Dendritic properties of hippocampal CA1 pyramidal neurons in the rat: Intracellular staining in vivo and in vitro

1998 ◽  
Vol 391 (3) ◽  
pp. 335-352 ◽  
Author(s):  
G.K. Pyapali ◽  
A. Sik ◽  
M. Penttonen ◽  
G. Buzsaki ◽  
D.A. Turner
Keyword(s):  
Pyramidal Neurons ◽  
Intracellular Staining ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1

scholarly journals Membrane Dysfunction Induced by In Vitro Ischemia in Rat Hippocampal CA1 Pyramidal Neurons

1999 ◽  
Vol 81 (4) ◽  
pp. 1872-1880 ◽  
Author(s):  
E. Tanaka ◽  
S. Yamamoto ◽  
H. Inokuchi ◽  
T. Isagai ◽  
H. Higashi
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Pyramidal Neurons ◽  
Membrane Surface ◽  
Bathing Medium ◽  
Ca1 Pyramidal Neurons ◽  
In Vitro Ischemia ◽  
Hippocampal Ca1 ◽  
Electrode Voltage

Membrane dysfunction induced by in vitro ischemia in rat hippocampal CA1 pyramidal neurons. Intracellular and single-electrode voltage-clamp recordings were made to investigate the process of membrane dysfunction induced by superfusion with oxygen and glucose-deprived (ischemia-simulating) medium in hippocampal CA1 pyramidal neurons of rat tissue slices. To assess correlation between potential change and membrane dysfunction, the recorded neurons were stained intracellularly with biocytin. A rapid depolarization was produced ∼6 min after starting superfusion with ischemia-simulating medium. When oxygen and glucose were reintroduced to the bathing medium immediately after generating the rapid depolarization, the membrane did not repolarize but depolarized further, the potential reaching 0 mV ∼5 min after the reintroduction. In single-electrode voltage-clamp recording, a corresponding rapid inward current was observed when the membrane potential was held at −70 mV. After the reintroduction of oxygen and glucose, the current induced by ischemia-simulating medium partially returned to preexposure levels. These results suggest that the membrane depolarization is involved with the membrane dysfunction. The morphological aspects of biocytin-stained neurons during ischemic exposure were not significantly different from control neurons before the rapid depolarization. On the other hand, small blebs were observed on the surface of the neuron within 0.5 min of generating the rapid depolarization, and blebs increased in size after 1 min. After 3 min, neurons became larger and swollen. The long and transverse axes and area of the cross-sectional cell body were increased significantly 1 and 3 min after the rapid depolarization. When Ca2+-free (0 mM) with Co2+ (2.5 mM)-containing medium including oxygen and glucose was applied within 1 min after the rapid depolarization, the membrane potential was restored completely to the preexposure level in the majority of neurons. In these neurons, the long axis was lengthened without any blebs being apparent on the membrane surface. These results suggest that the membrane dysfunction induced by in vitro ischemia may be due to a Ca2+-dependent process that commences ∼1.5 min after and is completed 3 min after the onset of the rapid depolarization. Because small blebs occurred immediately after the rapid depolarization and large blebs appeared 1.5–3 min after, it is likely that the transformation from small to large blebs may result in the observed irreversible membrane dysfunction.

Neuroprotective mechanisms of lidocaine against in vitro ischemic insult of the rat hippocampal CA1 pyramidal neurons

2005 ◽  
Vol 53 (3) ◽  
pp. 271-278 ◽  
Author(s):  
S. Niiyama ◽  
E. Tanaka ◽  
S. Tsuji ◽  
Y. Murai ◽  
M. Satani ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Ischemic Insult ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1

scholarly journals Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Matthieu Raveau ◽  
Denis Polygalov ◽  
Roman Boehringer ◽  
Kenji Amano ◽  
Kazuhiro Yamakawa ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Pyramidal Neurons ◽  
Chromosome 21 ◽  
Network Activity ◽  
Inhibitory Neurons ◽  
Spatial Coding ◽  
Extra Copy ◽  
Hippocampal Ca1

