Intrinsic Ca2+-dependent theta oscillations in apical dendrites of hippocampal CA1 pyramidal cells in vitro

2014 ◽  
Vol 112 (3) ◽  
pp. 631-643 ◽  
Author(s):  
Allan Kjeldsen Hansen ◽  
Steen Nedergaard ◽  
Mogens Andreasen
Keyword(s):  
Frequency Band ◽  
Pyramidal Cells ◽  
Sine Wave ◽  
Detectable Effect ◽  
Ca1 Pyramidal Cells ◽  
Theta Frequency ◽  
Voltage Dependent ◽  
Oscillatory Mechanism ◽  
Apical Dendrites

Behavior-associated theta-frequency oscillation in the hippocampal network involves a patterned activation of place cells in the CA1, which can be accounted for by a somatic-dendritic interference model predicting the existence of an intrinsic dendritic oscillator. Here we describe an intrinsic oscillatory mechanism in apical dendrites of in vitro CA1 pyramidal cells, which is induced by suprathreshold depolarization and consists of rhythmic firing of slow spikes in the theta-frequency band. The incidence of slow spiking (29%) increased to 78% and 100% in the presence of the β-adrenergic agonist isoproterenol (2 μM) or 4-aminopyridine (2 mM), respectively. Prior depolarization facilitated the induction of slow spiking. Applied electrical field polarization revealed a distal dendritic origin of slow spikes. The oscillations were largely insensitive to tetrodotoxin, but blocked by nimodipine (10 μM), indicating that they depend on activation of L-type Ca2+ channels. Antagonists of T-, R-, N-, and P/Q-type Ca2+ channels had no detectable effect. The slow spike dimension and frequency was sensitive to 4-aminopyridine (0.1–2 mM) and TEA (10 mM), suggesting the contribution from voltage-dependent K+ channels to the oscillation mechanism. α-Dendrotoxin (10 μM), stromatoxin (2 μM), iberiotoxin (0.2 μM), apamin (0.5 μM), linorpidine (30 μM), and ZD7288 (20 μM) were without effect. Oscillations induced by sine-wave current injection or theta-burst synaptic stimulation were voltage-dependently attenuated by nimodipine, indicating an amplifying function of L-type Ca2+ channels on imposed signals. These results show that the apical dendrites have intrinsic oscillatory properties capable of generating rhythmic voltage fluctuations in the theta-frequency band.

Propagating dendritic action potential mediates synaptic transmission in CA1 pyramidal cells in situ

1990 ◽  
Vol 64 (5) ◽  
pp. 1429-1441 ◽  
Author(s):  
O. Herreras
Keyword(s):  
Pyramidal Neurons ◽  
Current Source ◽  
Maximum Amplitude ◽  
Pyramidal Cells ◽  
Distal Portion ◽  
Ca1 Pyramidal Cells ◽  
Basal Dendrites ◽  
Voltage Dependent ◽  
Speed Of Propagation ◽  
Apical Dendrites

1. The events leading to the Schaffer collateral-induced discharge of CA1 pyramidal neurons were investigated in the hippocampus of anesthetized rats by current source-density (CSD) analysis. 2. The earliest evoked currents detected shortly after a stimulus were a sink in the zone where synapses are known to be located (300-350 microns ventral to the somatic layer) flanked by two smaller sources in the distal portion of the apical dendrites and in the somatic layer. This synaptic sink (SyS) extended over 75-100 microns; it lasted for 15-20 ms, and it reached its maximum amplitude some milliseconds after the population spike (PS) and remained in the same location. Stimuli submaximal and supramaximal for evoking a PS yielded the same pattern of current distribution for the SyS. Presynaptic fiber volleys were not detected in these recordings. 3. During the rising phase of the SyS a second sink appeared in a more proximal portion of the apical dendrites. This late dendritic sink (LS) extended over 50-75 microns and was centered 100-150 microns ventral to the somatic layer. This proximal dendritic sink was of amplitude comparable with the SyS; it outlasted the latter and was not necessarily followed by a somatic PS. The LS was extinguished with the appearance of a PS, whereas the SyS persisted regardless of the presence of a PS. 4. After maximal stimuli the LS grew until it exceeded a threshold amplitude, and then, it started to move somatopetally as a continuously propagating sink (PrS). The average speed of propagation was approximately 0.2 m/s. In 0.5-0.7 ms the PrS reached the cell-body layer displacing the passive source that moved into the basal dendrites. The PrS then became the intensive sink corresponding to the main (negative) phase of the somatic PS. This was followed by the development of an active source in the soma layer, probably corresponding to the repolarization phase of the PS. 5. From these observations it appears that the LS and PrS are active dendritic responses. It may be inferred that, shortly after the synaptic currents enter the dendrites, depolarization of adjacent membranes causes the opening of low-threshold, voltage-dependent, slowly inactivating channels that generate the LS. If the depolarization resulting from the LS current is intense enough, another population of channels open that are also voltage-dependent but of higher threshold and faster inactivation.(ABSTRACT TRUNCATED AT 400 WORDS)

