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1.
Early electrophysiological studies in the mammalian hippocampus reported that orthodromic depolarization of pyramidal cells evoked action potential discharge (presumed Na+ dependent) both at the axon hillock and at one or more sites in the dendritic arborization (Cragg and Hamlyn, 1955; Andersen, 1959, 1960; Spencer and Kandel, 1961; Andersen and Lomo, 1966). Although tetrodotoxin (TTX)-sensitive spikes have been recorded at the dendritic level (Wong et al., 1979; Benardo et al., 1982; Miyakawa and Kato, 1986; Turner et al., 1989), the site for initiation of these potentials has not yet been determined. In this study, we examine the site for initiation of Na+ spike discharge over the cell axis of rat hippocampal CA1 pyramidal neurons. Intrasomatic and intradendritic recordings were obtained from pyramidal neurons of hippocampal slices maintained in vitro. Spike discharge was evoked by alvear (antidromic) stimulation or orthodromically by stimulation of afferent inputs in stratum oriens (SO) or stratum radiatum (SR). Antidromic and orthodromic spikes were greatest in amplitude in somatic recordings and declined over the apical dendritic axis, while spike half-width was shortest at the cell body and increased with distance from stratum pyramidale. Measurements of orthodromic spike threshold revealed that the only location at which spikes discharged at a consistent membrane potential at threshold intensity (voltage threshold) was the cell body region. Finally, at threshold intensity, SR-evoked intradendritic spikes were blocked by local application of TTX in stratum pyramidale, while spike blockade at suprathreshold intensity required the diffusion of TTX into the apical dendritic region. These results indicate that, for threshold intensities of stimulation, antidromic and orthodromic spike discharge in CA1 pyramidal cells is initiated in the region of the cell body layer, subsequently conducting over the apical dendrites in a retrograde fashion. In contrast, SR-evoked orthodromic spike discharge exhibits an intensity-dependent shift in the site of origin up to 200 microns within the apical dendritic arborization.  相似文献   

2.
This study investigated the effects of antidromically conducted nerve impulses on the transmission of orthodromic volleys in primary afferents of the hindlimb in decerebrated paralyzed cats. Two protocols were used: (A) Single skin and muscle afferents (N=20) isolated from the distal part of cut dorsal rootlets (L7-S1) were recorded while stimulation was applied more caudally. The results showed that during the trains of three to 20 stimuli, the orthodromic firing frequency decreased or ceased, depending on the frequency of stimulation. Remarkably, subsequent to these trains, the occurrence of orthodromic spikes could be delayed for hundreds of ms (15/20 afferents) and sometimes stopped for several seconds (10/20 afferents). Longer stimulation trains, simulating antidromic bursts reported during locomotion, caused a progressive decrease, and a slow recovery of, orthodromic firing frequency (7/20 afferents), indicating a cumulative long-lasting depressing effect from successive bursts. (B) Identified stretch-sensitive muscle afferents were recorded intra-axonally and antidromic spikes were evoked by the injection of square pulses of current through the micropipette. In this case, one to three antidromic spikes were sufficient to delay the occurrence of the next orthodromic spike by more than one control inter-spike interval. If the control inter-spike interval was decreased by stretching the muscle, the delay evoked by antidromic spikes decreased proportionally. Overall, these findings suggest that antidromic activity could alter the mechanisms underlying spike generation in peripheral sensory receptors and modify the orthodromic discharges of afferents during locomotion.  相似文献   

