scholarly journals Interneuronal gap junctions increase synchrony and robustness of hippocampal ripple oscillations

2018 ◽  
Author(s):  
André Holzbecher ◽  
Richard Kempter
Keyword(s):  
Gap Junctions ◽  
Memory Consolidation ◽  
Field Potential ◽  
Neuronal Firing ◽  
Promoting Effect ◽  
Sharp Wave ◽  
Neuronal Firing Rate ◽  
Fast Spiking ◽  
Junction Coupling ◽  
Hippocampal Networks

1AbstractSharp wave-ripple (SWRs) are important for memory consolidation. Their signature in the hippocampal extracellular field potential (EFP) can be decomposed into a ≈ 100 ms long sharp wave superimposed by ≈ 200 Hz ripple oscillations. How ripple oscillations are generated is currently not well understood. A promising model for the genesis of ripple oscillations is based on recurrent interneuronal networks (INT-INT). According to this hypothesis, the INT-INT network in CA1 receives a burst of excitation from CA3 that generates the sharp wave, and recurrent inhibition leads to an ultrafast synchronization of the CA1 network causing the ripple oscillations; fast-spiking parvalbumin-positive basket cells (PV+BCs) may constitute the ripple-generating interneuronal network. PV+BCs are also coupled by gap junctions (GJs) but the function of GJs for ripple oscillations has not been quantified. Using simulations of CA1 hippocampal networks of PV+BCs, we show that GJs promote synchrony and increase the neuronal firing rate of the interneuronal ensemble, while the ripple frequency is only affected mildly. The promoting effect of GJs on ripple oscillations depends on fast GJ transmission (≲ 0.5 ms), which requires proximal gap junction coupling (≲ 100 μm from soma).

scholarly journals The gap junction blocker mefloquine impairs sleep-dependent declarative memory consolidation in humans

2019 ◽  
Author(s):  
Gordon B. Feld ◽  
Hong-Viet Ngo ◽  
Ernesto Durán ◽  
Sandra Gebhardt ◽  
Lisa Kleist ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Memory Consolidation ◽  
Information Transfer ◽  
Declarative Memory ◽  
Electrical Coupling ◽  
Procedural Memory ◽  
Neuronal Firing ◽  
Electrical Synapses ◽  
Brain Functions ◽  
Healthy Humans

AbstractDuring sleep, the time-compressed replay of engrams acquired during preceding wakefulness drives memory consolidation. We demonstrate in healthy humans that direct electrical coupling between neurons via gap junctions, i.e., electrical synapses, contributes to this beneficial effect of sleep. Twenty male participants learned a declarative word-pair task and a procedural finger sequence tapping task before receiving the antimalarial mefloquine that is known to block electrical synapses. Retrieval was tested after a retention interval of approximately 20.5 hours that included nocturnal sleep. As predicted, mefloquine given before sleep impaired the retention of declarative memory. In contrast, this effect was absent in control groups, which stayed awake or received mefloquine after sleep. Irrespective of sleep or administration time, mefloquine enhanced retention performance on the procedural memory control task. We conclude that sleep-dependent processes relying on electrical neuronal coupling enable hippocampus-dependent declarative memory consolidation, presumably via time-compressed hippocampal replay of memory traces within sharp-wave/ripple complexes. The recruitment of this understudied form of neuronal information transfer may be necessary to achieve fast-paced memory reprocessing during sleep. Considering that drugs targeting neurochemical synapses have recently fallen short of substantially advancing the treatment of memory impairments in Alzheimer’s disease, schizophrenia or during normal aging, unraveling the contribution of gap junctions to sleep-dependent declarative memory formation can be expected to open new therapeutic avenues.Significance statementSleep supports the strengthening and transformation of memory content via the active replay of previously encoded engrams. Surprisingly, blocking neurochemical synaptic transmission does not impair this function of sleep. Here we demonstrate that the direct electrical coupling between neurons via electrical synapses (gap junctions) is essential for the sleep-dependent formation of declarative memory, i.e., memory for episodes and facts. These findings are in line with the assumption that electrical synapses enable time-compressed neuronal firing patterns that emerge during sleep and drive declarative memory consolidation. Electrical synapses have so far not been linked to higher-order brain functions in humans; their contribution to sleep-dependent memory processing may provide a novel target for sleep-related clinical interventions.

scholarly journals A computational study of suppression of sharp wave ripple complexes by controlling calcium and gap junctions in pyramidal cells

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 2603-2615
Author(s):  
Muhammad Mushtaq ◽  
Rizwan ul Haq ◽  
Waqas Anwar ◽  
Lisa Marshall ◽  
Maxim Bazhenov ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Computational Study ◽  
Pyramidal Cells ◽  
Sharp Wave

Investigation of the roles of Ca2+ and InsP3 diffusion in the coordination of Ca2+ signals between connected hepatocytes

2001 ◽  
Vol 114 (11) ◽  
pp. 1999-2007
Author(s):  
Caroline Clair ◽  
Cécile Chalumeau ◽  
Thierry Tordjmann ◽  
Josiane Poggioli ◽  
Christophe Erneux ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Significant Role ◽  
Signaling Molecules ◽  
Rat Hepatocyte ◽  
Inositol 1,4,5 Trisphosphate ◽  
Gap Junction Coupling ◽  
Junction Coupling ◽  
Insp3 Receptor

