Stimulus-Evoked Modulation of Sensorimotor Pyramidal Neuron EPSPs

2002 ◽  
Vol 88 (6) ◽  
pp. 3331-3347 ◽  
Author(s):  
Adam Kohn ◽  
Carol Metz ◽  
Mark A. Tommerdahl ◽  
Barry L. Whitsel
Keyword(s):  
Electrical Stimulation ◽  
Membrane Potential ◽  
Conditioning Stimulus ◽  
Pyramidal Cells ◽  
Epsp Amplitude ◽  
Layer V ◽  
Layer I ◽  
Repetitive Stimulus ◽  
Layer Vi ◽  
Stimulation Of

Sensory cortical neurons display substantial receptive field dynamics during and after persistent sensory drive. Because a cell's response properties are determined by the inputs it receives, receptive field dynamics are likely to involve changes in the relative efficacy of different inputs to the cell. To test this hypothesis, we have investigated if brief repetitive stimulus drive in vitro alters the efficacy of two types of corticocortical inputs to layer V pyramidal cells. Specifically, we have used whole cell recordings to measure the effect of repetitive electrical stimulation at the layer VI/white matter (WM) border on the synaptic response of layer V pyramidal cells to corticocortical input evoked by electrical stimulation of layer I or layer II/III and emulated by local application of glutamate. Repetitive stimulation (10 Hz for 3 s) at the layer VI/WM border transiently potentiated excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of layer II/III by 97 ± 12% (mean ± SE). The recovery of EPSP amplitude to its preconditioning value was well-described by a single-term decaying exponential with a time constant of 7.2 s. The same layer VI/WM conditioning train that evoked layer II/III EPSP potentiation frequently caused an attenuation of layer I EPSPs. Similarly, subthreshold postsynaptic responses to local glutamate application in layers II/III and I were potentiated and attenuated, respectively, by the conditioning stimulus. Potentiation and attenuation could be evoked in the same cell by repositioning the glutamate puffer pipette in the appropriate layer. The conditioning stimulus that led to the transient modification of upper layer EPSP efficacy also evoked a slow depolarization in glial cells. The membrane potential of glial cells recovered with a time course similar to the dissipation of the potentiation effect, suggesting that stimulus-evoked changes in extracellular potassium (ECK) play a role in layer II/III EPSP potentiation. Consistent with this proposal, increasing the bath concentration of ECK caused a substantial increase of layer II/III EPSP amplitude. EPSP potentiation was sensitive to postsynaptic membrane potential and, more importantly, was significantly weaker for synaptic currents than for synaptic potentials, suggesting that it involves the recruitment of a postsynaptic voltage-dependent mechanism. Two observations suggest that layer II/III EPSP potentiation may involve the recruitment of postsynaptic sodium channels: EPSP potentiation was strongly reduced by intracellular application of N-(2,6-dimethyl-phenylcarbamoylmethyl) triethylammonium bromide (QX-314) and responses to local glutamate application were potentiated by high ECK in the presence of cadmium but not in the presence of tetrodotoxin. The results demonstrate a novel way in which brief periods of repetitive stimulus drive are accompanied by rapid, transient, and specific alterations in the functional connectivity and information processing characteristics of sensorimotor cortex.

Responses of medullary raphespinal neurons to electrical stimulation of thoracic sympathetic afferents, vagal afferents, and to other sensory inputs in cats

1991 ◽  
Vol 66 (6) ◽  
pp. 2084-2094 ◽  
Author(s):  
R. W. Blair ◽  
A. R. Evans
Keyword(s):  
Electrical Stimulation ◽  
Neuronal Activity ◽  
Vagal Stimulation ◽  
Discharge Rate ◽  
Stellate Ganglion ◽  
Cell Activity ◽  
Conditioning Stimulus ◽  
Vagal Afferents ◽  
Early Peak ◽  
Stimulation Of

