A hemicord locomotor network of excitatory interneurons: a simulation study

Locomotor burst generation is simulated using a full-scale network model of the unilateral excitatory interneuronal population. Earlier small-scale models predicted that a population of excitatory neurons would be sufficient to produce burst activity, and this has recently been experimentally confirmed. Here we simulate the hemicord activity induced under various experimental conditions, including pharmacological activation by NMDA and AMPA as well as electrical stimulation. The model network comprises a realistic number of cells and synaptic connectivity patterns. Using similar distributions of cellular and synaptic parameters, as have been estimated experimentally, a large variation in dynamic characteristics like firing rates, burst, and cycle durations were seen in single cells. On the network level an overall rhythm was generated because the synaptic interactions cause partial synchronization within the population. This network rhythm not only emerged despite the distributed cellular parameters but relied on this variability, in particular, in reproducing variations of the activity during the cycle and showing recruitment in interneuronal populations. A slow rhythm (0.4–2 Hz) can be induced by tonic activation of NMDA-sensitive channels, which are voltage dependent and generate depolarizing plateaus. The rhythm emerges through a synchronization of bursts of the individual neurons. A fast rhythm (4–12 Hz), induced by AMPA, relies on spike synchronization within the population, and each burst is composed of single spikes produced by different neurons. The dynamic range of the fast rhythm is limited by the ability of the network to synchronize oscillations and depends on the strength of synaptic connections and the duration of the slow after hyperpolarization. The model network also produces prolonged bouts of rhythmic activity in response to brief electrical activations, as seen experimentally. The mutual excitation can sustain long-lasting activity for a realistic set of synaptic parameters. The bout duration depends on the strength of excitatory synaptic connections, the level of persistent depolarization, and the influx of Ca²⁺ ions and activation of Ca²⁺-dependent K⁺ current.     

Investigation of burst generation by the electrically coupled cyberchron network in the snail Helisoma using a single-electrode voltage clamp

This paper describes the results of investigating burst generation by the cyberchron network in the snail Helisoma. The cyberchron network is composed of approximately 20 electrically coupled neurons and controls the feeding behavior of the snail. The electrical coupling between network members has made it particularly difficult to distinguish between the importance and involvement of single-cell and network properties in burst generation by this system. The present investigations utilized the new single-electrode voltage clamp to examine the membrane properties and network interactions of the cyberchron neurons: (1) A slow outward current is activated by moderately large depolarizing commands (?40 to 0 mV) and does not undergo inactivation decay (i.e., decline in magnitude) during a command potential step maintained for 10 sec or more. The lack of inactivation of the outward current in cyberchron neurons appears to be due to the dominating role of a Ca-dependent K current. (2) There are two functionally distinct classes of cyberchrons—current generator cyberchrons and follower cyberchrons. (3) Primary current generator cyberchrons have membrane properties similar to endogenous bursting neurons (e.g., persistent inward Ca current and negative resistance region in I–V plot) and appear to provide the main driving and timing current for the rest of the network. (4) The vast majority of cyberchrons are secondary current generator cyberchrons with membrane properties which exhibit inward-going rectification and appear to burst as a result of regenerative excitation with one another and the primary current generator cyberchrons. (5) The second class of cyberchrons are driven by the electrical synaptic input from the current generator cyberchrons, do not exhibit inward-going rectification, and are called follower cyberchrons. (6) Burst termination is due to activation of a slow outward tail current in most cyberchrons during the burst (probably Ca-activated K current) which causes a hyperpolarization in individual cyberchrons, terminating the burst. (7) Decay of the outward tail current causes the cyberchrons to depolarize, which activates the persistent inward Ca current in the primary current generator cyberchrons, starting the burst cycle anew.     