Barbiturate protection against hypoxic neuronal damage in vitro

1986 ◽  
Vol 65 (2) ◽  
pp. 230-232 ◽  
Author(s):  
Peter G. Aitken ◽  
Steven J. Schiff
Keyword(s):  
Neuronal Damage ◽  
Pyramidal Cells ◽  
Perfusion Medium ◽  
Tissue Slices ◽  
Content Type ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Tissue ◽  
Barbiturate Protection ◽  
Fine Print

✓ Hippocampal tissue slices in vitro were exposed to periods of hypoxia of different durations. Addition of pentobarbital to the perfusion medium significantly increased the duration of hypoxia that was survived by CA1 pyramidal cells.

scholarly journals A Classification Method to Distinguish Cell-Specific Responses Elicited by Current Pulses in Hippocampal CA1 Pyramidal Cells

2008 ◽  
Vol 20 (6) ◽  
pp. 1512-1536 ◽  
Author(s):  
José Ambros-Ingerson ◽  
Lawrence M. Grover ◽  
William R. Holmes
Keyword(s):  
Distance Measure ◽  
Network Models ◽  
Pyramidal Cells ◽  
Spike Timing ◽  
Voltage Gradient ◽  
Neural Function ◽  
Ca1 Pyramidal Cells ◽  
Current Pulses ◽  
Point Distance

The suprathreshold electrophysiological responses of pyramidal cells have been grouped into large classes such as bursting and spiking. However, it is not known whether, within a class, response variability ranges uniformly across all cells or whether each cell has a unique and consistent profile that can be differentiated. A major difficulty when comparing suprathreshold responses is that slight variations in spike timing in otherwise very similar traces render traditional metrics ineffective. To address these issues, we developed a novel distance measure based on fiducial points to quantify the similarity among traces with trains of action potentials and applied it together with classification techniques to a set of in vitro patch clamp recordings from CA1 pyramidal cells. We tested if responses to repeated current stimulation of a given cell would cluster together yet remain distinct from those of other cells. We found that depolarizing and hyperpolarizing current pulses elicited responses in each cell that clustered and were systematically distinguishable from responses in other cells. The fiducial-point distance measure was more effective than other methods based on spike times and voltage-gradient phase planes. Depolarizing traces were more reliably differentiated than hyperpolarizing traces, and combining both scores was even more effective. These results suggest that each CA1 pyramidal cell has unique properties that can be detected and quantified with methods discussed here. This uniqueness may be due to slight variations in morphology or membrane channel densities and kinetics, or to large, coordinated variations in these elements. Ascertaining the actual sources and their degree of variability is important when constructing network models of neural function to ensure that key mechanisms are robust in the face of variations within these ranges. The analytical tools presented here can assist in constructing detailed cell models to match experimental records to elucidate the sources of electrophysiological variability in neurons.

