scholarly journals Beyond spikes: Multiscale computational analysis of in vivo long-term recordings in the cockroach circadian clock

2019 ◽  
Vol 3 (4) ◽  
pp. 944-968 ◽  
Author(s):  
Pablo Rojas ◽  
Jenny A. Plath ◽  
Julia Gestrich ◽  
Bharath Ananthasubramaniam ◽  
Martin E. Garcia ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Field Potential ◽  
Dynamic Features ◽  
Pigment Dispersing Factor ◽  
Gamma Frequency ◽  
Accessory Medulla ◽  
Electrophysiological Recordings ◽  
Wide Range

The circadian clock of the nocturnal Madeira cockroach is located in the accessory medulla, a small nonretinotopic neuropil in the brain’s visual system. The clock comprises about 240 neurons that control rhythms in physiology and behavior such as sleep-wake cycles. The clock neurons contain an abundant number of partly colocalized neuropeptides, among them pigment-dispersing factor (PDF), the insects’ most important circadian coupling signal that controls sleep-wake rhythms. We performed long-term loose-patch clamp recordings under 12:12-hr light-dark cycles in the cockroach clock in vivo. A wide range of timescales, from milliseconds to seconds, were found in spike and field potential patterns. We developed a framework of wavelet transform–based methods to detect these multiscale electrical events. We analyzed frequencies and patterns of events with interesting dynamic features, such as mixed-mode oscillations reminiscent of sharp-wave ripples. Oscillations in the beta/gamma frequency range (20–40 Hz) were observed to rise at dawn, when PDF is released, peaking just before the onset of locomotor activity of the nocturnal cockroach. We expect that in vivo electrophysiological recordings combined with neuropeptide/antagonist applications and behavioral analysis will determine whether specific patterns of electrical activity recorded in the network of the cockroach circadian clock are causally related to neuropeptide-dependent control of behavior.

Correlation between magnesium and potassium contents in muscle: role of Na(+)-K+ pump

1993 ◽  
Vol 264 (2) ◽  
pp. C457-C463 ◽  
Author(s):  
I. Dorup ◽  
T. Clausen
Keyword(s):  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Deficient Diet ◽  
Young Rats ◽  
Wide Range ◽  
86Rb Influx

In young rats fed a Mg(2+)-deficient diet for 3 wk, Mg2+ and K+ contents in soleus and extensor digitorum longus muscles were significantly reduced and closely correlated. In isolated soleus muscles, Mg2+ depletion induced an even more pronounced loss of K+, and Mg2+ and K+ contents were correlated over a wide range (r = 0.95, P < 0.001). Extracellular Mg2+ (0-1.2 mM) caused no change in total or ouabain-suppressible 86Rb influx. After long-term incubation in Ca(2+)-Mg(2+)-free buffer with EDTA and EGTA, cellular Mg2+ and K+ contents were reduced by 35 and 15%, respectively, without any reduction in ATP and total or ouabain-suppressible 86Rb influx. In Mg(2+)-depleted muscles 42K efflux was increased by up to 42%, and repletion with Mg2+ produced a graded decrease. We conclude that Mg2+ and K+ contents are closely correlated in muscles Mg2+ depleted in vivo or in vitro and that neither extracellular nor moderate intracellular Mg2+ depletion affects total or Na(+)-K+ pump-mediated K+ influx. The reduced K+ content may rather be related to increased K+ efflux from the muscles.

scholarly journals Constitutive expression of bcl-2 in B cells causes a lethal form of lupuslike autoimmune disease after induction of neonatal tolerance to H-2b alloantigens.