1. Medullary raphespinal neurons antidromically activated from the T2-T5 segments were tested for responses to electrical stimulation of cervical vagal and thoracic sympathetic afferents (by stimulating the left stellate ganglion), somatic probing, auditory stimuli, and visual stimuli in cats anesthetized with alpha-chloralose. A total of 99 neurons in the raphe nuclei were studied; the locations of 76 cells were histologically confirmed. Neurons were located in raphe magnus (RM, 65%), raphe obscurus (RO, 32%), and raphe pallidus (RPa, 4%). The mean conduction velocity of these neurons was 62 +/- 2.9 (SE) m/s with a range of 1.1-121 m/s. 2. A total of 60/99 tested neurons responded to electrical stimulation of sympathetic afferents. Quantitation of responses was obtained for 55 neurons. With one exception, all responsive neurons were excited and exhibited an early burst of spikes with a mean latency of 16 +/- 1.2 ms. From a spontaneous discharge rate of 5.2 +/- 1.2 spikes/s, neuronal activity increased by 2.9 +/- 0.3 spikes/stimulus. In addition to an early peak, 15 neurons (25%) exhibited a late burst of spikes with a latency of 182 +/- 12.9 ms; neuronal activity increased by 5.0 +/- 1.3 spikes/stimulus. Duration of the late peak (130 +/- 18.5 ms) was longer than for the early peak (18 +/- 0.7 ms), but threshold voltages for eliciting each peak were comparable. Sixteen of 29 spontaneously active neurons exhibited a postexcitatory depression of activity that lasted for 163 +/- 19.1 ms. All but one tested neuron in RO responded to stimulation of sympathetic afferents, but 65% of neurons in RM responded to this stimulus. 3. In response to vagal afferent stimulation, 19% of 57 neurons exhibited inhibition only, 11% were only excited, and 9% were either excited or inhibited, depending on the stimulus paradigm used; the remaining 61% of neurons were unresponsive. From a spontaneous rate of 7.9 +/- 3.8 spikes/s, excited cells increased their discharge rate by 1.6 +/- 0.3 spikes/stimulus. Activity of inhibited cells was reduced from 21.3 +/- 5.8 to 7.8 +/- 3.1 spikes/s. The conditioning-test (CT) technique was used to assess 11 neurons' responses. Stellate ganglion stimulation was the test stimulus, and vagal stimulation the conditioning stimulus. Vagal stimulation reduced the neuronal responses to stellate ganglion stimulation by an average of 50% with a CT interval of 60-100 ms, and cell responses returned to control after 300 ms. With spontaneous cell activity, low frequencies of vagal stimulation were generally excitatory, and high frequencies (10-20 Hz) inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)

Spontaneous firing patterns and axonal projections of single corticostriatal neurons in the rat medial agranular cortex

1994 ◽  
Vol 71 (1) ◽  
pp. 17-32 ◽  
Author(s):  
R. L. Cowan ◽  
C. J. Wilson
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Superficial Layer ◽  
Common Type ◽  
Spontaneous Firing ◽  
Antidromic Activation ◽  
Axon Collaterals ◽  
Medial Agranular Cortex ◽  
Layer V ◽  
Layer I