Neuromodulation via conditional release of endocannabinoids in the spinal locomotor network

Endocannabinoids act as retrograde signals to modulate synaptic transmission. Little is known, however, about their significance in integrated network activity underlying motor behavior. We have examined the physiological effects of endocannabinoids in a neuronal network underlying locomotor behavior using the isolated lamprey spinal cord. Our results show that endocannabinoids are released during locomotor activity and participate in setting the baseline burst rate. They are released in response to mGluR1 activation and act as retrograde messengers. This conditional release of endocannabinoids can transform motoneurons and crossing interneurons into modulatory neurons by enabling them to regulate their inhibitory synaptic inputs and thus contribute to the modulation of the locomotor burst frequency. These results provide evidence that endocannabinoid retrograde signaling occurs within the locomotor network and contributes to motor pattern generation and regulation in the spinal cord.     

Modulation of Burst Frequency by Calcium-Dependent Potassium Channels in the Lamprey Locomotor System: Dependence of the Activity Level

It is crucial to determine the effects on the network level of a modulation of intrinsic membrane properties. The role calcium-dependent potassium channels, K_Ca, in the lamprey locomotor system has been investigated extensively. Earlier experimental studies have shown that apamin, which affects one type of K_Ca, increases the cycle duration of the locomotor network, due to effects on the burst termination. The effects of apamin were here larger when the network had a low level of activity (burst frequency 0.5 to 1 Hz) as compared to a higher rate (>2 Hz). By using a previously developed simulation model based on the lamprey locomotor network, we show that the model could account for the frequency dependence of the apamin modulation, if only the K_Ca conductance activated by Ca²⁺ entering during the action potential was altered and not the K_Ca conductance activated by Ca²⁺ entering through NMDA channels. The present simulation model of the spinal network in the lamprey can thus account for earlier experimental results with apamin on the network and cellular level that previously appeared enigmatic.     

The resonance frequency shift, pattern formation, and dynamical network reorganization via sub-threshold input

We describe a novel mechanism that mediates the rapid and selective pattern formation of neuronal network activity in response to changing correlations of sub-threshold level input. The mechanism is based on the classical resonance and experimentally observed phenomena that the resonance frequency of a neuron shifts as a function of membrane depolarization. As the neurons receive varying sub-threshold input, their natural frequency is shifted in and out of its resonance range. In response, the neuron fires a sequence of action potentials, corresponding to the specific values of signal currents, in a highly organized manner. We show that this mechanism provides for the selective activation and phase locking of the cells in the network, underlying input-correlated spatio-temporal pattern formation, and could be the basis for reliable spike-timing dependent plasticity. We compare the selectivity and efficiency of this pattern formation to a supra-threshold network activation and a non-resonating network/neuron model to demonstrate that the resonance mechanism is the most effective. Finally we show that this process might be the basis of the phase precession phenomenon observed during firing of hippocampal place cells, and that it may underlie the active switching of neuronal networks to locking at various frequencies.     

TTX-Resistant NMDA Receptor-Mediated Membrane Potential Oscillations in Neonatal Mouse Hb9 Interneurons

Conditional neuronal membrane potential oscillations have been identified as a potential mechanism to help support or generate rhythmogenesis in neural circuits. A genetically identified population of ventromedial interneurons, called Hb9, in the mouse spinal cord has been shown to generate TTX-resistant membrane potential oscillations in the presence of NMDA, serotonin and dopamine, but these oscillatory properties are not well characterized. Hb9 interneurons are rhythmically active during fictive locomotor-like behavior. In this study, we report that exogenous N-Methyl-D-Aspartic acid (NMDA) application is sufficient to produce membrane potential oscillations in Hb9 interneurons. In contrast, exogenous serotonin and dopamine application, alone or in combination, are not sufficient. The properties of NMDA-induced oscillations vary among the Hb9 interneuron population; their frequency and amplitude increase with increasing NMDA concentration. NMDA does not modulate the T-type calcium current (I_Ca(T)), which is thought to be important in generating locomotor-like activity, in Hb9 neurons. These results suggest that NMDA receptor activation is sufficient for the generation of TTX-resistant NMDA-induced membrane potential oscillations in Hb9 interneurons.     