Down syndrome, the leading genetic cause of intellectual disability, results from an extra-copy of chromosome 21. Mice engineered to model this aneuploidy exhibit Down syndrome-like memory deficits in spatial and contextual tasks. While abnormal neuronal function has been identified in these models, most studies have relied on in vitro measures. Here, using in vivo recording in the Dp(16)1Yey model, we find alterations in the organization of spiking of hippocampal CA1 pyramidal neurons, including deficits in the generation of complex spikes. These changes lead to poorer spatial coding during exploration and less coordinated activity during sharp-wave ripples, events involved in memory consolidation. Further, the density of CA1 inhibitory neurons expressing neuropeptide Y, a population key for the generation of pyramidal cell bursts, were significantly increased in Dp(16)1Yey mice. Our data refine the ‘over-suppression’ theory of Down syndrome pathophysiology and suggest specific neuronal subtypes involved in hippocampal dysfunction in these model mice.

scholarly journals Kv1.1 contributes to a rapid homeostatic plasticity of intrinsic excitability in CA1 pyramidal neurons in vivo

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Peter James Morgan ◽  
Romain Bourboulou ◽  
Caroline Filippi ◽  
Julie Koenig-Gambini ◽  
Jérôme Epsztein
Keyword(s):  
Pyramidal Neurons ◽  
Place Cells ◽  
Homeostatic Plasticity ◽  
Intrinsic Excitability ◽  
Memory Interference ◽  
Ca1 Pyramidal Neurons ◽  
Whole Cell Patch Clamp ◽  
Activity Dependent

In area CA1 of the hippocampus, the selection of place cells to represent a new environment is biased towards neurons with higher excitability. However, different environments are represented by orthogonal cell ensembles, suggesting that regulatory mechanisms exist. Activity-dependent plasticity of intrinsic excitability, as observed in vitro, is an attractive candidate. Here, using whole-cell patch-clamp recordings of CA1 pyramidal neurons in anesthetized rats, we have examined how inducing theta-bursts of action potentials affects their intrinsic excitability over time. We observed a long-lasting, homeostatic depression of intrinsic excitability which commenced within minutes, and, in contrast to in vitro observations, was not mediated by dendritic Ih. Instead, it was attenuated by the Kv1.1 channel blocker dendrotoxin K, suggesting an axonal origin. Analysis of place cells’ out-of-field firing in mice navigating in virtual reality further revealed an experience-dependent reduction consistent with decreased excitability. We propose that this mechanism could reduce memory interference.

scholarly journals Enhanced Neuronal Damage After Ischemic Insults in Mice Lacking Kir6.2-Containing ATP-Sensitive K+ Channels

2006 ◽  
Vol 95 (4) ◽  
pp. 2590-2601 ◽  
Author(s):  
Hong-Shuo Sun ◽  
Zhong-Ping Feng ◽  
Takashi Miki ◽  
Susumu Seino ◽  
Robert J. French
Keyword(s):  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Neuronal Damage ◽  
Focal Cerebral Ischemia ◽  
Hippocampal Slices ◽  
Immunocytochemical Staining ◽  
Sulfonylurea Receptor ◽  
Ca1 Pyramidal Neurons

Adenosine triphosphate (ATP)–sensitive potassium (KATP) channels, incorporating Kir6.x and sulfonylurea receptor subunits, are weak inward rectifiers that are thought to play a role in neuronal protection from ischemic insults. However, the involvement of Kir6.2-containing KATP channel in hippocampus and neocortex has not been tested directly. To delineate the physiological roles of Kir6.2 channels in the CNS, we used knockout (KO) mice that do not express Kir6.2. Immunocytochemical staining demonstrated that Kir6.2 protein was expressed robustly in hippocampal neurons of the wild-type (WT) mice and absent in the KO. To examine neuronal sensitivity to metabolic stress in vitro, and to ischemia in vivo, we 1) exposed hippocampal slices to transient oxygen and glucose deprivation (OGD) and 2) produced focal cerebral ischemia by middle cerebral artery occlusion (MCAO). Both slice and whole animal studies showed that neurons from the KO mice were severely damaged after anoxia or ischemia, whereas few injured neurons were observed in the WT, suggesting that Kir6.2 channels are necessary to protect neurons from ischemic insults. Membrane potential recordings from the WT CA1 pyramidal neurons showed a biphasic response to OGD; a brief hyperpolarization was followed by a small depolarization during OGD, with complete recovery within 30 min after returning to normoxic conditions. By contrast, CA1 pyramidal neurons from the KO mice were irreversibly depolarized by OGD exposure, without any preceding hyperpolarization. These data suggest that expression of Kir6.2 channels prevents prolonged depolarization of neurons resulting from acute hypoxic or ischemic insults, and thus protects these central neurons from the injury.

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