1996 ◽  
Vol 183 (6) ◽  
pp. 2523-2531 ◽  
Author(s):  
M López-Hoyos ◽  
R Carrió ◽  
R Merino ◽  
L Buelta ◽  
S Izui ◽  
...  
Keyword(s):  
B Cells ◽  
Autoimmune Disease ◽  
Constitutive Expression ◽  
Systemic Autoimmune Disease ◽  
Spleen Cells ◽  
Term Survival ◽  
F1 Hybrid ◽  
Wide Range

The bcl-2 protooncogene has been shown to provide a survival signal to self-reactive B cells, but it fails to override their developmental arrest after encounter with antigen. Furthermore, constitutive expression of bcl-2 in B cells does not promote the development of autoimmune disease in most strains of mice, indicating that signals other than those conferred by bcl-2 are required for long-term survival and differentiation of self-reactive B cells in vivo. To further examine the factors that are required for the pathogenesis of autoimmune disease, we have assessed the effect of bcl-2 overexpression on the development of host-versus-graft disease, a self-limited model of systemic autoimmune disease. In this model, injection of spleen cells from (C57BL/6 x BALB/c)F1 hybrid mice into BALB/c newborn parental mice induces immunological tolerance to donor tissues and activation of autoreactive F1 donor B cells through interactions provided by allogeneic host CD4+ T cells. BALB/c newborns injected with spleen cells from (C57BL/6 x BALB/c)F1 mice expressing a bcl-2 transgene in B cells developed high levels of anti-single-stranded DNA and a wide range of pathogenic autoantibodies that were not or barely detectable in mice injected with nontransgenic spleen cells. In mice injected with transgenic B cells, the levels of pathogenic autoantibodies remained high during the course of the study and were associated with long-term persistence of donor B cells, development of a severe autoimmune disease, and accelerated mortality. These results demonstrate that bcl-2 can provide survival signals for the maintenance and differentiation of autoreactive B cells, and suggest that both increased B cell survival and T cell help play critical roles in the development of certain forms of systemic autoimmune disease.

scholarly journals Enhanced LTP of population spikes in the dentate gyrus of mice haploinsufficient for neurobeachin

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Julia Muellerleile ◽  
Aline Blistein ◽  
Astrid Rohlmann ◽  
Frederieke Scheiwe ◽  
Markus Missler ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Granule Cell ◽  
Field Potential ◽  
Synaptic Function ◽  
Spatial Learning And Memory ◽  
Neurotransmitter Receptor ◽  
Cell Excitability ◽  
Neuronal Protein ◽  
Electrophysiological Recordings

Abstract Deletion of the autism candidate molecule neurobeachin (Nbea), a large PH-BEACH-domain containing neuronal protein, has been shown to affect synaptic function by interfering with neurotransmitter receptor targeting and dendritic spine formation. Previous analysis of mice lacking one allele of the Nbea gene identified impaired spatial learning and memory in addition to altered autism-related behaviours. However, no functional data from living heterozygous Nbea mice (Nbea+/−) are available to corroborate the behavioural phenotype. Here, we explored the consequences of Nbea haploinsufficiency on excitation/inhibition balance and synaptic plasticity in the intact hippocampal dentate gyrus of Nbea+/− animals in vivo by electrophysiological recordings. Based on field potential recordings, we show that Nbea+/− mice display enhanced LTP of the granule cell population spike, but no differences in basal synaptic transmission, synapse numbers, short-term plasticity, or network inhibition. These data indicate that Nbea haploinsufficiency causes remarkably specific alterations to granule cell excitability in vivo, which may contribute to the behavioural abnormalities in Nbea+/− mice and to related symptoms in patients.

The occurrence of a stable quinone radical accumulating in vivo during natural and induced senescence in a range of plants

1994 ◽  
Vol 102 ◽  
pp. 501-503 ◽  
Author(s):  
George A. F. Hendry ◽  
N. M. Atherton ◽  
Wendy Seel ◽  
Olivier Leprince
Keyword(s):  
Free Radical ◽  
Seed Viability ◽  
Biochemical Processes ◽  
Organic Free Radical ◽  
W Band ◽  
Wide Range ◽  
Electron Transport Chains ◽  
Long Term Studies

