scholarly journals α 2 Adrenergic Modulation of Hippocampal CA3 Network Activity

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Chris W.D. Jurgens ◽  
Jacob King ◽  
Sarah Boese ◽  
Jessica Lichter ◽  
Brian Nelson ◽  
...  
Keyword(s):  
Network Activity ◽  
Adrenergic Modulation ◽  
Hippocampal Ca3

Activation of Ih is necessary for patterning of mGluR and mAChR induced network activity in the hippocampal CA3 region

2003 ◽  
Vol 44 (3) ◽  
pp. 293-303 ◽  
Author(s):  
S.R. Cobb ◽  
P.M. Larkman ◽  
D.O. Bulters ◽  
L. Oliver ◽  
C.H. Gill ◽  
...  
Keyword(s):  
Network Activity ◽  
Hippocampal Ca3 ◽  
Ca3 Region

scholarly journals Development of schemas revealed by prior experience and NMDA receptor knock-out

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
George Dragoi ◽  
Susumu Tonegawa
Keyword(s):  
De Novo ◽  
Prior Experience ◽  
Anterograde Amnesia ◽  
Network Activity ◽  
Knock Out ◽  
Related Information ◽  
Neuronal Mechanisms ◽  
Hippocampal Ca3 ◽  
Mental Schemas ◽  
Neuronal Encoding

Prior experience accelerates acquisition of novel, related information through processes like assimilation into mental schemas, but the underlying neuronal mechanisms are poorly understood. We investigated the roles that prior experience and hippocampal CA3 N-Methyl-D-aspartate receptor (NMDAR)-dependent synaptic plasticity play in CA1 place cell sequence encoding and learning during novel spatial experiences. We found that specific representations of de novo experiences on linear environments were formed on a framework of pre configured network activity expressed in the preceding sleep and were rapidly, flexibly adjusted via NMDAR-dependent activity. This prior experience accelerated encoding of subsequent experiences on contiguous or isolated novel tracks, significantly decreasing their NMDAR-dependence. Similarly, de novo learning of an alternation task was facilitated by CA3 NMDARs; this experience accelerated subsequent learning of related tasks, independent of CA3 NMDARs, consistent with a schema-based learning. These results reveal the existence of distinct neuronal encoding schemes which could explain why hippocampal dysfunction results in anterograde amnesia while sparing recollection of old, schema-based memories.

β-Adrenergic modulation of spontaneous spatiotemporal activity patterns and synchrony in hyperexcitable hippocampal circuits

2012 ◽  
Vol 108 (2) ◽  
pp. 658-671 ◽  
Author(s):  
Anupam Hazra ◽  
Robert Rosenbaum ◽  
Bernhard Bodmann ◽  
Siyuan Cao ◽  
Krešimir Josić ◽  
...  
Keyword(s):  
Propagation Velocity ◽  
Activity Patterns ◽  
Pyramidal Cells ◽  
Network Activity ◽  
Neural Activation ◽  
Ca1 Pyramidal Cells ◽  
Spatiotemporal Characteristics ◽  
Adrenergic Modulation ◽  
Whole Cell Recordings

A description of healthy and pathological brain dynamics requires an understanding of spatiotemporal patterns of neural activity and characteristics of its propagation between interconnected circuits. However, the structure and modulation of the neural activation maps underlying these patterns and their propagation remain elusive. We investigated effects of β-adrenergic receptor (β-AR) stimulation on the spatiotemporal characteristics of emergent activity in rat hippocampal circuits. Synchronized epileptiform-like activity, such as interictal bursts (IBs) and ictal-like events (ILEs), were evoked by 4-aminopyridine (4-AP), and their dynamics were studied using a combination of electrophysiology and fast voltage-sensitive dye imaging. Dynamic characterization of the spontaneous IBs showed that they originated in dentate gyrus/CA3 border and propagated toward CA1. To determine how β-AR modulates spatiotemporal characteristics of the emergent IBs, we used the β-AR agonist isoproterenol (ISO). ISO significantly reduced the spatiotemporal extent and propagation velocity of the IBs and significantly altered network activity in the 1- to 20-Hz range. Dual whole cell recordings of the IBs in CA3/CA1 pyramidal cells and optical analysis of those regions showed that ISO application reduced interpyramidal and interregional synchrony during the IBs. In addition, ISO significantly reduced duration not only of the shorter duration IBs but also the prolonged ILEs in 4-AP. To test whether the decrease in ILE duration was model dependent, we used a different hyperexcitability model, zero magnesium (0 Mg2+). Prolonged ILEs were readily formed in 0 Mg2+, and addition of ISO significantly reduced their durations. Taken together, these novel results provide evidence that β-AR activation dynamically reshapes the spatiotemporal activity patterns in hyperexcitable circuits by altering network rhythmogenesis, propagation velocity, and intercellular/regional synchronization.

