scholarly journals Network burst activity in hippocampal neuronal cultures: the role of synaptic and intrinsic currents

2016 ◽  
Vol 115 (6) ◽  
pp. 3073-3089 ◽  
Author(s):  
Jyothsna Suresh ◽  
Mihailo Radojicic ◽  
Lorenzo L. Pesce ◽  
Anita Bhansali ◽  
Janice Wang ◽  
...  

The goal of this work was to define the contributions of intrinsic and synaptic mechanisms toward spontaneous network-wide bursting activity, observed in dissociated rat hippocampal cell cultures. This network behavior is typically characterized by short-duration bursts, separated by order of magnitude longer interburst intervals. We hypothesize that while short-timescale synaptic processes modulate spectro-temporal intraburst properties and network-wide burst propagation, much longer timescales of intrinsic membrane properties such as persistent sodium (Nap) currents govern burst onset during interburst intervals. To test this, we used synaptic receptor antagonists picrotoxin, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and 3-(2-carboxypiperazine-4-yl)propyl-1-phosphonate (CPP) to selectively block GABAA, AMPA, and NMDA receptors and riluzole to selectively block Napchannels. We systematically compared intracellular activity (recorded with patch clamp) and network activity (recorded with multielectrode arrays) in eight different synaptic connectivity conditions: GABAA+ NMDA + AMPA, NMDA + AMPA, GABAA+ AMPA, GABAA+ NMDA, AMPA, NMDA, GABAA, and all receptors blocked. Furthermore, we used mixed-effects modeling to quantify the aforementioned independent and interactive synaptic receptor contributions toward spectro-temporal burst properties including intraburst spike rate, burst activity index, burst duration, power in the local field potential, network connectivity, and transmission delays. We found that blocking intrinsic Napcurrents completely abolished bursting activity, demonstrating their critical role in burst onset within the network. On the other hand, blocking different combinations of synaptic receptors revealed that spectro-temporal burst properties are uniquely associated with synaptic functionality and that excitatory connectivity is necessary for the presence of network-wide bursting. In addition to confirming the critical contribution of direct excitatory effects, mixed-effects modeling also revealed distinct combined (nonlinear) contributions of excitatory and inhibitory synaptic activity to network bursting properties.

2020 ◽  
Vol 51 (3) ◽  
pp. 149-156
Author(s):  
Andrew H. Hales ◽  
Kipling D. Williams

Abstract. Ostracism has been shown to increase openness to extreme ideologies and groups. We investigated the consequences of this openness-to-extremity from the perspective of potential ostracizers. Does openness-to-extremity increase one’s prospects of being ostracized by others who are not affiliated with the extreme group? Participants rated willingness to ostracize 40 targets who belong to activist groups that vary in the type of goals/cause they support (prosocial vs. antisocial), and the extremity of their actions (moderate vs. extreme). Mixed-effects modeling showed that people are more willing to ostracize targets whose group engages in extreme actions. This effect was unexpectedly stronger for groups pursuing prosocial causes. It appears openness-to-extremity entails interpersonal cost, and could increase reliance on the extreme group for social connection.


2011 ◽  
Vol 109 (1) ◽  
pp. 166-175 ◽  
Author(s):  
Emilia Biffi ◽  
Andrea Menegon ◽  
Francesco Piraino ◽  
Alessandra Pedrocchi ◽  
Gianfranco B. Fiore ◽  
...  

2019 ◽  
Vol 13 ◽  
pp. 408-414 ◽  
Author(s):  
Edinéia A.S. Galvanin ◽  
Raquel Menezes ◽  
Murilo H.X. Pereira ◽  
Sandra M.A.S. Neves

1996 ◽  
Vol 75 (6) ◽  
pp. 2654-2657 ◽  
Author(s):  
W. Jarolimek ◽  
H. Brunner ◽  
A. Lewen ◽  
U. Misgeld

1. Spontaneous synaptic activity in networks formed by dissociated neurons from embryonic rat midbrain was analyzed in tight seal whole cell recordings. 2. Application of furosemide (0.5 mM) to the cell and its surrounding area increased the frequency of spontaneous synaptic currents. Incubation of the culture with furosemide resulted in “rhythmic” burst activity. 3. Furosemide (0.1-0.5 mM) changed equilibrium potentials of inhibitory postsynaptic currents, gamma-aminobutyric acid-A (GABAA) or glycine receptor-mediated Cl- currents by a blockade of Cl(-)-outward transport. Furosemide did not alter the slope conductance of GABAA receptor-mediated currents. Membrane conductance and cell excitability were also unaffected. 4. We conclude that furosemide locked the activity of the network in “burst activity” mode through impairment of inhibition resulting from the disturbance of Cl- homeostasis.


1994 ◽  
Vol 72 (2) ◽  
pp. 1032-1036 ◽  
Author(s):  
M. R. Pelletier ◽  
J. J. Hablitz

1. Neocortical brain slices were prepared from rats (35–50 days of age) and maintained in vitro. Intracellular recordings were obtained from neurons in cortical layers II/III. The effect of bath application of cyclothiazide (CYZ), a potent blocker of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor desensitization, on evoked synaptic activity and passive membrane properties was investigated. 2. Bath application of CYZ did not significantly affect resting membrane potential, input resistance, or repetitive firing. CYZ increased both the amplitude and duration of evoked excitatory postsynaptic potentials (EPSPs). Polysynaptic responses were also augumented. These effects persisted after the blockade of N-methyl-D-aspartate (NMDA) receptors with D-2-amino-5-phosphonovaleric acid (D-APV). The magnitude of these effects appeared to vary directly with stimulation intensity and presumably, amount of glutamate release. 3. Epileptiform activity was induced by bath application of bicuculline methiodide. The amplitude and duration of evoked paroxysmal discharges were increased by CYZ. Similar results were seen in presence of D-APV. 4. These results indicate that CYZ has significant effects on synaptic transmission. Desensitization of non-NMDA receptors may be an important mechanism for determining the time course of EPSPs and in curtailing epileptiform responses in the rat neocortex.


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