1. Spontaneous fluctuations of membrane potential, patterns of spontaneous firing, dendritic branching patterns, and intracortical and striatal axonal arborizations were compared for two types of corticostriatal neurons in the medial agranular cortex of urethan-anesthetized rats: 1) pyramidal tract (PT) cells identified by antidromic activation from the medullary pyramid and 2) crossed corticostriatal (CST) neurons identified by antidromic activation from the contralateral neostriatum. The ipsilateral corticostriatal projections of intracellularly stained PT neurons as well as contralateral corticostriatal neurons were confirmed after labeling by intracellular injection of biocytin. 2. All well-stained PT neurons had intracortical and intrastriatal collaterals. The more common type (6 of 8) was a large, deep layer V neuron that had an extensive intracortical axon arborization but a limited axon arborization in the neostriatum. The less common type of PT neuron (2 of 8) was a medium-sized, superficial layer V neuron that had a limited intracortical axon arborization but a larger and more dense intrastriatal axonal arborization. Both subclasses of PT neurons had anatomic and physiological properties associated with slow PT cells in cats and monkeys and conduction velocities < 10 m/s. All of the PT cells but one were regular spiking cells. The exception cell fired intrinsic bursts. 3. Intracellularly stained CST neurons were located in the superficial half of layer V and the deep part of layer III. Their layer I apical dendrites were few and sparsely branched. Their axons gave rise to an extensive arbor of local axon collaterals that distributed in the region of the parent neuron, frequently extending throughout the more superficial layers, including layer I. Axon collaterals were also traced to the corpus callosum, as expected from their contralateral projections, and they contributed axon collaterals to the ipsilateral neostriatum. In the neostriatum, these axons formed extended arborizations sparsely occupying a large volume of striatal tissue. All CST neurons were regular spiking cells. 4. Both types of cells displayed spontaneous membrane fluctuations consisting of a polarized state (-60 to -90 mV) that was interrupted by 0.1- to 3.0-s periods of depolarization (-55 to -45 mV) accompanied by action potentials. The membrane potential was relatively constant in each state, and transitions between the depolarized and hyperpolarized states were sometimes periodic with a frequency of 0.3–1.5 Hz. A much faster (30-45 Hz) subthreshold oscillation of the membrane potential was observed only in the depolarized state and triggered action potentials that locked to the depolarizing peaks of this rhythm.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Cannabinoids Modulate Synaptic Strength and Plasticity at Glutamatergic Synapses of Rat Prefrontal Cortex Pyramidal Neurons

2000 ◽  
Vol 83 (6) ◽  
pp. 3287-3293 ◽  
Author(s):  
Nathalie Auclair ◽  
Satoru Otani ◽  
Philippe Soubrie ◽  
Francis Crepel
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Transmission ◽  
Cannabinoid Receptors ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Type I ◽  
Glutamatergic Synaptic Transmission ◽  
Layer V ◽  
Stimulation Of

Cannabinoids receptors have been reported to modulate synaptic transmission in many structures of the CNS, but yet little is known about their role in the prefrontal cortex where type I cannabinoid receptor (CB-1) are expressed. In this study, we tested first the acute effects of selective agonists and antagonist of CB-1 on glutamatergic excitatory postsynaptic currents (EPSCs) in slices of rat prefrontal cortex (PFC). EPSCs were evoked in patch-clamped layer V pyramidal cells by stimulation of layer V afferents. Monosynaptic EPSCs were strongly depressed by bath application (1 μM) of the cannabinoid receptors agonists WIN55212-2 (−50.4 ± 8.8%) and CP55940 (−42.4 ± 10.9%). The CB-1 antagonist SR141716A reversed these effects. Unexpectedly, SR141716A alone produced a significant increase of glutamatergic synaptic transmission (+46.9 ± 11.2%), which could be partly reversed by WIN55212-2. In the presence of strontium in the bath, the frequency but not the amplitude of asynchronous synaptic events evoked in layer V pyramidal cells by stimulating layer V afferents, was markedly decreased (−54.2 ± 8%), indicating a presynaptic site of action of cannabinoids at these synapses. Tetanic stimulation (100 pulses at 100 Hz, 4 trains) induced in control condition, no changes ( n = 7/18), long-term depression (LTD; n = 6/18), or long-term potentiation (LTP; n = 5/18) of monosynaptic EPSCs evoked by stimulation of layer V afferents. When tetanus was applied in the presence of WIN 55,212-2 or SR141716-A (1 μM) in the bath, the proportion of “nonplastic” cells were not significantly changed ( n = 7/15 in both cases). For the plastic ones ( n = 8 in both cases), WIN 55,212-2 strongly favored LTD ( n = 7/8) at the apparent expense of LTP ( n = 1/8), whereas the opposite effect was observed with SR141716-A (7/8 LTP; 1/8 LTD). These results demonstrate that cannabinoids influence glutamatergic synaptic transmission and plasticity in the PFC of rodent.

