Noradrenergic modulation determines respiratory network activity during temperature changes in the in vitro brainstem of bullfrogs

2018 ◽  
Vol 258 ◽  
pp. 25-31 ◽  
Author(s):  
Mauricio Vallejo ◽  
Joseph M. Santin ◽  
Lynn K. Hartzler
2008 ◽  
Vol 99 (5) ◽  
pp. 2114-2125 ◽  
Author(s):  
Andrew K. Tryba ◽  
Fernando Peña ◽  
Steven P. Lieske ◽  
Jean-Charles Viemari ◽  
Muriel Thoby-Brisson ◽  
...  

Many networks generate distinct rhythms with multiple frequency and amplitude characteristics. The respiratory network in the pre-Bötzinger complex (pre-Böt) generates both the low-frequency, large-amplitude sigh rhythm and a faster, smaller-amplitude eupneic rhythm. Could the same set of pacemakers generate both rhythms? Here we used an in vitro respiratory brainslice preparation. We describe a subset of synaptically isolated pacemakers that spontaneously generate two distinct bursting patterns. These two patterns resemble network activity including sigh-like bursts that occur at low frequencies and have large amplitudes and eupneic-like bursts with higher frequency and smaller amplitudes. Cholinergic neuromodulation altered the network and pacemaker bursting: fictive sigh frequency is increased dramatically, whereas fictive eupneic frequency is drastically lowered. The data suggest that timing and amplitude characteristics of fictive eupneic and sigh rhythms are set by the same set of pacemakers that are tuned by changes in the neuromodulatory state.


2002 ◽  
Vol 87 (6) ◽  
pp. 2964-2971 ◽  
Author(s):  
Dawn M. Blitz ◽  
Jan-Marino Ramirez

Neural networks that produce rhythmic behaviors require flexibility to respond to changes in the internal and external state of the animal. It is important to not only understand how a network responds during such perturbations but also how the network recovers. For example, the respiratory network needs to respond to and recover from temporary changes in oxygen level that can occur during sleep, exercise, and respiratory disorders. During a temporary decrease in oxygen level, there is an increase in respiratory frequency followed by a depression that can lead to complete apnea. Here we used a mouse brain stem slice preparation as a model system to examine the recovery of respiratory network activity after brief episodes of anoxia. We found the respiratory network recovers from a single anoxic episode with a transient increase in fictive respiratory frequency. Although repetitive anoxia does not elicit a greater frequency increase, it does elicit a longer lasting frequency increase persisting ≤90 min. Thus there is a centrally mediated long-lasting influence on the respiratory network elicited by decreased oxygen levels. This modulation occurs as a prolonged facilitation of fictive respiratory frequency after brief repetitive but not single anoxic exposure. These data are important to consider in the context of disorders such as sleep apnea in which brief periodic anoxic episodes are experienced.


2021 ◽  
Author(s):  
Maryna Psol ◽  
Sofia Guerin Darvas ◽  
Kristian Leite ◽  
Sameehan U Mahajani ◽  
Mathias Bähr ◽  
...  

Abstract ß-Synuclein (ß-Syn) has long been considered to be an attenuator for the neuropathological effects caused by the Parkinson’s disease-related α-Synuclein (α-Syn) protein. However, recent studies demonstrated that overabundant ß-Syn can form aggregates and induce neurodegeneration in CNS neurons in vitro and in vivo, albeit at a slower pace as compared to α-Syn. Here we demonstrate that ß-Syn mutants V70M, detected in a sporadic case of Dementia with Lewy Bodies (DLB), and P123H, detected in a familial case of DLB, robustly aggravate the neurotoxic potential of ß-Syn. Intriguingly, the two mutations trigger mutually exclusive pathways. ß-Syn V70M enhances morphological mitochondrial deterioration and degeneration of dopaminergic and non-dopaminergic neurons, but has no influence on neuronal network activity. Conversely, ß-Syn P123H silences neuronal network activity, but does not aggravate neurodegeneration. ß-Syn WT, V70M and P123H formed proteinase K (PK) resistant intracellular fibrils within neurons, albeit with less stable C-termini as compared to α-Syn. Under cell free conditions, ß-Syn V70M demonstrated a much slower pace of fibril formation as compared to WT ß-Syn, and P123H fibrils present with a unique phenotype characterized by large numbers of short, truncated fibrils. Thus, it is possible that V70M and P123H cause structural alterations in ß-Syn, that are linked to their distinct neuropathological profiles. The extent of the lesions caused by these neuropathological profiles is almost identical to that of overabundant α-Syn, and thus likely to be directly involved into etiology of DLB. Over all, this study provides insights into distinct disease mechanisms caused by mutations of ß-Syn.