SynopsisA correlation has been firmly established, in a wide range of plants, between environmental stress, the onset of senescence, loss of viability in seeds and the development and accumulation of a stable organic free radical. On the basis of the EPR response obtained at 95 GHz (W-band) and ENDOR spectra, and comparisons with quinone radical anions, we present evidence from contrasted plant species, plant tissues and sub-cellular fractions that this stable radical originates from one or more quinones possibly, though perhaps not exclusively, associated with stressed or age-impaired photosynthetic and respiratory electron transport chains. The radical appears to be ubiquitously associated with sub-lethal stress-induced damage and with senescence and arises during the sub-cellular structural and biochemical processes associated with the final phases of metabolism prior to death. As the free radical persists for some considerable time after death, it may have value in long-term studies of seed viability and in broader areas of plant pathology and stress physiology.

scholarly journals The ionic mechanism of gamma resonance in rat striatal fast-spiking neurons

2011 ◽  
Vol 106 (6) ◽  
pp. 2936-2949 ◽  
Author(s):  
Giuseppe Sciamanna ◽  
Charles J. Wilson
Keyword(s):  
Firing Rate ◽  
Firing Pattern ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Repetitive Firing ◽  
Spike Threshold ◽  
Gamma Frequency ◽  
Subthreshold Oscillations ◽  
Fast Spiking

Striatal fast-spiking (FS) cells in slices fire in the gamma frequency range and in vivo are often phase-locked to gamma oscillations in the field potential. We studied the firing patterns of these cells in slices from rats ages 16–23 days to determine the mechanism of their gamma resonance. The resonance of striatal FS cells was manifested as a minimum frequency for repetitive firing. At rheobase, cells fired a doublet of action potentials or doublets separated by pauses, with an instantaneous firing rate averaging 44 spikes/s. The minimum rate for sustained firing was also responsible for the stuttering firing pattern. Firing rate adapted during each episode of firing, and bursts were terminated when firing was reduced to the minimum sustainable rate. Resonance and stuttering continued after blockade of Kv3 current using tetraethylammonium (0.1–1 mM). Both gamma resonance and stuttering were strongly dependent on Kv1 current. Blockade of Kv1 channels with dendrotoxin-I (100 nM) completely abolished the stuttering firing pattern, greatly lowered the minimum firing rate, abolished gamma-band subthreshold oscillations, and slowed spike frequency adaptation. The loss of resonance could be accounted for by a reduction in potassium current near spike threshold and the emergence of a fixed spike threshold. Inactivation of the Kv1 channel combined with the minimum firing rate could account for the stuttering firing pattern. The resonant properties conferred by this channel were shown to be adequate to account for their phase-locking to gamma-frequency inputs as seen in vivo.

scholarly journals In vivo brain activity imaging of interactively locomoting mice

2017 ◽  
Author(s):  
Shigenori Inagaki ◽  
Masakazu Agetsuma ◽  
Shinya Ohara ◽  
Toshio Iijima ◽  
Tetsuichi Wazawa ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Brain Activity ◽  
Field Potential ◽  
Brain Functions ◽  
Wide Range ◽  
Novel Method ◽  
Freely Moving ◽  
Voltage Indicator

AbstractElectrophysiological field potential dynamics have been widely used to investigate brain functions and related psychiatric disorders. Conversely, however, various technical limitations of conventional recording methods have limited its applicability to freely moving subjects, especially when they are in a group and socially interacting with each other. Here, we propose a new method to overcome these technical limitations by introducing a bioluminescent voltage indicator called LOTUS-V. Using our simple and fiber-free recording method, named “SNIPA,” we succeeded in capturing brain activity in freely-locomotive mice, without the need for complicated instruments. This novel method further allowed us to simultaneously record from multiple independently-locomotive animals that were interacting with one another. Further, we successfully demonstrated that the primary visual cortex was activated during the interaction. This methodology will further facilitate a wide range of studies in neurobiology and psychiatry.

scholarly journals Decoys reveal the genetic and biochemical roles of redundant plant E3 ubiquitin ligases