Synaptic triggering of epileptiform discharges in CA1 pyramidal cells in vitro

1981 ◽  
Vol 113 (2) ◽  
pp. 245-252 ◽  
Author(s):  
L. GJERSTAD ◽  
P. ANDERSEN ◽  
I. A. LANGMOEN ◽  
A. LUNDERVOLD ◽  
J. HABLITZ
Keyword(s):  
Pyramidal Cells ◽  
Ca1 Pyramidal Cells ◽  
Epileptiform Discharges

Efects of corticosterone on the electrophysiology of hippocampal CA1 pyramidal Cells in vitro

1984 ◽  
Vol 12 (4) ◽  
pp. 349-353 ◽  
Author(s):  
Craig T. Reiheld ◽  
Timothy J. Teyler ◽  
Richard M. Vardaris
Keyword(s):  
Pyramidal Cells ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1

Role of norepinephrine in seizurelike activity of hippocampal pyramidal cells maintained in vitro: alteration by 6-hydroxydopamine lesions of norepinephrine-containing systems

1983 ◽  
Vol 61 (8) ◽  
pp. 841-846 ◽  
Author(s):  
I. Mody ◽  
P. Leung ◽  
J. J. Miller
Keyword(s):  
Epileptiform Activity ◽  
Pyramidal Cells ◽  
Population Spike ◽  
Stratum Radiatum ◽  
Excitatory Postsynaptic Potential ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Population Spike Amplitude ◽  
6 Hydroxydopamine

Perfusion of 50 μM norepinephrine (NE) produced a marked, reversible decrease (range 20–28%) of the extracellular population spike and excitatory postsynaptic potential (EPSP) responses of the CA1 region evoked by stratum radiatum stimulation in the rat hippocampal slice preparation. The effects of NE were dramatically altered in slices obtained from animals which were previously treated with intracerebral or intraventricular injections of 6-hydroxydopamine (6-OHDA) to destroy forebrain catecholamine systems. In the latter preparations NE produced a reduction in the inhibition of the EPSP (50%), enhancement of the population spike amplitude, and multiple spike discharges characteristic of ongoing epileptiform activity. The reversal of NE-induced inhibition and the generation of seizurelike activity in 6-OHDA-treated animals suggests that NE may, in part, act upon interneurons to produce a disinhibition of CA1 pyramidal cells.

Fiberoptic System for Recording Dendritic Calcium Signals in Layer 5 Neocortical Pyramidal Cells in Freely Moving Rats

2007 ◽  
Vol 98 (3) ◽  
pp. 1791-1805 ◽  
Author(s):  
Masanori Murayama ◽  
Enrique Pérez-Garci ◽  
Hans-Rudolf Lüscher ◽  
Matthew E. Larkum
Keyword(s):  
Pyramidal Neurons ◽  
Calcium Influx ◽  
Signal To Noise Ratio ◽  
Pyramidal Cells ◽  
Cellular Mechanisms ◽  
Novel Approach ◽  
Specific Loading ◽  
Apical Dendrites

Calcium influx into the dendritic tufts of layer 5 neocortical pyramidal neurons modifies a number of important cellular mechanisms. It can trigger local synaptic plasticity and switch the firing properties from regular to burst firing. Due to methodological limitations, our knowledge about Ca2+ spikes in the dendritic tuft stems mostly from in vitro experiments. However, it has been speculated that regenerative Ca2+ events in the distal dendrites correlate with distinct behavioral states. Therefore it would be most desirable to be able to record these Ca2+ events in vivo, preferably in the behaving animal. Here, we present a novel approach for recording Ca2+ signals in the dendrites of populations of layer 5 pyramidal neurons in vivo, which ensures that all recorded fluorescence changes are due to intracellular Ca2+ signals in the apical dendrites. The method has two main features: 1) bolus loading of layer 5 with a membrane-permeant Ca2+ dye resulting in specific loading of pyramidal cell dendrites in the upper layers and 2) a fiberoptic cable attached to a gradient index lens and a prism reflecting light horizontally at 90° to the angle of the apical dendrites. We demonstrate that the in vivo signal-to-noise ratio recorded with this relatively inexpensive and easy-to-implement fiberoptic-based device is comparable to conventional camera-based imaging systems used in vitro. In addition, the device is flexible and lightweight and can be used for recording Ca2+ signals in the distal dendritic tuft of freely behaving animals.

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