Neural mechanisms potentially contributing to the intersegmental phase lag in lamprey

Factors contributing to the production of a phase lag along chains of oscillatory networks consisting of Hodgkin-Huxley type neurons are analyzed by means of simulations. Simplified network configurations are explored consisting of the basic building blocks of the spinal central pattern generator (CPG) generating swimming in the lamprey. It consists of reciprocally coupled crossed inhibitory C interneurons and ipsilateral excitatory E interneurons that activate C neurons and other E neurons. Oscillatory activity in the model network can, in the simplest case, be produced by a pair of reciprocally coupled C interneurons oscillating through an escape mechanism. Different levels of tonic excitation drive the network over a wide burst frequency range. In this type of network, powerful frequency-regulating factors are the effective inhibition produced by the active side, in combination with the tendency of the inactive side to escape from the inhibition. These two mechanisms can be affected by several factors, e.g. spike frequency adaptation (calcium-dependent K(+) channels), N-methyl-D-aspartate membrane properties as well as presence of low-voltage activated calcium channels. A rostrocaudal phase lag can be produced either by extending the contralateral inhibitory projections or the ipsilateral excitatory projections relatively more in the caudal than the rostral direction, since both an increased inhibition and a phasic excitation slow down the receiving network. The phase lag becomes decreased if the length of the intersegmental projections is increased or if the projections are extended symmetrically in both the rostral and the caudal directions. The simulations indicate that the conditions in the ends of an oscillator chain may significantly affect sign, magnitude and constancy of the phase lag. Also, with short and relatively weak intersegmental connections, the network remains robust against perturbations as well as intrinsic frequency differences along the chain. The phase lag (percentage of cycle duration) increases, however, with burst frequency also when the coupling strength is comparatively weak. The results are discussed and compared with previous "phase pulling" models as well as relaxation oscillators.     

Simulation and Parameter Estimation Study of a Simple Neuronal Model of Rhythm Generation: Role of NMDA and Non-NMDA Receptors

Simple neural network models of the Xenopus embryo swimming CPG, based on the one originally developed by Roberts and Tunstall (1990), were used to investigate the role of the voltage-dependent N-methyl-D-aspartate (NMDA) receptor channels, in conjunction with faster non-NMDA components of synaptic excitation, in rhythm generation. The voltage-dependent NMDA current "follows" the membrane potential, leading to a postinhibitory rebound that is more efficient than one without voltage dependency and allows neurons to fire more than one action potential per cycle. Furthermore, the model demonstrated limited rhythmic activity in the absence of synaptic inhibition, supporting the hypothesis that the NMDA channels provide a basic mechanism for rhythmicity. However, the rhythmic properties induced by the NMDA current were observed only when there was moderate activation of the non-NMDA synaptic channels, suggesting a modulatory role for this component. The simulations also show that the voltage dependency of the NMDA conductance, as well as the fast non-NMDA current, stabilizes the alternation pattern versus synchrony. To verify that these effects and their implications on the mechanism of swimming and transition to other types of activity take place in the real preparation, constraints on parameter values have to be specified. A method to estimate synaptic parameters was tested with generated data. It is shown that a global analysis, based on multiple iterations of the optimization process (Foster et al., 1993), gives a better understanding of the parameter subspace describing network activity than a standard fit with a sensitivity analysis for an individual solution.     

