Physiological consequences of selective suppression of synaptic transmission in developing cerebral cortical networks in vitro: Differential effects on intrinsically generated bioelectric discharges in a living ‘model’ system for slow-wave sleep activity

Corner, M.A.; Baker, Robert E.; Pelt, Jaap van

doi:10.1016/j.neubiorev.2008.06.008

Cited by 19 publications

(27 citation statements)

References 458 publications

(846 reference statements)

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“…Interestingly, it has recently been shown [36] that a neuromodulator cocktail including CCh, NA, serotonin, histamine, dopamine and orexin applied to cortical networks similar to those used here, both suppresses network synchrony and drives widespread changes in gene expression, which do not fully revert even when synchrony spontaneously reemerges. These experimental observations, along with the emergence of synchrony in so many different conditions (prenatal and postnatal development [99,100], NREM sleep, anesthesia), systems (acute, organotypic and cell culture preparations [22][23][24][25][27][28][29][30][31][32][33][34][35][36][37][38]89]) and modeling studies [39,40,48,49] support the possibility that the parameter space for synchrony emergence is quite large, and that avoiding its emergence might be something of a balancing act.…”

Section: Adaptation To Prolonged Neuromodulation: An Inevitable Returmentioning

confidence: 79%

“…All these (and others) have been previously shown to be affected by (cholinergic) neuromodulation in complex and intricate manners [26,40,55,57,62,65,83,[91][92][93][94][95] which differ from one cell type to another [96]. Consequently, the (homeostatic) recovery [25,38] of one or more of these finely tuned factors, in one or more neuronal types, might move the system back into a parameter space within which synchrony naturally emerges [49]. In line with this possibility, we observed that recovery from prolonged neuromodulatory input was often associated with changes in global network activity levels, burst rates and burst intensities (Figure 3, Additional file 6: Figure S5; see also [35,36]).…”

Section: Adaptation To Prolonged Neuromodulation: An Inevitable Returmentioning

confidence: 99%

“…In contrast, reduced activity of these systems, which occurs mainly during periods of NREM (non rapid eye movement) sleep, is associated with the prominent appearance of network synchrony as defined above. Importantly, however, neither these forms of network synchrony nor their modulation by acetylcholine (ACh) and noradrenaline (NA) are limited to the intact cortex, as similar activity patterns occur in brain slabs [21], acute and organotypic cortical preparations (for example, [22][23][24][25][26]) and even in networks of dissociated cortical neurons (for example, [27][28][29][30][31][32][33][34][35][36][37]; reviewed in [38]). …”

Section: Introductionmentioning

confidence: 99%

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Adaptation to prolonged neuromodulation in cortical cultures: an invariable return to network synchrony

2014

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Background: Prolonged neuromodulatory regimes, such as those critically involved in promoting arousal and suppressing sleep-associated synchronous activity patterns, might be expected to trigger adaptation processes and, consequently, a decline in neuromodulator-driven effects. This possibility, however, has rarely been addressed. Results: Using networks of cultured cortical neurons, acetylcholine microinjections and a novel closed-loop 'synchrony-clamp' system, we found that acetylcholine pulses strongly suppressed network synchrony. Over the course of many hours, however, synchrony invariably reemerged, even when feedback was used to compensate for declining cholinergic efficacy. Network synchrony also reemerged following its initial suppression by noradrenaline, but this did not occlude the suppression of synchrony or its gradual reemergence following subsequent cholinergic input. Importantly, cholinergic efficacy could be restored and preserved over extended time scales by periodically withdrawing cholinergic input. Conclusions: These findings indicate that the capacity of neuromodulators to suppress network synchrony is constrained by slow-acting, reactive processes. A multiplicity of neuromodulators and ultimately neuromodulator withdrawal periods might thus be necessary to cope with an inevitable reemergence of network synchrony.