scholarly journals Local oxygen homeostasis during various neuronal network activity states in the mouse hippocampus

2017 ◽  
Vol 39 (5) ◽  
pp. 859-873 ◽  
Author(s):  
Justus Schneider ◽  
Nikolaus Berndt ◽  
Ismini E Papageorgiou ◽  
Jana Maurer ◽  
Sascha Bulik ◽  
...  
Keyword(s):  
Gamma Oscillations ◽  
Network Activity ◽  
Synaptic Excitation ◽  
Sharp Wave ◽  
Oxygen Homeostasis ◽  
Neuronal Network Activity ◽  
Hippocampal Ca3 ◽  
The Brain ◽  
Local Oxygen ◽  
Brain Energy

Cortical information processing comprises various activity states emerging from timed synaptic excitation and inhibition. However, the underlying energy metabolism is widely unknown. We determined the cerebral metabolic rate of oxygen (CMRO2) along a tissue depth of <0.3 mm in the hippocampal CA3 region during various network activities, including gamma oscillations and sharp wave-ripples that occur during wakefulness and sleep. These physiological states associate with sensory perception and memory formation, and critically depend on perisomatic GABA inhibition. Moreover, we modelled vascular oxygen delivery based on quantitative microvasculature analysis. (1) Local CMRO2 was highest during gamma oscillations (3.4 mM/min), medium during sharp wave-ripples, asynchronous activity and isoflurane application (2.0–1.6 mM/min), and lowest during tetrodotoxin application (1.4 mM/min). (2) Energy expenditure of axonal and synaptic signaling accounted for >50% during gamma oscillations. (3) CMRO2 positively correlated with number and synchronisation of activated synapses, and neural multi-unit activity. (4) The median capillary distance was 44 µm. (5) The vascular oxygen partial pressure of 33 mmHg was needed to sustain oxidative phosphorylation during gamma oscillations. We conclude that gamma oscillations featuring high energetics require a hemodynamic response to match oxygen consumption of respiring mitochondria, and that perisomatic inhibition significantly contributes to the brain energy budget.

Desynchronization of Glutamate Release Prolongs Synchronous CA3 Network Activity

2007 ◽  
Vol 97 (5) ◽  
pp. 3812-3818 ◽  
Author(s):  
Jethro Jones ◽  
Elizabeth A. Stubblefield ◽  
Timothy A. Benke ◽  
Kevin J. Staley
Keyword(s):  
Glutamate Release ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Network Activity ◽  
Neural Population ◽  
Axon Terminals ◽  
Rate Of Spread ◽  
Hippocampal Ca3 ◽  
Recurrent Collateral

Periodic bursts of activity in the disinhibited in vitro hippocampal CA3 network spread through the neural population by the glutamatergic recurrent collateral axons that link CA3 pyramidal cells. It was previously proposed that these bursts of activity are terminated by exhaustion of releasable glutamate at the recurrent collateral synapses so that the next periodic burst of network activity cannot occur until the supply of glutamate has been replenished. As a test of this hypothesis, the rate of glutamate release at CA3 axon terminals was reduced by substitution of extracellular Ca2+ with Sr2+. Reduction of the rate of glutamate release reduces the rate of depletion and should thereby prolong bursts. Here we demonstrate that Sr2+ substitution prolongs spontaneous bursts in the disinhibited adult CA3 hippocampal slices to 37.2 ± 7.6 (SE) times the duration in control conditions. Sr2+ also decreased the probability of burst initiation and the rate of burst onset, consistent with reduced synchrony of glutamate release and a consequent reduced rate of spread of excitation through the slice. These findings support the supply of releasable glutamate as an important determinant of the probability and duration of synchronous CA3 network activity.