2017 ◽  
Author(s):  
Chin-Mei Lee ◽  
Ann Feke ◽  
Christopher Adamchek ◽  
Kristofor Webb ◽  
José Pruneda-Paz ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Mammalian Cells ◽  
E3 Ligase ◽  
Ubiquitin Ligases ◽  
E3 Ubiquitin Ligases ◽  
Genetic Redundancy ◽  
Clock Period ◽  
E3 Ligases ◽  
Wide Range

AbstractThe ubiquitin proteasome system (UPS) is the main cellular route for protein degradation in plants and is important for a wide range of biological processes including daily and seasonal timing. The UPS relies on the action of E3 ubiquitin ligases to specifically recognize substrate proteins and facilitate their ubiquitylation. In plants, there are three major challenges that inhibit studies of E3 ligase function: 1) rampant genetic redundancy, 2) labile interactions between an E3 ligase and its cognate substrates, and 3) a lack of tools for rapid validation of bona fide substrates. To overcome these 3 challenges, we have developed a decoy method that allows for rapid genetic analysis of E3 ligases, in vivo identification of substrates using immunoprecipitation followed by mass spectrometry, and reconstitution of the ubiquitylation reaction in mammalian cells to rapidly validate potential substrates. We employ the strategy to study the plant F-box proteins, ZTL, LKP2, and FKF1 revealing differential genetic impacts on circadian clock period and seasonal flowering. We identify a group of circadian clock transcriptional regulators that interact with ZTL, LKP2, and FKF1 in vivo providing a host of potential substrates that have not been seen previously. We then validate one substrate of ZTL, the plant circadian clock transcription factor CHE, and show that ZTL mediates CHE ubiquitylation and that the levels of the CHE protein cycle in daily timecourses. This work further untangles the complicated genetic roles of this family of E3 ligases and suggests that ZTL is a master regulator of a diverse set of critical clock transcription factors. Furthermore, the method that is validated here can be tool employed widely to overcome traditional challenges in studying redundant plant E3 ubiquitin ligases.

scholarly journals Wireless, battery-free, and fully implantable electrical neurostimulation in freely moving rodents

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Alex Burton ◽  
Sang Min Won ◽  
Arian Kolahi Sohrabi ◽  
Tucker Stuart ◽  
Amir Amirhossein ◽  
...  
Keyword(s):  
Small Animal ◽  
Platinum Electrodes ◽  
Mechanistic Investigation ◽  
Wide Range ◽  
Rapid Dissemination ◽  
Therapeutic Mechanisms ◽  
Freely Moving ◽  
Control Stimulation

AbstractImplantable deep brain stimulation (DBS) systems are utilized for clinical treatment of diseases such as Parkinson’s disease and chronic pain. However, long-term efficacy of DBS is limited, and chronic neuroplastic changes and associated therapeutic mechanisms are not well understood. Fundamental and mechanistic investigation, typically accomplished in small animal models, is difficult because of the need for chronic stimulators that currently require either frequent handling of test subjects to charge battery-powered systems or specialized setups to manage tethers that restrict experimental paradigms and compromise insight. To overcome these challenges, we demonstrate a fully implantable, wireless, battery-free platform that allows for chronic DBS in rodents with the capability to control stimulation parameters digitally in real time. The devices are able to provide stimulation over a wide range of frequencies with biphasic pulses and constant voltage control via low-impedance, surface-engineered platinum electrodes. The devices utilize off-the-shelf components and feature the ability to customize electrodes to enable broad utility and rapid dissemination. Efficacy of the system is demonstrated with a readout of stimulation-evoked neural activity in vivo and chronic stimulation of the medial forebrain bundle in freely moving rats to evoke characteristic head motion for over 36 days.

scholarly journals Investigating the Association between Motor Function, Neuroinflammation, and Recording Metrics in the Performance of Intracortical Microelectrode Implanted in Motor Cortex