Current and calcium responses to local activation of axonal NMDA receptors in developing cerebellar molecular layer interneurons

In developing cerebellar molecular layer interneurons (MLIs), NMDA increases spontaneous GABA release. This effect had been attributed to either direct activation of presynaptic NMDA receptors (preNMDARs) or an indirect pathway involving activation of somato-dendritic NMDARs followed by passive spread of somatic depolarization along the axon and activation of axonal voltage dependent Ca(2+) channels (VDCCs). Using Ca(2+) imaging and electrophysiology, we searched for preNMDARs by uncaging NMDAR agonists either broadly throughout the whole field or locally at specific axonal locations. Releasing either NMDA or glutamate in the presence of NBQX using short laser pulses elicited current transients that were highly sensitive to the location of the spot and restricted to a small number of varicosities. The signal was abolished in the presence of high Mg(2+) or by the addition of APV. Similar paradigms yielded restricted Ca(2+) transients in interneurons loaded with a Ca(2+) indicator. We found that the synaptic effects of NMDA were not inhibited by blocking VDCCs but were impaired in the presence of the ryanodine receptor antagonist dantrolene. Furthermore, in voltage clamped cells, bath applied NMDA triggers Ca(2+) elevations and induces neurotransmitter release in the axonal compartment. Our results suggest the existence of preNMDARs in developing MLIs and propose their involvement in the NMDA-evoked increase in GABA release by triggering a Ca(2+)-induced Ca(2+) release process mediated by presynaptic Ca(2+) stores. Such a mechanism is likely to exert a crucial role in various forms of Ca(2+)-mediated synaptic plasticity.     

The dynamical stability of reverberatory neural circuits

The concept of reverberation proposed by Lorente de Nó and Hebb is key to understanding strongly recurrent cortical networks. In particular, synaptic reverberation is now viewed as a likely mechanism for the active maintenance of working memory in the prefrontal cortex. Theoretically, this has spurred a debate as to how such a potentially explosive mechanism can provide stable working-memory function given the synaptic and cellular mechanisms at play in the cerebral cortex. We present here new evidence for the participation of NMDA receptors in the stabilization of persistent delay activity in a biophysical network model of conductance-based neurons. We show that the stability of working-memory function, and the required NMDA/AMPA ratio at recurrent excitatory synapses, depend on physiological properties of neurons and synaptic interactions, such as the time constants of excitation and inhibition, mutual inhibition between interneurons, differential NMDA receptor participation at excitatory projections to pyramidal neurons and interneurons, or the presence of slow intrinsic ion currents in pyramidal neurons. We review other mechanisms proposed to enhance the dynamical stability of synaptically generated attractor states of a reverberatory circuit. This recent work represents a necessary and significant step towards testing attractor network models by cortical electrophysiology.     

Intrinsic and network rhythmogenesis in a reduced traub model for CA3 neurons

We have developed a two-compartment, eight-variable model of a CA3 pyramidal cell as a reduction of a complex 19-compartment cable model [Traub et al, 1991]. Our reduced model segregates the fast currents for sodium spiking into a proximal, soma-like, compartment and the slower calcium and calcium-mediated currents into a dendrite-like compartment. In each model periodic bursting gives way to repetitive soma spiking as somatic injected current increases. Steady dendritic stimulation can produce periodic bursting of significantly higher frequency (8–20 Hz) than can steady somatic input (<8 Hz). Bursting in our model occurs only for an intermediate range of electronic coupling conductance. It depends on the segregation of channel types and on the coupling current that flows back-and-forth between compartments. When the soma and dendrite are tightly coupled electrically, our model reduces to a single compartment and does not burst. Network simulations with our model using excitatory AMPA and NMDA synapses (without inhibition) give results similar to those obtained with the complex cable model [Traub et al, 1991; Traub et al, 1992]. Brief stimulation of a single cell in a resting network produces multiple synchronized population bursts, with fast AMPA synapses providing the dominant synchronizing mechanism. The number of bursts increases with the level of maximal NMDA conductance. For high enough maximal NMDA conductance synchronized bursting repeats indefinitely. We find that two factors can cause the cells to desynchronize when AMPA synapses are blocked: heterogeneity of properties amongst cells and intrinsically chaotic burst dynamics. But even when cells are identical, they may synchronize only approximately rather than exactly. Since our model has a limited number of parameters and variables, we have studied its cellular and network dynamics computationally with relative ease and over wide parameter ranges. Thereby, we identify some qualitative features that parallel or are distinguished from those of other neuronal systems; e.g., we discuss how bursting here differs from that in some classical models.     