3.
The number of orthodromically evoked population spikes was used to classify brain slice tissue from the dentate gyrus of temporal lobe epileptic patients as “more excitable” (multiple population spikes) or “less excitable” (a single population spike). During orthodromic stimulation, “more excitable” tissue exhibited less paired-pulse depression in comparison to “less excitable” tissue. During antidromic stimulaltion, both multiple population spikes and paired-pulse depression were observed in “more excitable” tissue. “Less excitable” tissue exhibited a single antidromic spike and often on antidromically evoked paired-pulse depression. The strength of antidromic paired-pulse depression was correlated positively with the number of antidromic spikes and was correlated negatively with orthodromic paired-pulse depression. Although orthodromic and antidromic paired-pulse depression were correlated to the number of orthodromically evoked populaltion spikes, this correlation was not as strong as that between orthodromic paired-pulse depression, antidromic paired-pulse depression, and number of antidromically evoked population spikes. The antidromic paired-pulse depression observed in tissue exhibiting antidromically evoked multiple population spikes was enhanced rather than blocked by bicuculline. In addition, the blockade of the antidromic paired-pulse depression by CNQX indicated that this inhibition is mediated by an AMPA-type glutamatergic synapse. We suggest that alterations in circuitry occur in the dentate gyrus of some temporal lobe epileptic patients and were manifested by both a loss of inhibitory input as well as an increase of inhibition, which was dependent on the pathway of stimulaltion. The results of pairing antidromic and orthodromic stimuli were consistent with these conclusions. © 1994 Wiley-Liss, Inc.  相似文献   

4.
Extracellular spikes were recorded from the cell bodies of antidromically activated callosal axons in rabbit visual cortex. Callosal axons were stimulated near their terminals in the contralateral cortex. The primary method for differentiating antidromic from synaptic activation was the test for collision of impulses. Additional tests provided further confirmation of antidromic activation. A decrease in antidromic latency always occurred when an antidromic volley followed either a spontaneous spike or a preceding antidromically elicited spike at appropriate intervals. The time course and magnitude of the latency decrease coincided with that of a threshold decrease at the site of electrical stimulation. The antidromic latency decrease was primarily due to an increase in axon conduction velocity. These systematic variations in conduction velocity and stimulus threshold strongly suggest that an afterdepolarization follows the activation of callosal axons. While such afterpotentials are known to occur in unmyelinated C fibers, the present evidence suggests that they also occur in the smallest of myelinated axons.  相似文献   

5.
M E Westecker  D Manns 《Brain research》1983,288(1-2):119-130
Spikes with bimodal and occasional trimodal latencies were recorded from neurons in the olfactory bulb of rabbits in response to lateral olfactory tract (LOT) stimulation at one site. Among neurons with bimodal spike latencies, two types have to be distinguished. In the case of type I neurons long-latency second-mode spikes were suppressed by short-latency first-mode spikes. Due to this suppression the long-latency second-mode spike could be investigated only, when its threshold was lower than that of the short-latency spike. In the case of type II neurons the long-latency second-mode spike was not suppressed. The collision test was applied to type I bimodal spikes. All short-latency first-mode and long-latency second-mode spikes were suppressed by spontaneous spikes. The suppression time indicated the likelihood of collision in most cases, but one could not entirely exclude the possibility, that short-latency first-mode spikes were suppressed due to refractoriness and long-latency second-mode spikes due to inhibition. To allow a more definite interpretation of collision a multiple collision test was applied, by stimulating axons at several LOT sites. A parallel rise of latency values and suppression time values was measured for 3 and more axonal spikes with different latencies, indicating collision and antidromic activation more definitely. Antidromically activated short-latency first-mode spikes were interpreted to be due to axonal stimulation and antidromically activated long-latency second-mode spikes to be due to axon collateral stimulation. No evidence for any postsynaptic activation of type I short-latency first-mode or long-latency second-mode spikes was gained. An indicator for collision of an antidromic spike with a spontaneous spike is the value collision time minus latency (c-l). The c-l values of axonal spikes ranged from 0.2 to 1.8 ms with a mean of 0.7 ms (n = 25), and c-l values of axon collateral spikes from 0.2 to 2.5 ms, with a mean of 1.1 ms (n = 13). The interpretation of c-l values is discussed. In the multiple collision test the c-l deviations from the lowest c-l value of each neuron ranged for axonal spikes between 0.0 and 0.7 ms (n = 25), with 38% not exceeding 0.1 ms and 81% not exceeding 0.4 ms. Spikes activated via axon collaterals had c-l deviations between 0.0 and 2.0 ms (n = 13). The c-l deviations above 2 ms were remote from other values and considered to be possibly inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)  相似文献   

