Effects of dithiothreitol, a sulfhydryl reducing agent, on CA1 pyramidal cells of the guinea pig hippocampus in vitro

1988 ◽  
Vol 456 (1) ◽  
pp. 49-56 ◽  
Author(s):  
J.M. Tolliver ◽  
T.C. Pellmar
1986 ◽  
Vol 65 (2) ◽  
pp. 230-232 ◽  
Author(s):  
Peter G. Aitken ◽  
Steven J. Schiff

✓ 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.


2008 ◽  
Vol 20 (6) ◽  
pp. 1512-1536 ◽  
Author(s):  
José Ambros-Ingerson ◽  
Lawrence M. Grover ◽  
William R. Holmes

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.


2014 ◽  
Vol 112 (3) ◽  
pp. 631-643 ◽  
Author(s):  
Allan Kjeldsen Hansen ◽  
Steen Nedergaard ◽  
Mogens Andreasen

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.


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

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

1983 ◽  
Vol 61 (8) ◽  
pp. 841-846 ◽  
Author(s):  
I. Mody ◽  
P. Leung ◽  
J. J. Miller

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.


1994 ◽  
Vol 72 (1) ◽  
pp. 131-138 ◽  
Author(s):  
R. Bianchi ◽  
R. K. Wong

1. Carbachol effects on CA3 hippocampal cells were studied in the absence of ionotropic glutamatergic and GABAergic transmission with intracellular and extracellular recordings from guinea pig septohippocampal slices. 2. In all experiments the perfusing solution contained ionotropic glutamate and gamma-aminobutyric acid (GABA) receptor blockers [6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10–20 microM), 3-((+/-)-2-carboxypiperazin-4-il)propyl-1-phosphonic acid (CPP, 10–20 microM), and picrotoxin (50 microM), respectively]. Under these conditions, the excitatory and early inhibitory postsynaptic potentials, evoked in CA3 pyramidal cells by mossy fiber stimulation before the addition of the blockers, were completely suppressed. 3. Carbachol (50 microM) introduced via bath perfusion or pulse application elicited a series of rhythmic bursts with overriding action potentials. Each rhythmic burst lasted up to 30 s and repeated at intervals of 0.7–6 min. Rhythmic bursts were blocked by atropine (1 microM). 4. At membrane potentials more depolarized than -70 mV, carbachol also elicited a sustained depolarization associated with an increase in membrane input resistance and action-potential firing. This response was blocked by atropine (1 microM). 5. Carbachol can induce both rhythmic bursts and sustained depolarizations in the same cell. Rhythmic bursts were elicited when the membrane potential of the cell was more hyperpolarized than -70 mV; sustained depolarizing responses were activated by carbachol when the cell membrane potential was more depolarized than -70 mV. 6. Extracellular field potential responses in the CA3 region occurred simultaneously with rhythmic bursts, indicating the synchronization of the event in the CA3 field. Dual intracellular recordings confirmed that rhythmic bursts occurred simultaneously in CA3 hippocampal pyramidal cells.(ABSTRACT TRUNCATED AT 250 WORDS)


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