Glycogenolytic agonists induce coordinated Ca2+ oscillations in multicellular rat hepatocyte systems as well as in the intact liver. The coordination of intercellular Ca2+ signals requires functional gap-junction coupling. The mechanisms ensuring this coordination are not precisely known. We investigated possible roles of Ca2+ or inositol 1,4,5-trisphosphate (InsP3) as a coordinating messengers for Ca2+ spiking among connected hepatocytes. Application of ionomycin or of supra-maximal concentrations of agonists show that Ca2+ does not significantly diffuse between connected hepatocytes, although gap junctions ensure the passage of small signaling molecules, as demonstrated by FRAP experiments. By contrast, coordination of Ca2+ spiking among connected hepatocytes can be favored by a rise in the level of InsP3, via the increase of agonist concentrations, or by a shift in the affinity of InsP3 receptor for InsP3. In the same line, coordination cannot be achieved if the InsP3 is rapidly metabolized by InsP3-phosphatase in one cell of the multiplet. These results demonstrate that even if small amounts of Ca2+ diffuse across gap junctions, they most probably do not play a significant role in inducing a coordinated Ca2+ signal among connected hepatocytes. By contrast, coordination of Ca2+ oscillations is fully dependent on the diffusion of InsP3 between neighboring cells.

scholarly journals Zinc and Flunitrazepam Modulation of GABA-Mediated Currents in Rat Suprachiasmatic Neurons

1999 ◽  
Vol 81 (1) ◽  
pp. 184-191 ◽  
Author(s):  
G. J. Strecker ◽  
W. K. Park ◽  
F. E. Dudek
Keyword(s):  
Cell Voltage ◽  
Neuronal Firing ◽  
Similar Degree ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Pressure Application ◽  
Neuronal Firing Rate ◽  
Old Rats ◽  
Receptor Modulators ◽  
Hypothalamic Slices

Strecker, G. J., W. K. Park, and F. E. Dudek. Zinc and flunitrazepam modulation of GABA-mediated currents in rat suprachiasmatic neurons. J. Neurophysiol. 81: 184–191, 1999. The suprachiasmatic nucleus (SCN) of the hypothalamus is responsible for generating circadian rhythms in mammals, and GABA is the predominant neurotransmitter in the SCN. Properties of γ-aminobutyric acid-A (GABAA) responses in SCN neurons were examined in acutely prepared hypothalamic slices from 3- to 8-wk-old rats with the use of whole cell voltage-clamp techniques. Zn2+ reduced the amplitude of GABAA-mediated spontaneous inhibitory postsynaptic currents (sIPSCs) in a concentration-dependent manner ranging from a reduction of control amplitude to 88% at 10 μM to 27% at 1,000 μM. Zn2+ reduced IPSC amplitude to a similar degree in the presence of tetrodotoxin and also significantly reduced the amplitude of currents evoked by application of exogenous GABA (100 μM, pressure applied). Zn2+ increased the frequency of IPSCs at lower concentrations and decreased it at higher ones. Flunitrazepam (100 nM) usually failed to potentiate the amplitude of sIPSCs, but prolonged sIPSC kinetics. Two exponential components were normally resolved in the sIPSC decay constants, and flunitrazepam significantly increased those two components. Thus flunitrazepam increased the duration of sIPSCs and potentiated the amplitude of currents evoked by pressure application of GABA. Zn2+ and benzodiazepine each modulated the effect of GABA in nearly all cells, suggesting that most SCN neurons have a similar GABAA receptor subunit composition in this respect. Zn2+ also affected sIPSC frequency, which suggests that Zn2+ increased neuronal firing rate at lower concentrations. These results begin to define the cellular roles that these GABAA receptor modulators might play in circadian regulation.

scholarly journals Estimation of neuronal firing rate using Bayesian Adaptive Kernel Smoother (BAKS)

2017 ◽  
Author(s):  
Nur Ahmadi ◽  
Timothy G. Constandinou ◽  
Christos-Savvas Bouganis
Keyword(s):  
Firing Rate ◽  
Spike Train ◽  
Prior Distribution ◽  
Kernel Smoothing ◽  
Neuronal Firing ◽  
Gaussian Kernel ◽  
Single Trial ◽  
Adaptive Kernel ◽  
Neuronal Firing Rate ◽  
Spike Train Data

AbstractNeurons use sequences of action potentials (spikes) to convey information across neuronal networks. In neurophysiology experiments, information about external stimuli or behavioral tasks has been frequently characterized in term of neuronal firing rate. The firing rate is conventionally estimated by averaging spiking responses across multiple similar experiments (or trials). However, there exist a number of applications in neuroscience research that require firing rate to be estimated on a single trial basis. Estimating firing rate from a single trial is a challenging problem and current state-of-the-art methods do not perform well. To address this issue, we develop a new method for estimating firing rate based on kernel smoothing technique that considers the bandwidth as a random variable with prior distribution that is adaptively updated under a Bayesian framework. By carefully selecting the prior distribution together with Gaussian kernel function, an analytical expression can be achieved for the kernel bandwidth. We refer to the proposed method as Bayesian Adaptive Kernel Smoother (BAKS). We evaluate the performance of BAKS using synthetic spike train data generated by biologically plausible models: inhomogeneous Gamma (IG) and inhomogeneous inverse Gaussian (IIG). We also apply BAKS to real spike train data from non-human primate (NHP) motor and visual cortex. We benchmark the proposed method against the established and previously reported methods. These include: optimized kernel smoother (OKS), variable kernel smoother (VKS), local polynomial fit (Locfit), and Bayesian adaptive regression splines (BARS). Results using both synthetic and real data demonstrate that the proposed method achieves better performance compared to competing methods. This suggests that the proposed method could be useful for understanding the encoding mechanism of neurons in cognitive-related tasks. The proposed method could also potentially improve the performance of brain-machine interface (BMI) decoder that relies on estimated firing rate as the input.

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