6.
Leung LS  Peloquin P 《Hippocampus》2006,16(4):388-407
Spike backpropagation has been proposed to enhance dendritic depolarization and synaptic plasticity. However, relatively little is known about the inhibitory control of spike backpropagation in vivo. In this study, the backpropagation of the antidromic spike into the dendrites of CA1 pyramidal cells was studied by extracellular recording in urethane-anesthetized rats. The population antidromic spike (pAS) in CA1 following stimulation of the alveus was recorded simultaneously with a 16-channel silicon probe and analyzed as current source density (CSD). The pAS current sink was shown to sequentially invade the soma and then the apical and basal dendrites. When the pAS was preceded <400 ms by a conditioning orthodromic CA3 stimulus, the apical and basal dendritic spike sinks were reduced and delayed. Dendritic spike suppression was large after a high-intensity CA3 conditioning stimulus that evoked a population spike, small after a low-intensity CA3 conditioning stimulus, and weak after conditioning by another pAS. The late (150-400 ms latency) inhibition of the backpropagating pAS at the apical and basal dendrites was partially relieved by a GABA(B) receptor antagonist, CGP35348 or CGP56999A, given intracerebroventricularly (icv). CGP35348 icv also decreased the latency of the antidromic spike sinks at all depths. A compartment cable model of a CA1 pyramidal cell with excitable dendrites, combined with a model of extracellular potential generation, confirms that GABA(B) receptor activation delays a backpropagating spike and blocks distal dendritic spikes. GABA(B) receptor-mediated conductance increase and hyperpolarization, amplified by removing dendritic I(A) inactivation, contribute to conditioned dendritic spike suppression. In addition, the model shows that slow Na(+) channel inactivation also participates in conditioned spike suppression, which may partly explain the small dendritic spike suppression after conditioning with a weak orthodromic stimulus or another antidromic spike. Thus, both theory and experiment confirm an important role of the GABA(B) receptors in controlling dendritic spike backpropagation.  相似文献   

7.
Electrophysiological studies on preganglionic neurons (PGNs) in the dorsal motor nucleus (DMN) of the vagus nerve has been hampered by technical limitations. Conventional electrical stimulation of the vagus nerve with cathodal square-wave pulses activates both preganglionic and afferent fibers. Thus, some PGNs cannot be identified because the anticipated antidromic responses would be blocked due to collision with those orthodromic responses evoked with shorter latencies by activation of fast-conducting afferent fibers. Projections of vagus afferent fibers to PGNs are difficult to analyse with conventional methods because a preceding antidromic response may affect an orthodromic response which has a slightly longer latency. A new stimulation method was designed, consisting of anodal triangular pulse stimulation and spontaneous-spike triggered stimulation. In chlorase-urethane-anesthetized rats, unitary responses of the DMN to electrical stimulation of the ipsilateral vagus nerve were recorded. When only an orthodromic response by a DMN neuron was recorded with conventional stimulation, application of anodal triangular pulse stimulation revealed an antidromic response, so that the cell in question could be identified as a PGN. Some neurons that produced only an antidromic response to conventional stimulation, revealed an orthodromic response on spontaneous-spike triggered stimulation, which blocked the antidromic response due to collision. With these procedures, orthodromic responses due to vagus afferent projections were recorded in 35% of the identified PGNs, mostly due to C and partly, A fiber activations. All these projections were polysynaptic in nature. In conclusion, one-third of the PGNs of the DMN are involved in vagovagal reflexes, which occur through multisynaptic pathways.  相似文献   