Spatiotemporally differential inhibition of pyramidal cells in the cat motor cortex

1994 ◽  
Vol 71 (1) ◽  
pp. 280-293 ◽  
Author(s):  
Y. Kang ◽  
T. Kaneko ◽  
H. Ohishi ◽  
K. Endo ◽  
T. Araki
Keyword(s):  
Motor Cortex ◽  
Rise Time ◽  
Pyramidal Cells ◽  
Spatiotemporal Pattern ◽  
Stimulation Site ◽  
Time To Peak ◽  
Early Portion ◽  
Layer V ◽  
Apical Dendrites ◽  
Stimulation Of

1. The spatiotemporal pattern of inhibition in the cat motor cortex was studied in in vitro slice preparations in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 2-amino-5-phosphonovaleric acid (APV). 2. After intracortical microstimulation (0.5–6 microA), fast and slow inhibitory postsynaptic potentials (IPSPs) were produced in layers II–VI pyramidal cells and selectively reduced with bicuculline methiodide and phaclofen, respectively. 3. Fast IPSPs were maximally produced by stimulation of the same layer where their cell bodies were located, and they decreased in amplitude as the more superficial layer was stimulated. In contrast, slow IPSPs were maximally produced by stimulation of layer II regardless of the location of the recorded pyramidal cell and decreased in amplitude as the deeper layer was stimulated. 4. The reduction of amplitude of fast IPSPs, in response to a vertical shift of the stimulation site toward more superficial layers, was always correlated with an increase in rise time and with a shift of the reversal potential to a more hyperpolarized level. 5. When the stimulation site was moved horizontally to the more lateral site, fast IPSPs increased in latency and decreased in amplitude gradually without appreciable changes in rise time. Fast IPSPs could be evoked from horizontally remote sites of up to 800–1,200 microns. 6. Inhibitory interneurons, which are responsible for evoking fast IPSPs, appear to be distributed through almost all layers to send horizontally spreading parallel axons making synaptic contacts at different electrotonic distances along apical dendrites of single pyramidal cells. 7. Horizontal spreads were much less in slow IPSPs (< 340–680 microns). The time-to-peak of slow IPSPs produced in layer V pyramidal cells (159.5 +/- 6.8 ms, mean +/- SD, n = 10) was significantly (P < 0.0001) longer than that in layers II and III pyramidal cells (128.5 +/- 7.5 ms, n = 7). Asymmetric reversal properties of slow IPSPs were seen, suggesting the spatial dispersion of synaptic inputs along apical dendrites of pyramidal cells. 8. In layer V pyramidal cells, the time-to-peak of slow IPSPs decreased with increasing membrane hyperpolarization, indicating that the later portion of slow IPSPs was more sensitive to the membrane-potential change than the early portion. This further indicates that the late portion of slow IPSPs is generated at synapses on the more proximal dendrite of pyramidal cells than the early portion, contrary to that expected from the Rall's model of passive dendrite under the condition of synchronous inputs.(ABSTRACT TRUNCATED AT 400 WORDS)

Layer I neurons of rat neocortex. I. Action potential and repetitive firing properties

1996 ◽  
Vol 76 (2) ◽  
pp. 651-667 ◽  
Author(s):  
F. M. Zhou ◽  
J. J. Hablitz
Keyword(s):  
Membrane Potential ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Repetitive Firing ◽  
Bathing Solution ◽  
Maximal Amplitude ◽  
Frequency Adaptation ◽  
Rat Neocortex ◽  
Layer I ◽  
Firing Properties

