Calcium currents in rat entorhinal cortex layer II stellate and layer III pyramidal neurons in acute brain slice

The lateral entorhinal cortex (LEC) provides information about multi-sensory environmental cues to the hippocampus through direct inputs to the distal dendrites of CA1 pyramidal neurons. A growing body of work suggests that LEC neurons perform important functions for episodic memory processing, coding for contextually-salient elements of an environment or the experience within it. However, we know little about the functional circuit interactions between LEC and the hippocampus. In this study, we combine functional circuit mapping and computational modeling to examine how long-range glutamatergic LEC projections modulate compartment-specific excitation-inhibition dynamics in hippocampal area CA1. We demonstrate that glutamatergic LEC inputs can drive local dendritic spikes in CA1 pyramidal neurons, aided by the recruitment of a disinhibitory vasoactive intestinal peptide (VIP)-expressing inhibitory neuron microcircuit. Our circuit mapping further reveals that, in parallel, LEC also recruits cholecystokinin (CCK)-expressing inhibitory neurons, which our model predicts act as a strong suppressor of dendritic spikes. These results provide new insight into a cortically-driven GABAergic microcircuit mechanism that gates non-linear dendritic computations, which may support compartment-specific coding of multi-sensory contextual features within the hippocampus.

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Specificity in the Interaction of HVA Ca2+ Channel Types With Ca2+-Dependent AHPs and Firing Behavior in Neocortical Pyramidal Neurons

Journal of Neurophysiology ◽

10.1152/jn.1998.79.5.2522 ◽

1998 ◽

Vol 79 (5) ◽

pp. 2522-2534 ◽

Cited By ~ 72

Author(s):

Juan Carlos Pineda ◽

Robert S. Waters ◽

Robert C. Foehring

Keyword(s):

Brain Slice ◽

Pyramidal Neurons ◽

Repetitive Firing ◽

Channel Blockers ◽

Firing Behavior ◽

Inward Currents ◽

Functional Consequences ◽

P Type ◽

Brain Slice Preparation ◽

Neocortical Pyramidal Neurons

Pineda, Juan Carlos, Roberts S. Waters, and Robert C. Foehring. Specificity in the interaction of HVA Ca2+ channel types with Ca2+-dependent AHPs and firing behavior in neocortical pyramidal neurons. J. Neurophysiol. 79: 2522–2534, 1998. Intracellular recordings and organic and inorganic Ca2+ channel blockers were used in a neocortical brain slice preparation to test whether high-voltage–activated (HVA) Ca2+ channels are differentially coupled to Ca2+-dependent afterhyperpolarizations (AHPs) in sensorimotor neocortical pyramidal neurons. For the most part, spike repolarization was not Ca2+ dependent in these cells, although the final phase of repolarization (after the fast AHP) was sensitive to block of N-type current. Between 30 and 60% of the medium afterhyperpolarization (mAHP) and between ∼80 and 90% of the slow AHP (sAHP) were Ca2+ dependent. Based on the effects of specific organic Ca2+ channel blockers (dihydropyridines, ω-conotoxin GVIA, ω-agatoxin IVA, and ω-conotoxin MVIIC), the sAHP is coupled to N-, P-, and Q-type currents. P-type currents were coupled to the mAHP. L-type current was not involved in the generation of either AHP but (with other HVA currents) contributes to the inward currents that regulate interspike intervals during repetitive firing. These data suggest different functional consequences for modulation of Ca2+ current subtypes.

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Calcium Currents in Retrogradely Labeled Pyramidal Cells From Rat Sensorimotor Cortex

Journal of Neurophysiology ◽

10.1152/jn.2000.83.4.2349 ◽

2000 ◽

Vol 83 (4) ◽

pp. 2349-2354 ◽

Cited By ~ 9

Author(s):

Ansalan Stewart ◽

Robert C. Foehring

Keyword(s):

Pyramidal Neurons ◽

Pyramidal Cells ◽

Cell Types ◽

Calcium Currents ◽

Patch Clamp Technique ◽

Whole Cell ◽

Multiple Populations ◽

Whole Cell Patch Clamp ◽

The Mean ◽

P Type

Our previous studies of calcium (Ca2+) currents in cortical pyramidal cells revealed that the percentage contribution of each Ca2+ current type to the whole cell Ca2+ current varies from cell to cell. The extent to which these currents are modulated by neurotransmitters is also variable. This study was directed at testing the hypothesis that a major source of this variability is recording from multiple populations of pyramidal cells. We used the whole cell patch-clamp technique to record from dissociated corticocortical, corticostriatal, and corticotectal projecting pyramidal cells. There were significant differences between the three pyramidal cell types in the mean percentage of L-, P-, and N-type Ca2+ currents. For both N- and P-type currents, the range of percentages expressed was small for corticostriatal and corticotectal cells as compared with cells which project to the corpus callosum or to the general population. The variance was significantly different between cell types for N- and P-type currents. These results suggest that an important source of the variability in the proportions of Ca2+ current types present in neocortical pyramidal neurons is recording from multiple populations of pyramidal cells.

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

Journal of Neurophysiology ◽

10.1152/jn.00014.2010 ◽

2011 ◽

Vol 105 (3) ◽

pp. 1372-1379 ◽

Cited By ~ 12

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.

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