held (CoH). This giant glutamatergic terminal forms an axosomatic synapse with a single principal neuron located in the MNTB. The NG2 glia, as postsynaptic principal neurons, establish synapse-like structures with the CoH terminal. In contrast to the principal neurons, which are known to receive excitatory as well as inhibitory inputs, the NG2 glia receive mostly, if not exclusively, α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor–mediated evoked and spontaneous synaptic input. Simultaneous recordings from neurons and NG2 glia indicate that they partially receive synchronized spontaneous input. This shows that an NG2+ glial cell and a postsynaptic neuron share presynaptic terminals.

Electrophysiology of Acanthocephalan Body Wall Muscles

1979 ◽  
Vol 82 (1) ◽  
pp. 273-280
Author(s):  
B. S. WONG ◽  
DONALD M. MILLER ◽  
T. T. DUNAGAN
Keyword(s):  
Light Microscopy ◽  
Intracellular Recording ◽  
Body Wall ◽  
Membrane Potentials ◽  
The Body ◽  
Spontaneous Potential ◽  
Body Wall Muscles ◽  
Macracanthorhynchus Hirudinaceus ◽  
Anterior Posterior

Body wall muscles of an acanthocephalan Macracanthorhynchus hirudinaceus were studied by means of scanning and light microscopy and intracellular recording of potentials. Three types of spontaneous potential changes were found: larger (L) potentials which usually exhibited overshoot and were as large as 65 mV; smaller symmetric (A) potentials approximately 15 mV in amplitude; and even smaller asymmetric (S) potentials which sometimes reached 10 mV. The potentials recorded depended upon the position of the electrode in the anterior-posterior, as well as the medialateral, axis. Tetrodotoxin eliminated L but not S potentials. Ouabain lengthened the time for depolarization of L potentials and depolarized the membrane potentials. It is suggested that the rete system activates the body wall muscles in Acanthocephala.

scholarly journals Does a Unique Type of CA3 Pyramidal Cell in Primates Bypass the Dentate Gate?

2005 ◽  
Vol 94 (1) ◽  
pp. 896-900 ◽  
Author(s):  
Paul S. Buckmaster
Keyword(s):  
Dentate Gyrus ◽  
Entorhinal Cortex ◽  
Synaptic Input ◽  
Granule Cells ◽  
Molecular Layer ◽  
Pyramidal Cells ◽  
Dendritic Morphology ◽  
Dentate Granule Cells ◽  
Excitatory Synaptic Input ◽  
Ca3 Pyramidal Cells

The predominant excitatory synaptic input to the hippocampus arises from entorhinal cortical axons that synapse with dentate granule cells, which in turn synapse with CA3 pyramidal cells.Thus two highly excitable brain areas—the entorhinal cortex and the CA3 field—are separated by dentate granule cells, which have been proposed to function as a gate or filter. However, unlike rats, primates have “dentate” CA3 pyramidal cells with an apical dendrite that extends into the molecular layer of the dentate gyrus, where they could receive strong, monosynaptic, excitatory synaptic input from the entorhinal cortex. To test this possibility, the dentate gyrus molecular layer was stimulated while intracellular recordings were obtained from CA3 pyramidal cells in hippocampal slices from neurologically normal macaque monkeys. Stimulus intensity of the outer molecular layer of the dentate gyrus was standardized by the threshold intensity for evoking a dentate gyrus field potential population spike. Recorded proximal CA3 pyramidal cells were labeled with biocytin, processed with diaminobenzidine for visualization, and classified according to their dendritic morphology. In response to stimulation of the dentate gyrus molecular layer, action potential thresholds were similar in proximal CA3 pyramidal cells with different dendritic morphologies. These findings do not support the hypothesis that dentate CA3 pyramidal cells receive stronger synaptic input from the entorhinal cortex than do other proximal CA3 pyramidal cells.

Principal Cell Spiking, Postsynaptic Excitation, and Oxygen Consumption in the Rat Cerebellar Cortex

2009 ◽  
Vol 102 (3) ◽  
pp. 1503-1512 ◽  
Author(s):  
Kirsten Thomsen ◽  
Henning Piilgaard ◽  
Albert Gjedde ◽  
Gilles Bonvento ◽  
Martin Lauritzen
Keyword(s):  
Oxygen Consumption ◽  
Action Potential ◽  
Neuronal Activity ◽  
Cerebellar Cortex ◽  
Synaptic Input ◽  
Large Fraction ◽  
A Priori ◽  
Synaptic Activity ◽  
Principal Cell ◽  
Excitatory Synaptic Input

One contention within the field of neuroimaging concerns the character of the depicted activity: Does it represent neuronal action potential generation (i.e., spiking) or postsynaptic excitation? This question is related to the metabolic costs of different aspects of neurosignaling. The cerebellar cortex is well suited for addressing this problem because synaptic input to and spiking of the principal cell, the Purkinje cell (PC), are spatially segregated. Also, PCs are pacemakers, able to generate spikes endogenously. We examined the contributions to cerebellar cortical oxygen consumption (CMRO2) of postsynaptic excitation and PC spiking during evoked and ongoing neuronal activity in the rat. By inhibiting excitatory synaptic input using ionotropic glutamate receptor blockers, we found that the increase in CMRO2 evoked by parallel fiber (PF) stimulation depended entirely on postsynaptic excitation. In contrast, PC spiking was largely responsible for the increase in CMRO2 when ongoing neuronal activity was increased by γ-aminobutyric acid type A receptor blockade. In this case, CMRO2 increased equally during PC spiking with excitatory synaptic activity as during PC pacemaker spiking without excitatory synaptic input. Subsequent inhibition of action potential propagation and neurotransmission by blocking voltage-gated Na+-channels eliminated the increases in CMRO2 due to PF stimulation and increased PC spiking, but left a large fraction of CMRO2, i.e., basal CMRO2, intact. In conclusion, whereas basal CMRO2 in anesthetized animals did not seem to be related to neurosignaling, increases in CMRO2 could be induced by all aspects of neurosignaling. Our findings imply that CMRO2 responses cannot a priori be assigned to specific neuronal activities.

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