Cell-type specificity of mGluR activation in striatal neuronal subtypes

Summary. The effects of metabotropic glutamate receptor (mGluR) activation were studied in medium spiny neurons and large aspiny (LA) interneurons by means of electrophysiological and optical recordings. DCG-IV and L-SOP, agonists for group II and III mGluRs, respectively, produced a presynaptic inhibitory effect on corticostriatal glutamatergic excitatory postsynaptic potentials (EPSPs) in both spiny and LA cells. Activation of group I mGluRs by the selective agonist 3,5-DHPG produced no effect on membrane properties and glutamatergic transmission in spiny neurons, whereas it did cause a membrane depolarization in LA interneurons coupled to increased input resistance. In combined optical and electrophysiological experiments, in spiny neurons 3,5-DHPG enhanced membrane depolarization and intracellular calcium (Ca²⁺) levels induced by NMDA applications, but not in LA interneurons. These data suggest the existence of a positive interaction between NMDA and group I mGlu receptors only in medium spiny cells which might, at least partially, account for the differential vulnerability to excitotoxic damage observed in striatal neuronal subtypes. Accepted September 20, 1999     

Intersegmental coordination in the lamprey: simulations using a network model without segmental boundaries

Swimming in vertebrates such as eel and lamprey involves the coordination of alternating left and right activity in each segment. Forward swimming is achieved by a lag between the onset of activity in consecutive segments rostrocaudally along the spinal cord. The intersegmental phase lag is approximately 1% of the cycle duration per segment and is independent of the swimming frequency. Since the lamprey has approximately 100 spinal segments, at any given time one wave of activity is propagated along the body. Most previous simulations of intersegmental coordination in the lamprey have treated the cord as a chain of coupled oscillators or well-defined segments. Here a network model without segmental boundaries is described which can produce coordinated activity with a phase lag. This ‘continuous’ pattern-generating network is composed of a column of 420 excitatory interneurons (E1 to E420) and 300 inhibitory interneurons (C1 to C300) on each half of the simulated spinal cord. The interneurons are distributed evenly along the simulated spinal cord, and their connectivity is chosen to reflect the behavior of the intact animal and what is known about the length and strength of the synaptic connections. For example, E100 connects to all interneurons between E51 and E149, but at varying synaptic strengths, while E101 connects to all interneurons between E52 and E150. This unsegmented E-C network generates a motor pattern that is sampled by output elements similar to motoneurons (M cells), which are arranged along the cell column so that they receive input from seven E and five C interneurons. The M cells thus represent the summed excitatory and inhibitory input at different points along the simulated spinal cord and can be regarded as representing the ventral root output to the myotomes along the spinal cord. E and C interneurons have five simulated compartments and Hodgkin-Huxley based dynamics. The simulated network produces rhythmic output over a wide range of frequencies (1–11 Hz) with a phase lag constant over most of the length, with the exception of the ‘cut’ ends due to reduced synaptic input. As the inhibitory C interneurons in the simulation have more extensive caudal than rostral projections, the output of the simulation has positive phase lags, as occurs in forward swimming. However, unlike the biological network, phase lags in the simulation increase significantly with burst frequency, from 0.5% to 2.3% over the range of frequencies of the simulation. Local rostral or caudal increases in excitatory drive in the simulated network are sufficient to produce motor patterns with increased or decreased phase lags, respectively. Received: 15 December 1995 / Accepted in revised form: 17 September 1996     

Generation of locomotion rhythms without inhibition in vertebrates: the search for pacemaker neurons