1. Whole cell patch-clamp techniques, combined with direct visualization of neurons, were used to study action potential (AP) and repetitive firing properties of layer I neurons in slices of rat neocortex. 2. Layer I neurons had resting membrane potentials (RMP) of -59.8 +/- 4.7 mV (mean +/- SD) and input resistances (RN) of 592 +/- 284 M Omega. Layer II/III pyramidal neurons had RMPs and RNs of -61.5 +/- 5.6 mV and 320 +/- 113 M omega, respectively. A double exponential function was needed to describe the charging curves of both neuron types. In layer I neurons, tau(0) was 45 +/- 22 ms and tau(1) was 5 +/- 3.3 ms whereas in layer II/III pyramidal neurons, tau(0) was 41 +/- 11 ms and tau(1) was 3 +/- 2.6 ms. Estimates of specific membrane resistance (Rm) for layer I and layer II/III cells were 45 +/- 22 and 41 +/- 11 k omega cm2, respectively (Cm was assumed to be 1 microF/cm2). 3. AP threshold was -41 +/- 2 mV in layer I neurons. Spike amplitudes, measured from threshold to peak, were 90.6 +/- 7.7 mV. AP durations, measured both at the base and half maximal amplitude, were 2.5 +/- 0.4 and 1.1 +/- 0.2 ms, respectively. AP 10-90% rise and repolarization times were 0.6 +/- 0.1 and 1.1 +/- 0.2 ms, respectively. In layer II/III pyramidal neurons, AP threshold was -41 +/- 2.5 mV and spike amplitude was 97 +/- 9.7 mV. AP duration at base and half maximal amplitude was 5.4 +/- 1.1 ms and 1.8 +/- 0.2 ms, respectively. AP 10-90% rise and decay times were 0.6 +/- 0.1 ms and 2.8 +/- 0.6 ms, respectively. 4. Layer I neurons were fast spiking cells that showed little frequency adaptation, a large fast afterhyperpolarization (fAHP), and no slow afterhyperpolarization (sAHP). Some cells had a medium afterhyperpolarization (mAHP) and a slow afterdepolarization (sADP). All pyramidal cells in layer II/III and "atypical" pyramidal neurons in upper layer II showed regular spiking behavior, prominent frequency adaptation, and marked sAHPs. 5. In both layer I neurons and layer II/III pyramidal neurons, changes in membrane potential did not greatly alter AP properties. The duration of APs evoked from -50 to -60 mV was only slightly longer, from -80 to -90 mV. The latency to first spike also was not solely dependent on membrane potential. 6. During repetitive firing, APs broadened in both layer I neurons and layer II/III pyramidal neurons. This was most prominent in pyramidal cells. Broadening was dependent on spike frequency and appeared to result from partial inactivation of both outward potassium and inward sodium currents. 7. In layer I neurons, removing Ca2+ from the bathing solution slightly prolonged spike duration and modestly increased AP firing frequency. These results indicate minimal involvement of Ca2+-dependent K+ currents in AP repolarization. fAHPs were reduced whereas sADPs were abolished. In layer II/III pyramidal neurons, removing Ca2+ reduced or blocked mAHPs and sAHPs and decreased or abolished frequency adaptation. 8. Low concentrations (50 microM) of 4-aminopyridine (4-AP) prolonged APs and induced burst-like firing in layer I neurons. In the presence of 4-AP, the spiking behavior of layer I neurons resembled that of regular spiking layer II/III pyramidal cells. At high concentrations (4 mM), 4-AP could induce a delayed depolarization (DD) after each spike in layer I neurons and in a minority of pyramidal neurons. 9. All layer I neurons had a prominent fAHP that was absent or very small in layer II/III pyramidal neurons. fAHP amplitude was inversely related to AP duration. The reduction of fAHPs by 4-AP or during repetitive firing was accompanied by AP prolongation, suggesting that the current underlying fAHP played an essential role in AP repolarization. The fAHP of layer I neurons could be effectively blocked by 4-AP but only slightly reduced by removing Ca2+ from bathing solution, indicating that the fAHP was mediated primarily by a voltage-dependent transient outward current.(ABSTRACT TRUNCATED)

scholarly journals Relative electrical conductivity measurements of the rat frontal cortex and the influence on current source density