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Section: Adaptation To Prolonged Neuromodulation: An Inevitable Returmentioning

confidence: 79%

Section: Adaptation To Prolonged Neuromodulation: An Inevitable Returmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adaptation to prolonged neuromodulation in cortical cultures: an invariable return to network synchrony

2014

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“…We have shown that matured cortical cultures also fire with a typical burst-pause low-frequency pattern. Undisturbed cultures show this unique electrical activity (default mode) that can only be altered by electrical or chemical stimulation (Van Pelt et al, 2004;Corner, 2008;Corner et al, 2008). However, as opposed to the cortex of living animals, no activity in delta frequency range (1-4 Hz) was observed in cortical cultures, although during recovery after stimulation, the frequency of bursting activity reached the lower (0.5-0.6 Hz) delta frequency range.…”

Section: Discussionmentioning

confidence: 99%

“…Cortical cultures have been used previously to study firing properties of cortical networks and MEA recordings revealed spontaneous synchronized bursting across culture resembling slowwave sleep (Van Pelt et al, 2004;Corner, 2008;Corner et al, 2008). To verify the activity of cortical neurons in vitro, embryonic dissociated cortical neurons were cultured on MEAs and their firing activity was recorded over the course of maturation (Fig.…”

Section: Sleep As a Default State Of Mature Neuronal Assemblies In Vitromentioning

confidence: 99%

Key Electrophysiological, Molecular, and Metabolic Signatures of Sleep and Wakefulness Revealed in Primary Cortical Cultures

et al. 2012

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Although sleep is defined as a behavioral state, at the cortical level sleep has local and use-dependent features suggesting that it is a property of neuronal assemblies requiring sleep in function of the activation experienced during prior wakefulness. Here we show that mature cortical cultured neurons display a default state characterized by synchronized burst-pause firing activity reminiscent of sleep. This default sleep-like state can be changed to transient tonic firing reminiscent of wakefulness when cultures are stimulated with a mixture of waking neurotransmitters and spontaneously returns to sleep-like state. In addition to electrophysiological similarities, the transcriptome of stimulated cultures strikingly resembles the cortical transcriptome of sleep-deprived mice, and plastic changes as reflected by AMPA receptors phosphorylation are also similar. We used our in vitro model and sleep-deprived animals to map the metabolic pathways activated by waking. Only a few metabolic pathways were identified, including glycolysis, aminoacid, and lipids. Unexpectedly large increases in lysolipids were found both in vivo after sleep deprivation and in vitro after stimulation, strongly suggesting that sleep might play a major role in reestablishing the neuronal membrane homeostasis. With our in vitro model, the cellular and molecular consequences of sleep and wakefulness can now be investigated in a dish.

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Inflammatory cytokine-associated depression

Lotrich

2015

Brain Research

145

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Inflammatory cytokines can sometimes trigger depression in humans, are often associated with depression, and can elicit some behaviors in animals that are homologous to major depression. Moreover, these cytokines can affect monoaminergic and glutamatergic systems, supporting an overlapping pathoetiology with major depression. This suggests that there could be a specific major depression subtype, inflammatory cytokine-associated depression (ICAD), which may require different therapeutic approaches. However, most people do not develop depression, even when exposed to sustained elevations in inflammatory cytokines. Thus several vulnerabilities and sources of resilience to inflammation-associated depression have been identified. These range from genetic differences in neurotrophic and serotonergic systems to sleep quality and omega-3 fatty acid levels. Replicating these sources of resilience as treatments could be one approach for preventing “ICAD”.

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Physiological consequences of selective suppression of synaptic transmission in developing cerebral cortical networks in vitro: Differential effects on intrinsically generated bioelectric discharges in a living ‘model’ system for slow-wave sleep activity

Cited by 19 publications

References 458 publications

Adaptation to prolonged neuromodulation in cortical cultures: an invariable return to network synchrony

Adaptation to prolonged neuromodulation in cortical cultures: an invariable return to network synchrony

Key Electrophysiological, Molecular, and Metabolic Signatures of Sleep and Wakefulness Revealed in Primary Cortical Cultures

Inflammatory cytokine-associated depression

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