Locomotion rhythms are thought to be generated by neurons in the central-pattern-generator (CPG) circuit in the spinal cord. Synaptic connections in the CPG and pacemaker properties in certain CPG neurons, both may contribute to generation of the rhythms. In the half-center model proposed by Graham Brown a century ago, reciprocal inhibition plays a critical role. However, in all vertebrate preparations examined, rhythmic motor bursts can be induced when inhibition is blocked in the spinal cord. Without inhibition, neuronal pacemaker properties may become more important in generation of the rhythms. Pacemaker properties have been found in motoneurons and some premotor interneurons in different vertebrates and they can be dependent on N-Methyl-d-aspartate (NMDA) receptors (NMDAR) or rely on other ionic currents like persistent inward currents. In the swimming circuit of the hatchling Xenopus tadpole, there is substantial evidence that emergent network properties can give rise to swimming rhythms. During fictive swimming, excitatory interneurons (dINs) in the caudal hindbrain fire earliest on each swimming cycle and their spikes drive the firing of other CPG neurons. Regenerative dIN firing itself relies on reciprocal inhibition and background excitation. We now find that the activation of NMDARs can change dINs from firing singly at rest to current injection to firing repetitively at swimming frequencies. When action potentials are blocked, some intrinsic membrane potential oscillations at about 10 Hz are revealed, which may underlie repetitive dIN firing during NMDAR activation. In confirmation of this, dIN repetitive firing persists in NMDA when synaptic transmission is blocked by Cd(2+). When inhibition is blocked, only dINs and motoneurons are functional in the spinal circuit. We propose that the conditional intrinsic NMDAR-dependent pacemaker firing of dINs can drive the production of swimming-like rhythms without the participation of inhibitory neurotransmission.     

Inhibitory network of spiking neurons may express a sharp peak of synchrony at low frequency band

Spike synchronization remains an important issue in neuroscience, and inhibitory networks are the best candidates to provide such synchrony. Increasing evidence indicates that in many brain area inhibitory interneurons of similar properties make reciprocal connections. We found that a hybrid, as well as model network, consisting of two reciprocally inhibitory spiking neurons may express a peak of synchronization in a narrow range of low spiking frequencies in addition to classically described plateau of synchrony at a wide range of high frequencies. Occurrence of the low frequency peak of synchrony requires a moderate-to-strong inhibitory coupling and relatively fast synapses. This novel possibility of synchronization in a narrow range of network parameters may have an important implication in discrimination and encoding of signals of precise intensity, as well as in altering network ability to process information.     

Localization and interaction of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors of lamprey spinal neurons.

Small volumes of N-Methyl-D-Aspartate (NMDA) and non-NMDA excitatory amino acid receptor agonists were applied to localized regions of the dendritic trees of lamprey spinal neurons along their medial-lateral axis to obtain a spatial map of glutamate receptor distribution. Voltage clamp and frequency domain methods were used to obtain quantitative kinetic data of the voltage dependent ionic channels located both on the soma and on highly branched dendritic membranes. Pressure pulses of NMDA applied to the most peripheral regions of the dendritic tree elicited large somatic impedance increases, indicating that the most peripheral dendrites are well supplied with NMDA receptors. Experiments done with kainate did not elicit somatic responses to agonist applications on peripheral dendrites. The data obtained are consistent with the hypothesis that the activation of NMDA receptors by exogenous glutamate is significantly modified by the simultaneous activation of non-NMDA receptors, which shunts the NMDA response. The non-NMDA shunting hypothesis was tested by a combined application of kainate and NMDA to mimic the action of glutamate showing that the shunting effect of non-NMDA receptor activation virtually abolished the marked voltage dependency typical of NMDA receptor activation. These data were interpreted with a compartmental neuronal model having both NMDA and non-NMDA receptors.     