Alpha2A adrenergic receptor‐mediated inhibition of mouse hippocampal CA3 network activity

2008 ◽  
Vol 22 (S2) ◽  
pp. 98-98
Author(s):  
Elizabeth Luger ◽  
Kylie Davis ◽  
Brianna Goldenstein ◽  
Brian Nelson ◽  
Ke Xu ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Network Activity ◽  
Hippocampal Ca3

Calcium-Activated Afterhyperpolarizations Regulate Synchronization and Timing of Epileptiform Bursts in Hippocampal CA3 Pyramidal Neurons

2006 ◽  
Vol 96 (6) ◽  
pp. 3028-3041 ◽  
Author(s):  
David Fernández de Sevilla ◽  
Julieta Garduño ◽  
Emilio Galván ◽  
Washington Buño
Keyword(s):  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Epileptiform Activity ◽  
Network Activity ◽  
Cellular Mechanisms ◽  
Burst Frequency ◽  
Potassium Conductances ◽  
Hippocampal Ca3 ◽  
Ca3 Pyramidal Neurons

Calcium-activated potassium conductances regulate neuronal excitability, but their role in epileptogenesis remains elusive. We investigated in rat CA3 pyramidal neurons the contribution of the Ca2+-activated K+-mediated afterhyperpolarizations (AHPs) in the genesis and regulation of epileptiform activity induced in vitro by 4-aminopyridine (4-AP) in Mg2+-free Ringer. Recurring spike bursts terminated by prolonged AHPs were generated. Burst synchronization between CA3 pyramidal neurons in paired recordings typified this interictal-like activity. A downregulation of the medium afterhyperpolarization (mAHP) paralleled the emergence of the interictal-like activity. When the mAHP was reduced or enhanced by apamin and EBIO bursts induced by 4-AP were increased or blocked, respectively. Inhibition of the slow afterhyperpolarization (sAHP) with carbachol, t-ACPD, or isoproterenol increased bursting frequency and disrupted burst regularity and synchronization between pyramidal neuron pairs. In contrast, enhancing the sAHP by intracellular dialysis with KMeSO4 reduced burst frequency. Block of GABAA–B inhibitions did not modify the abnormal activity. We describe novel cellular mechanisms where 1) the inhibition of the mAHP plays an essential role in the genesis and regulation of the bursting activity by reducing negative feedback, 2) the sAHP sets the interburst interval by decreasing excitability, and 3) bursting was synchronized by excitatory synaptic interactions that increased in advance and during bursts and decreased throughout the subsequent sAHP. These cellular mechanisms are active in the CA3 region, where epileptiform activity is initiated, and cooperatively regulate the timing of the synchronized rhythmic interictal-like network activity.

β1 Adrenergic Receptor-Mediated Enhancement of Hippocampal CA3 Network Activity

2005 ◽  
Vol 314 (2) ◽  
pp. 552-560 ◽  
Author(s):  
Chris W. D. Jurgens ◽  
Katie E. Rau ◽  
Chris A. Knudson ◽  
Jacob D. King ◽  
Patrick A. Carr ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Network Activity ◽  
Hippocampal Ca3

scholarly journals Alpha‐2A adrenergic receptor activation inhibits rat hippocampal CA3 network activity

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Kylie Davis ◽  
Jessica Lichter ◽  
Brian Nelson ◽  
Brianna Goldenstein ◽  
Sarah Boese ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Network Activity ◽  
Hippocampal Ca3
Sign in / Sign up

Export Citation Format

Share Document