scholarly journals 5-HT1A Receptor Agonists Enhance Pyramidal Cell Firing in Prefrontal Cortex Through a Preferential Action on GABA Interneurons

2011 ◽  
Vol 22 (7) ◽  
pp. 1487-1497 ◽  
Author(s):  
L. Llado-Pelfort ◽  
N. Santana ◽  
V. Ghisi ◽  
F. Artigas ◽  
P. Celada
Keyword(s):  
Prefrontal Cortex ◽  
Pyramidal Cell ◽  
Receptor Agonists ◽  
Cell Firing

scholarly journals Why are pyramidal cell firing rates increased with aging, and what can we do about it?

2008 ◽  
Vol 9 (S1) ◽  
Author(s):  
A Yadav ◽  
Christina M Weaver ◽  
Yuan Z Gao ◽  
Jennifer I Luebke ◽  
Susan L Wearne
Keyword(s):  
Pyramidal Cell ◽  
Firing Rates ◽  
Cell Firing

Effects of prefrontal cortex microinjection of neurotensin-(8-13) on midbrain dopamine and non-dopamine cell firing

2000 ◽  
Vol 876 (1-2) ◽  
pp. 196-200 ◽  
Author(s):  
Maria D Fatigati ◽  
Roberta M Anderson ◽  
Pierre-Paul Rompré
Keyword(s):  
Prefrontal Cortex ◽  
Cell Firing ◽  
Midbrain Dopamine ◽  
Dopamine Cell

Deciphering how interneuron specific 3 cells control oriens lacunosum-moleculare cells to contribute to circuit function

2021 ◽  
Author(s):  
Alexandre Guet-McCreight ◽  
Frances K Skinner
Keyword(s):  
Pyramidal Cell ◽  
Inhibitory Interneuron ◽  
Cell Type ◽  
Cell Recruitment ◽  
External Modulation ◽  
Theta Frequency ◽  
Cell Firing ◽  
Circuit Function

The wide diversity of inhibitory cells across the brain makes them suitable to contribute to network dynamics in specialized fashions. However, the contributions of a particular inhibitory cell type in a behaving animal are challenging to untangle as one needs to both record cellular activities and identify the cell type being recorded. Thus, using computational modeling and theory to predict and hypothesize cell-specific contributions is desirable. Here, we examine potential contributions of interneuron-specific 3 (I-S3) cells - an inhibitory interneuron found in CA1 hippocampus that only targets other inhibitory interneurons - during simulated theta rhythms. We use previously developed multi-compartment models of oriens lacunosum-moleculare (OLM) cells, the main target of I-S3 cells, and explore how I-S3 cell inputs during in vitro and in vivo scenarios contribute to theta. We find that I-S3 cells suppress OLM cell spiking, rather than engender its spiking via post-inhibitory rebound mechanisms, and contribute to theta frequency spike resonance during simulated in vivo scenarios. To elicit recruitment similar to in vitro experiments, inclusion of disinhibited pyramidal cell inputs is necessary, implying that I-S3 cell firing broadens the window for pyramidal cell disinhibition. Using in vivo virtual networks, we show that I-S3 cells contribute to a sharpening of OLM cell recruitment at theta frequencies. Further, shifting the timing of I-S3 cell spiking due to external modulation shifts the timing of the OLM cell firing and thus disinhibitory windows. We propose a specialized contribution of I-S3 cells to create temporally precise coordination of modulation pathways.

Depth distribution and mechanism of changes in extracellular K+ and Ca2+ concentrations in the hippocampus

1982 ◽  
Vol 60 (12) ◽  
pp. 1658-1671 ◽  
Author(s):  
K. Krnjević ◽  
M. E. Morris ◽  
R. J. Reiffenstein ◽  
N. Ropert
Keyword(s):  
Pyramidal Cell ◽  
Time Course ◽  
Depth Distribution ◽  
Close Correlation ◽  
Pyramidal Layer ◽  
Wide Range ◽  
Anaesthetized Rats ◽  
Inward Currents ◽  
Cell Firing ◽  
Ca1 Area

In the CA1 area of the hippocampus of urethane-anaesthetized rats, the greatest Δ[K+]o and Δ[Ca2+]o evoked by repetitive fimbrial – commissural stimulation were always found in the pyramidal cell layer; but there were large increases in [K+]o over a wide range of depth, whereas a major fall in [Ca2+]o was localized almost exclusively to the level of the pyramidal layer. A sustained focal negative potential was also evoked by fimbrial stimulation; it resembled Δ[K+]o in time course and depth distribution and therefore probably reflected cellular depolarization caused by increased [K+]o. The close correlation between Δ[Ca2+]o and Δ[K+]o and the appearance of population spikes (especially in bursts of three to four spikes) indicate that pyramidal cell firing and corresponding K-outward and Ca-inward currents are mainly responsible for the accumulation of [Formula: see text] and the depletion of [Formula: see text]. In CA3 pyramidal areas, Δ[K+]o and Δ[Ca2+]o were comparable in magnitude and distribution to changes seen in CA1, but they occurred after a longer latency, and the major Δ[Ca2+]o had a longer duration, consistent with a more prolonged Ca2+ current.

Joro spider toxin (JSTX) selectively blocks pyramidal cell loss in the hippocampal CA3 subfields induced by non-NMDA receptor agonists

1992 ◽  
Vol 17 ◽  
pp. 104
Author(s):  
Hirohiko Kanai ◽  
Nobuya Ishida ◽  
Akira Masui ◽  
Keiji Satoh ◽  
Terumi Nakajima ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Pyramidal Cell ◽  
Cell Loss ◽  
Receptor Agonists ◽  
Spider Toxin ◽  
Hippocampal Ca3

Impact of Heterogeneous Perisomatic IPSC Populations on Pyramidal Cell Firing Rates

2004 ◽  
Vol 91 (6) ◽  
pp. 2849-2858 ◽  
Author(s):  
Ildiko Aradi ◽  
Vijayalakshmi Santhakumar ◽  
Ivan Soltesz
Keyword(s):  
Computational Modeling ◽  
Pyramidal Cell ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Decay Kinetics ◽  
Potential Oscillations ◽  
Firing Rates ◽  
Ca1 Pyramidal Cells ◽  
Cell Firing ◽  
Modeling Data

Previous computational modeling studies suggested a set of rules underlying the modulation of principal cell firing rates by heterogeneity in the synaptic parameters (peak amplitude and decay kinetics) of populations of GABAergic inputs. Here we performed dynamic clamp experiments in CA1 hippocampal pyramidal cells to test these ideas in biological neurons. In agreement with the simulation studies, the effects of increasing the event-to-event variance in a population of perisomatically injected inhibitory postsynaptic current (IPSC) peak conductances caused either an increase, decrease, or no change in the firing rates of CA1 pyramidal cells depending on the mean around which the scatter was introduced, the degree of the scatter, the depolarization that the pyramidal cell received, and the IPSC reversal potential. In contrast to CA1 pyramidal cells, both model and biological CA3 pyramidal cells responded with bursts of action potentials to sudden, step-wise alterations in input heterogeneity. In addition, injections of 40-Hz IPSC conductances together with θ-modulated depolarizing current inputs to CA1 pyramidal cells demonstrated that the principles underlying the modulation of pyramidal cell excitability by heterogeneous IPSC populations also apply during membrane potential oscillations. Taken together, these experimental results and the computational modeling data show the existence of simple rules governing the interactions of heterogeneous interneuronal inputs and principal cells.

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