Intrinsic bursting enhances the robustness of a neural network model of sequence generation by avian brain area HVC

Avian brain area HVC is known to be important for the production of birdsong. In zebra finches, each RA-projecting neuron in HVC emits a single burst of spikes during a song motif. The population of neurons is activated in a precisely timed, stereotyped sequence. We propose a model of these burst sequences that relies on two hypotheses. First, we hypothesize that the sequential order of bursting is reflected in the excitatory synaptic connections between neurons. Second, we propose that the neurons are intrinsically bursting, so that burst duration is set by cellular properties. Our model generates burst sequences similar to those observed in HVC. If intrinsic bursting is removed from the model, burst sequences can also be produced. However, they require more fine-tuning of synaptic strengths, and are therefore less robust. In our model, intrinsic bursting is caused by dendritic calcium spikes, and strong spike frequency adaptation in the soma contributes to burst termination.     

Modulation in firing pattern and oscillation in nerve cells of Lymnaea during network reconstruction

The modulation and reconstruction of the cardio-respiratory neural circuit of Lymnaea stagnalis L. was compared to that of Helix ponatia L. where the input variation and signal molecules were found to have primary importance in network reorganization. From the cardio-respiratory circuit only neurons connected by afferent or efferent pathways to the peripheral chemosensory organ, the osphradium, were used. It was shown that, the general principles of the network reorganization is similar in the two species. The firing pattern of the neurons altered in Lymnaea depending on the input activation or presence of signal molecules in the vicinity of the neurons. The responses of the neurons to the same sensory information, originating from osphradium varied depending on their firing patterns. On central neurones the generation of phasic pattern and/or oscillation was an indicator of network disintegration leading to insensibility to the osphradial sensory inputs. Co-application of signal molecules (5HT, DA, GABA with opioid peptides) to the neurons caused a phasic firing pattern and/or oscillation leading to disintegration of one network and activation of another one. The effect of mu-opioid peptides on GABA-induced and voltage activated ion currents were shown to be the cellular target in reconstruction of neural networks in Lymnaea. The neural network reconstruction in vertebrate brain evoked by signal molecules can be compared to that observed in the identified network of Lymnaea stagnalis making this latter a useful model in further studies, too.     

Role of type-specific neuron properties in a spinal cord motor network

Recent recordings from spinal neurons in hatchling frog tadpoles allow their type-specific properties to be defined. Seven main types of neuron involved in the control of swimming have been characterized. To investigate the significance of type-specific properties, we build models of each neuron type and assemble them into a network using known connectivity between: sensory neurons, sensory pathway interneurons, central pattern generator (CPG) interneurons and motoneurons. A single stimulus to a sensory neuron initiates swimming where modelled neuronal and network activity parallels physiological activity. Substitution of firing properties between neuron types shows that those of excitatory CPG interneurons are critical for stable swimming. We suggest that type-specific neuronal properties can reflect the requirements for involvement in one particular network response (like swimming), but may also reflect the need to participate in more than one response (like swimming and slower struggling). Action Editor: Eberhard E. Fetz     

大脑皮层神经元NMDA受体的单通道特性

本文用膜片箝技术对机械分离培养的大鼠大脑皮层神经元胞体上的ＮＭＤＡ受体的单通道特性进行了研究,实验用细胞贴附和内面向外两种形式记录单离子通道的活动。电极液内含有ＮＭＤＡ或Ｌ－门冬氨酸时,在皮层神经元上常见电导为３５ｐＳ的离子通道。通道对Ｎａ＋,Ｋ＋非选择性通透,对Ｃｌ－不通透,其平均开放时间和开放概率随超极化程度增大而降低。开放、关闭时间及ｂｕｒｓｔ时程的分布直方图均需双指数拟合。Ｍｇ２＋以电压和浓度依赖性的方式减小通道开放时间,ＡＰＶ能阻断通道活动,温度降低使通道开放时间延长及电流幅度减小。本文结果表明大脑皮层神经元上ＮＭＤＡ受体通道活动自身具有电压依赖性,因此提示ＮＭＤＡ受体通道的正常功能活动可能依赖于某些细胞内调控过程的存在。