2017 ◽  
Author(s):  
Yevgenij Yanovsky ◽  
Jurij Brankačk
Keyword(s):  
Electrical Conductivity ◽  
Current Source ◽  
Pyramidal Cells ◽  
Field Potentials ◽  
Source Density ◽  
Deep Layers ◽  
Layer V ◽  
Relative Electrical Conductivity ◽  
Conductivity Gradient ◽  
Layer Vi

summaryThe relative electrical conductivity gradient with depth was estimated in the frontal cortex of anaesthetized rats. Current source density (CSD) approximations of field potentials evoked by ventromedial thalamic stimulations with an assumed homogeneous electrical conductivity of the neocortical tissue were compared to those with correction for the estimated conductivity gradient. In spite of the cellular heterogeneity the electrical conductivity of the frontal cortical tissue was found to be fairly homogeneous inside the superficial (layers I through IV) or deep layers (V- VI). The relative conductivity increased twofold at the transition between superficial and deep layers. Regardless of this changes CSD analysis of the field potentials evoked by ventromedial thalamic stimulation revealed negligible differences between estimations ignoring the conductivity and those taking the conductivity into account. No sinks or sources appeared or disappeared. Both CSD approximations revealed: 1) a strong sink in layer I representing most likely summed monosynaptic EPSPs of the ventromedial thalamic afferents; 2) a strong sink in layer VI, probably representing summed disynaptic EPSPs on dendrites of layer VI pyramidal cells, generated by axons of upper layer pyramidal cells; and 3) a sink in lower layer V representing probably threesynaptic summed EPSPs on dendrites of layer V pyramidal cells.

Use-dependent depression of IPSPs in rat hippocampal pyramidal cells in vitro

1985 ◽  
Vol 53 (2) ◽  
pp. 557-571 ◽  
Author(s):  
M. McCarren ◽  
B. E. Alger
Keyword(s):  
Membrane Potential ◽  
Conditioning Stimulus ◽  
Pyramidal Cells ◽  
Repetitive Stimulation ◽  
Stratum Radiatum ◽  
Resting Potential ◽  
Masking Effect ◽  
Extracellular Potassium ◽  
Gamma Aminobutyric Acid ◽  
Hippocampal Pyramidal Cells

We have used intracellular recording techniques to study the use-dependence of evoked inhibitory postsynaptic potentials (IPSPs) in rat CA1 hippocampal pyramidal cells. We determined reversal potentials and conductance changes associated with IPSPs and responses to directly applied gamma-aminobutyric acid (GABA). The IPSP depression could be seen after a single conditioning stimulus. This depression appeared to be due primarily to a 50% decrease in IPSP conductance (gIPSP). Trains of stimulating pulses (50 pulses at 5 or 10 Hz) produced more pronounced effects than a single conditioning pulse. Suprathreshold repetitive stimulation of stratum radiatum (SR) produced epileptiform burst firing and greater depression of IPSPs than did alvear (ALV) or subthreshold SR stimulation. During suprathreshold SR stimulation the IPSP was nearly abolished and the membrane potential could become less negative than the resting potential. A masking effect of facilitated depolarizing potentials on IPSPs was unlikely since IPSPs accompanied by little or no depolarizing potential were also depressed by SR trains. The 75% reduction in IPSP conductance found after repetitive stimulation confirmed that an overlapping conductance was not responsible for the depression of the IPSP. The GABA-induced conductance increase was not depressed by identical trains. Trains of stimulation induced depolarizing shifts in equilibrium potentials for the IPSP (EIPSP) and GABA (EGABA) of approximately 10 mV. These shifts were always greater after SR trains than after ALV trains. Simultaneous recordings of membrane potential and extracellular potassium concentration ([K+]o) with K+-sensitive microelectrodes revealed a direct correlation between the two during a stimulus train. Membrane potential depolarized as much as 18 mV from the peak of the IPSP and [K+]o could increase to a maximum of 10 mM during some trains. A depressant effect (of approximately 50%) of K+ on IPSPs was demonstrated by brief pressure ejection of K+ near the soma. We conclude that repetitive stimulation depresses gIPSP and shifts EIPSP in the depolarizing direction. Whereas gIPSP began to decline after a single conditioning pulse, the additional depression of IPSPs produced by stimulus trains was due in large part to shifts in EIPSP. Depression of gIPSP was not due to desensitization or block of ionic conductances, since gGABA was not reduced. The EIPSP may change as a result of increases in [K+]o.