Micromachines ◽  
2020 ◽  
Vol 11 (9) ◽  
pp. 838
Author(s):  
Evon S. Ereifej ◽  
Youjun Li ◽  
Monika Goss-Varley ◽  
Youjoung Kim ◽  
Seth M. Meade ◽  
...  
Keyword(s):  
Cell Activation ◽  
Motor Behavior ◽  
Formal Concept ◽  
Neuronal Density ◽  
Glial Cell Activation ◽  
Electrophysiological Recordings ◽  
Analysis Scheme ◽  
Wide Range ◽  
Third Dimension

Long-term reliability of intracortical microelectrodes remains a challenge for increased acceptance and deployment. There are conflicting reports comparing measurements associated with recording quality with postmortem histology, in attempts to better understand failure of intracortical microelectrodes (IMEs). Our group has recently introduced the assessment of motor behavior tasks as another metric to evaluate the effects of IME implantation. We hypothesized that adding the third dimension to our analysis, functional behavior testing, could provide substantial insight on the health of the tissue, success of surgery/implantation, and the long-term performance of the implanted device. Here we present our novel analysis scheme including: (1) the use of numerical formal concept analysis (nFCA) and (2) a regression analysis utilizing modern model/variable selection. The analyses found complimentary relationships between the variables. The histological variables for glial cell activation had associations between each other, as well as the neuronal density around the electrode interface. The neuronal density had associations to the electrophysiological recordings and some of the motor behavior metrics analyzed. The novel analyses presented herein describe a valuable tool that can be utilized to assess and understand relationships between diverse variables being investigated. These models can be applied to a wide range of ongoing investigations utilizing various devices and therapeutics.

scholarly journals Inhibitory Control of Basolateral Amygdalar Transmission to the Prefrontal Cortex by Local Corticotrophin Type 2 Receptor

2019 ◽  
Vol 23 (2) ◽  
pp. 108-116 ◽  
Author(s):  
Hector E Yarur ◽  
Ignacio Vega-Quiroga ◽  
Marcela P González ◽  
Verónica Noches ◽  
Daniel R Thomases ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Inhibitory Control ◽  
Glutamate Release ◽  
Field Potential ◽  
Behavioral Responses ◽  
Long Term Potentiation ◽  
In Vivo Microdialysis ◽  
Electrophysiological Recordings

Abstract Background Basolateral amygdalar projections to the prefrontal cortex play a key role in modulating behavioral responses to stress stimuli. Among the different neuromodulators known to impact basolateral amygdalar-prefrontal cortex transmission, the corticotrophin releasing factor (CRF) is of particular interest because of its role in modulating anxiety and stress-associated behaviors. While CRF type 1 receptor (CRFR1) has been involved in prefrontal cortex functioning, the participation of CRF type 2 receptor (CRFR2) in basolateral amygdalar-prefrontal cortex synaptic transmission remains unclear. Methods Immunofluorescence anatomical studies using rat prefrontal cortex synaptosomes devoid of postsynaptic elements were performed in rats with intra basolateral amygdalar injection of biotinylated dextran amine. In vivo microdialysis and local field potential recordings were used to measure glutamate extracellular levels and changes in long-term potentiation in prefrontal cortex induced by basolateral amygdalar stimulation in the absence or presence of CRF receptor antagonists. Results We found evidence for the presynaptic expression of CRFR2 protein and mRNA in prefrontal cortex synaptic terminals originated from basolateral amygdalar. By means of microdialysis and electrophysiological recordings in combination with an intra-prefrontal cortex infusion of the CRFR2 antagonist antisauvagine-30, we were able to determine that CRFR2 is functionally positioned to limit the strength of basolateral amygdalar transmission to the prefrontal cortex through presynaptic inhibition of glutamate release. Conclusions Our study shows for the first time to our knowledge that CRFR2 is expressed in basolateral amygdalar afferents projecting to the prefrontal cortex and exerts an inhibitory control of prefrontal cortex responses to basolateral amygdalar inputs. Thus, changes in CRFR2 signaling are likely to disrupt the functional connectivity of the basolateral amygdalar-prefrontal cortex pathway and associated behavioral responses.

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