scholarly journals Distance- and activity-dependent modulation of spike back-propagation in layer V pyramidal neurons of the medial entorhinal cortex

2011 ◽  
Vol 105 (3) ◽  
pp. 1372-1379 ◽  
Author(s):  
Sonia Gasparini
Keyword(s):  
Entorhinal Cortex ◽  
High Speed ◽  
Pyramidal Neurons ◽  
Back Propagation ◽  
Medial Entorhinal Cortex ◽  
Type K ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Layer V ◽  
Activity Dependent

Layer V principal neurons of the medial entorhinal cortex receive the main hippocampal output and relay processed information to the neocortex. Despite the fundamental role hypothesized for these neurons in memory replay and consolidation, their dendritic features are largely unknown. High-speed confocal and two-photon Ca2+ imaging coupled with somatic whole cell patch-clamp recordings were used to investigate spike back-propagation in these neurons. The Ca2+ transient associated with a single back-propagating action potential was considerably smaller at distal dendritic locations (>200 μm from the soma) compared with proximal ones. Perfusion of Ba2+ (150 μM) or 4-aminopyridine (2 mM) to block A-type K+ currents significantly increased the amplitude of the distal, but not proximal, Ca2+ transients, which is strong evidence for an increased density of these channels at distal dendritic locations. In addition, the Ca2+ transients decreased with each subsequent spike in a 20-Hz train; this activity-dependent decrease was also more prominent at more distal locations and was attenuated by the perfusion of the protein kinase C activator phorbol-di-acetate. These data are consistent with a phosphorylation-dependent control of back-propagation during trains of action potentials, attributable mainly to an increase in the time constant of recovery from voltage-dependent inactivation of dendritic Na+ channels. In summary, dendritic Na+ and A-type K+ channels control spike back-propagation in layer V entorhinal neurons. Because the activity of these channels is highly modulated, the extent of the dendritic Ca2+ influx is as well, with important functional implications for dendritic integration and associative synaptic plasticity.

Stimulation of 5-HT2 Receptors in Prefrontal Pyramidal Neurons Inhibits Cav1.2 L-Type Ca2+Currents Via a PLCβ/IP3/Calcineurin Signaling Cascade

2002 ◽  
Vol 87 (5) ◽  
pp. 2490-2504 ◽  
Author(s):  
Michelle Day ◽  
Patricia A. Olson ◽  
Josef Platzer ◽  
Joerg Striessnig ◽  
D. James Surmeier
Keyword(s):  
Pyramidal Neurons ◽  
Inositol Trisphosphate ◽  
Cell Voltage ◽  
Signaling Cascade ◽  
Channel Modulation ◽  
Receptor Modulation ◽  
Bath Application ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Layer V

There is growing evidence linking alterations in serotonergic signaling in the prefrontal cortex to the etiology of schizophrenia. Prefrontal pyramidal neurons are richly innervated by serotonergic fibers and express high levels of serotonergic 5-HT2-class receptors. It is unclear, however, how activation of these receptors modulates cellular activity. To help fill this gap, whole cell voltage-clamp and single-cell RT-PCR studies of acutely isolated layer V–VI prefrontal pyramidal neurons were undertaken. The vast majority (>80%) of these neurons had detectable levels of 5-HT2A or 5-HT2C receptor mRNA. Bath application of 5-HT2 agonists inhibited voltage-dependent Ca2+ channel currents. L-type Ca2+ channels were a particularly prominent target of this signaling pathway. The L-type channel modulation was blocked by disruption of Gαq signaling or by inhibition of phospholipase Cβ. Antagonism of intracellular inositol trisphosphate signaling, chelation of intracellular Ca2+, or depletion of intracellular Ca2+ stores also blocked this modulation. Inhibition of the Ca2+-dependent phosphatase calcineurin prevented receptor-mediated modulation of L-type currents. Last, the 5-HT2 receptor modulation was robustly expressed in neurons from Cav1.3 knockout mice. These findings argue that 5-HT2receptors couple through Gαq proteins to trigger a phospholipase Cβ/inositol trisphosphate signaling cascade resulting in the mobilization of intracellular Ca2+, activation of calcineurin, and inhibition of Cav1.2 L-type Ca2+currents. This modulation and its blockade by atypical neuroleptics could have wide-ranging effects on synaptic integration and long-term gene expression in deep-layer prefrontal pyramidal neurons.

scholarly journals Cholinergic Modulation of the Resonance Properties of Stellate Cells in Layer II of Medial Entorhinal Cortex