8.
Impulse activity has been reported in neuronal dendrites in several regions of the central nervous system, where it is believed to assist in boosting transmission of signals from remote dendritic sites to the cell body. We have studied this activity in the dendrites of mitral cells in an isolated preparation of the turtle olfactory bulb. Intracellular recordings have been obtained from mitral cells responding to single volleys in the olfactory nerves or lateral olfactory tract. In addition to the large somatic spike, a small fast prepotential (FPP) was present in nearly all cells in response to an orthodromic volley in the olfactory nerves, but it was never seen in antidromic responses from the lateral olfactory tract. Collision tests using antidromic and orthodromic volleys showed that the EPP does not propagate into the axon. Hyperpolarizing current injections caused delay and blocking of the soma spike with little effect on the FPP response. These and other tests provided evidence to localize the EPP in the dendrites and to distinguish it from injury potentials and from spikes in the axon hillock or axonal initial segment. These results suggest that one function of the impulse in mitral cell dendrites is the classical one of boosting transmission of synaptic responses from the glomerular tuft to the cell body. In addition, it si well established that mitral cell dendrites are presynaptic to the dendrites of interneurons within the bulb and that these connections provide pathways for recurrent inhibition of the mitral cells. It therefore appears that the dendritic impulse in mitral cells acts as a booster for local dendritic synaptic output. These results provide further evidence for the multiple state-dependent input-output functions of cells with presynaptic dendrites.  相似文献   

9.
Spontaneous rhythmic antidromic discharges have previously been recorded in proximal stumps of cut dorsal roots during locomotion (real and fictive). The goals of the present study were to elucidate (1) whether both orthodromic and antidromic discharges occur in the same dorsal root filament and (2) whether orthodromic discharges have an influence upon antidromic discharges of units in the same filament. Unitary activity was recorded in 70 uncut dorsal root filaments (L6-S1) in 15 decerebrate cats using bipolar Ag/AgCl electrodes. Spikes with similar wave shapes were considered to represent the activity of single units. Spike-triggered averaging (STA), local anaesthesia and transection of filaments were used to determine the direction of propagation of spikes. Spikes with different initial electrical polarities were found in most of the filaments and shown to propagate in opposite directions at rest and during fictive locomotion. On average, there were 38%±S.D. 23% antidromically discharging units per filament and their mean conduction velocity was 55 m/s±S.D. 25 m/s. After blocking orthodromic activity of the whole filament by a transection or local anesthesia applied distally to the recording site, changes were seen in the antidromic discharges of some units suggesting that spontaneous orthodromic discharges normally seen in the filament may influence the antidromic discharges of some units. Moreover, out of 27 antidromic units recorded during fictive locomotion, 12 were rhythmically modulated with peak discharges occurring in various parts of the locomotor cycle. We conclude that, in uncut dorsal roots, there is a normal coexistence of spontaneous orthodromic and antidromic discharges revealed by STA and that there is an interaction between spontaneous orthodromic and antidromic discharges.  相似文献   

10.
M Isokawa  D M Finch 《Brain research》1991,551(1-2):94-103
Synaptic responses of commissurally activated rat subicular and entorhinal neurons were studied intracellularly in vivo by stimulating the contralateral dentate gyrus. The most prominent synaptic responses in both subicular and entorhinal neurons were inhibitory postsynaptic potentials (IPSPs). IPSPs were generated in combination with antidromic spikes and/or excitatory postsynaptic potentials (EPSPs) and orthodromic spikes. No dependency between any two response types were found. Commissurally projecting subicular neurons (identified by the presence of antidromic spikes evoked by contralateral stimulation) were found, extending previous anatomical studies. Commissurally projecting entorhinal neurons were found in layer II, confirming previous anatomical studies. Positive correlations between antidromic spike latency and depth of recording sites supported the interpretation that axons projected along the fiber bundles of the hippocampal commissures and angular bundle to distribute to their targets. Possible circuits that could have mediated the excitatory and inhibitory responses of these retrohippocampal neurons are considered.  相似文献   

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