Dendrosomatic Voltage and Charge Transfer in Rat Neocortical Pyramidal Cells In Vitro

2000 ◽  
Vol 84 (3) ◽  
pp. 1445-1452 ◽  
Author(s):  
Daniel Ulrich ◽  
Christian Stricker
Keyword(s):  
Membrane Potential ◽  
Time Course ◽  
Cutoff Frequency ◽  
Pyramidal Cells ◽  
Apical Dendrite ◽  
Resting Membrane Potential ◽  
Excitatory Postsynaptic Potential ◽  
Transfer Characteristics ◽  
Layer V

Most excitatory synapses on neocortical pyramidal cells are located on dendrites, which are endowed with a variety of active conductances. The main origin for action potentials is thought to be at the initial segment of the axon, although local regenerative activity can be initiated in the dendrites. The transfer characteristics of synaptic voltage and charge along the dendrite to the soma remains largely unknown, although this is an essential determinant of neural input-output transformations. Here we perform dual whole-cell recordings from layer V pyramidal cells in slices from somatosensory cortex of juvenile rats. Steady-state and sinusoidal current injections are applied to characterize the voltage transfer characteristics of the apical dendrite under resting conditions. Furthermore, dendrosomatic charge and voltage transfer are determined by mimicking synapses via dynamic current-clamping. We find that around rest, the dendrite behaves like a linear cable. The cutoff frequency for somatopetal current transfer is around 4 Hz, i.e., synaptic inputs are heavily low-pass filtered. In agreement with linearity, transfer resistances are reciprocal in opposite directions, and the centroids of the synaptic time course are on the order of the membrane time constant. Transfer of excitatory postsynaptic potential (EPSP) charge, but not peak amplitude, is positively correlated with membrane potential. We conclude that the integrative properties of dendrites in infragranular neocortical pyramidal cells appear to be linear near resting membrane potential. However, at polarized potentials charge transferred is voltage-dependent with a loss of charge at hyperpolarized and a gain of charge at depolarized potentials.

scholarly journals Homer 1a Suppresses Neocortex Long-Term Depression in a Cortical Layer-Specific Manner

2008 ◽  
Vol 99 (2) ◽  
pp. 950-957 ◽  
Author(s):  
Yoshifumi Ueta ◽  
Ryo Yamamoto ◽  
Shigeki Sugiura ◽  
Kaoru Inokuchi ◽  
Nobuo Kato
Keyword(s):  
Metabotropic Glutamate Receptors ◽  
Pyramidal Cells ◽  
Cortical Layer ◽  
Long Term Depression ◽  
Group I ◽  
Specific Manner ◽  
Group I Mglurs ◽  
Layer V ◽  
Layer Vi