2010 ◽  
Vol 104 (1) ◽  
pp. 258-270 ◽  
Author(s):  
James G. Heys ◽  
Lisa M. Giocomo ◽  
Michael E. Hasselmo
Keyword(s):  
Patch Clamp ◽  
Resonance Frequency ◽  
Entorhinal Cortex ◽  
Stellate Cells ◽  
Cholinergic Modulation ◽  
Medial Entorhinal Cortex ◽  
Whole Cell ◽  
Whole Cell Patch Clamp ◽  
Resonance Properties

In vitro whole cell patch-clamp recordings of stellate cells in layer II of medial entorhinal cortex show a subthreshold membrane potential resonance in response to a sinusoidal current injection of varying frequency. Physiological recordings from awake behaving animals show that neurons in layer II medial entorhinal cortex, termed “grid cells,” fire in a spatially selective manner such that each cell's multiple firing fields form a hexagonal grid. Both the spatial periodicity of the grid fields and the resonance frequency change systematically in neurons along the dorsal to ventral axis of medial entorhinal cortex. Previous work has also shown that grid field spacing and acetylcholine levels change as a function of the novelty to a particular environment. Using in vitro whole cell patch-clamp recordings, our study shows that both resonance frequency and resonance strength vary as a function of cholinergic modulation. Furthermore, our data suggest that these changes in resonance properties are mediated through modulation of h-current and m-current.

scholarly journals Activity-dependent downregulation of D-type K+channel subunit Kv1.2 in rat hippocampal CA3 pyramidal neurons

2013 ◽  
Vol 591 (22) ◽  
pp. 5525-5540 ◽  
Author(s):  
Jung Ho Hyun ◽  
Kisang Eom ◽  
Kyu-Hee Lee ◽  
Won-Kyung Ho ◽  
Suk-Ho Lee
Keyword(s):  
Pyramidal Neurons ◽  
K Channel ◽  
Type K ◽  
Hippocampal Ca3 ◽  
Ca3 Pyramidal Neurons ◽  
Activity Dependent

scholarly journals The Role of NMDA Receptor Subtypes in Short-Term Plasticity in the Rat Entorhinal Cortex

2008 ◽  
Vol 2008 ◽  
pp. 1-13 ◽  
Author(s):  
Sophie E. L. Chamberlain ◽  
Jian Yang ◽  
Roland S. G. Jones
Keyword(s):  
Entorhinal Cortex ◽  
Glutamate Release ◽  
Receptor Subtypes ◽  
Short Term ◽  
Low Frequencies ◽  
Short Term Plasticity ◽  
Whole Cell Patch Clamp ◽  
Layer V ◽  
Presynaptic Nmda Receptors

We have previously shown that spontaneous release of glutamate in the entorhinal cortex (EC) is tonically facilitated via activation of presynaptic NMDA receptors (NMDAr) containing the NR2B subunit. Here we show that the same receptors mediate short-term plasticity manifested by frequency-dependent facilitation of evoked glutamate release at these synapses. Whole-cell patch-clamp recordings were made from layer V pyramidal neurones in rat EC slices. Evoked excitatory postsynaptic currents showed strong facilitation at relatively low frequencies (3 Hz) of activation. Facilitation was abolished by an NR2B-selective blocker (Ro 25-6981), but unaffected by NR2A-selective antagonists (Zn2+, NVP-AAM077). In contrast, postsynaptic NMDAr-mediated responses could be reduced by subunit-selective concentrations of all three antagonists. The data suggest that NMDAr involved in presynaptic plasticity in layer V are exclusively NR1/NR2B diheteromers, whilst postsynaptically they are probably a mixture of NR1/NR2A, NR1/NR2B diheteromers and NR1/NR2A/NR2B triheteromeric receptors.

Input from the presubiculum to dendrites of layer-V neurons of the medial entorhinal cortex of the rat

2004 ◽  
Vol 1013 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Floris G Wouterlood ◽  
Theo van Haeften ◽  
Maartje Eijkhoudt ◽  
Luciënne Baks-te-Bulte ◽  
Peter H Goede ◽  
...  
Keyword(s):  
Entorhinal Cortex ◽  
Medial Entorhinal Cortex ◽  
Layer V

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.

Ca2+-independent muscarinic excitation of rat medial entorhinal cortex layer V neurons

2003 ◽  
Vol 18 (12) ◽  
pp. 3343-3351 ◽  
Author(s):  
Alexei V. Egorov ◽  
Plamena R. Angelova ◽  
Uwe Heinemann ◽  
Wolfgang Muller
Keyword(s):  
Entorhinal Cortex ◽  
Medial Entorhinal Cortex ◽  
Layer V
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