Homer1a/Vesl-1S is an activity-dependently induced member of the scaffold protein family Homer/Vesl, which is known to link group I metabotropic glutamate receptors (mGluRs) to endoplasmic calcium release channels and to regulate them. Here we studied roles of Homer 1a in inducing long-term depression (LTD) in rat visual cortex slices. Homer 1a protein was injected by diffusion from whole cell patch pipettes. In layer VI pyramidal cells, LTD was reduced in magnitude with Homer 1a. LTD in layer VI was suppressed by applying antagonists of mGluR5, a subtype of group I mGluRs expressed with higher density than mGluR1 in neocortex pyramidal cells, or inositol-1,4,5-triphosphate receptors (IP3Rs) but not that against N-methyl-d-aspartate receptors (NMDARs). In layer II/III or layer V, Homer 1a injection was unable to affect LTD, which is mostly dependent on NMDARs and not on group I mGluRs in these layers. To examine the effects of endogenous Homer 1a, electroconvulsive shock (ECS) was applied. Homer 1a thereby induced, as did Homer 1a injection, reduced LTD magnitude in layer VI pyramidal cells and failed to do so in layer II/III or layer V pyramidal cells. These results indicate that both exo- and endogenous Homer 1a suppressed LTD in a cortical layer-specific manner, and its layer-specificity may be explained by the high affinity of Homer 1a to group I mGluRs.

Electrophysiological and morphological characteristics of layer VI pyramidal cells in the cat motor cortex

1994 ◽  
Vol 72 (2) ◽  
pp. 578-591 ◽  
Author(s):  
Y. Kang ◽  
F. Kayano
Keyword(s):  
Motor Cortex ◽  
Action Potentials ◽  
Morphological Characteristics ◽  
Pyramidal Cells ◽  
Apical Dendrite ◽  
Current Pulses ◽  
Axon Collaterals ◽  
Layer V ◽  
Apical Dendrites ◽  
Layer Vi

1. Intracellular recordings were made from layer VI pyramidal cells in in vitro slice preparations of the cat motor cortex (area 4 gamma). Layer VI pyramidal cells were identified morphologically by intracellular injection of biocytin. 2. Of 22 layer VI pyramidal cells examined, single action potentials were followed by depolarizing afterpotentials (DAP) in 9 cells, but were not followed by DAP in the remaining 13 cells. The amplitude of DAP was 3.4 +/- 1.4 mV (mean +/- SD, n = 9) when measured from the negative peak of fast afterhyperpolarization to the peak of DAP. 3. In response to depolarizing current pulses with a duration of 300–400 ms, pyramidal cells showing DAP displayed a train of action potentials in a phasic-tonic pattern without any appreciable adaptation in the tonic firing, whereas pyramidal cells lacking DAP exhibited a weak adaptation after phasic firing. Anomalous rectification was seen in both pyramidal cells showing DAP and those lacking DAP. 4. Repetitive doublet or triplet spiking was induced in DAP-showing pyramidal cells in response to a depolarizing current pulse after injecting strong depolarizing current pulses of 400 ms duration at 1 Hz for 30–60 s, but was never induced in DAP-lacking pyramidal cells. Doublet/triplet spiking lasted 5–10 min and returned to the original single spiking. An application of CsCl induced a burst firing in DAP-showing pyramidal cells. 5. In the nine pyramidal cells showing DAP, seven cells had shorter apical dendrites that arborized extensively at layer V and terminated in the middle part of layer III. In the 13 pyramidal cells lacking DAP, 11 cells had longer apical dendrites that arborized less frequently and extended into layer II or I. Main axons could be traced into the deep white matter in 17 of the 22 layer VI pyramidal cells examined. 6. Ascending recurrent axon collaterals were more prominent in pyramidal cells with longer apical dendrites than in pyramidal cells with shorter apical dendrites. The terminal bouton-like swelling observed along the recurrent axon collaterals arising from the pyramidal cells with longer apical dendrite were distributed most densely at the level between the bottom part of layer III and the top part of layer V. In contrast, those arising from the pyramidal cells with shorter apical dendrite were distributed mainly at the levels of layers V and VI.(ABSTRACT TRUNCATED AT 400 WORDS)

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