10.2341/05-26 ◽  
2006 ◽  
Vol 31 (2) ◽  
pp. 261-265 ◽  
Author(s):  
A. R. Yazici ◽  
A. Müftü ◽  
G. Kugel ◽  
R. D. Perry

Clinical Relevance The thickness of the residual dentin is a critical factor in the reducing thermal transfer to pulp, and this transfer varies with the curing unit used.


2008 ◽  
Vol 99 (3) ◽  
pp. 1394-1407 ◽  
Author(s):  
Sarah Potez ◽  
Matthew E. Larkum

Understanding the impact of active dendritic properties on network activity in vivo has so far been restricted to studies in anesthetized animals. However, to date no study has been made to determine the direct effect of the anesthetics themselves on dendritic properties. Here, we investigated the effects of three types of anesthetics commonly used for animal experiments (urethane, pentobarbital and ketamine/xylazine). We investigated the generation of calcium spikes, the propagation of action potentials (APs) along the apical dendrite and the somatic firing properties in the presence of anesthetics in vitro using dual somatodendritic whole cell recordings. Calcium spikes were evoked with dendritic current injection and high-frequency trains of APs at the soma. Surprisingly, we found that the direct actions of anesthetics on calcium spikes were very different. Two anesthetics (urethane and pentobarbital) suppressed dendritic calcium spikes in vitro, whereas a mixture of ketamine and xylazine enhanced them. Propagation of spikes along the dendrite was not significantly affected by any of the anesthetics but there were various changes in somatic firing properties that were highly dependent on the anesthetic. Last, we examined the effects of anesthetics on calcium spike initiation and duration in vivo using high-frequency trains of APs generated at the cell body. We found the same anesthetic-dependent direct effects in addition to an overall reduction in dendritic excitability in anesthetized rats with all three anesthetics compared with the slice preparation.


1983 ◽  
Vol 245 (1) ◽  
pp. R32-R37
Author(s):  
P. J. Walsh ◽  
T. W. Moon

The effects of acclimation temperature and acute temperature changes on the intracellular pH (pHi) of hepatocytes isolated from the American eel, Anguilla rostrata, were studied by the measurement of the distribution ratio of dimethyloxizolidinedione (DMO). Varying the concentration of DMO (10(-7) to 10(-4) M) did not affect estimates of pHi, indicating that DMO acts as an ideal pHi probe in eel hepatocytes. In vitro studies yielded values of liver cell pHi identical to those previously measured in vivo (in vitro pHi = 7.556 +/- 0.010; in vivo pHi = 7.570 +/- 0.049 at 20 degrees C); hepatocyte pHi varied inversely with acclimation temperature (5-20 degrees C) in a manner consistent with alphastat regulation (delta pH/delta T = -0.0182 +/- 0.021). During acute temperature increases (5-20 degrees C) and decreases (20-5 degrees C) hepatocytes regulated pHi to the appropriate (acclimated) value within 30-45 min posttransfer under conditions of constant medium pH (pHe). The effects of medium pH were also studied, and although patterns of pHi regulation differed between 5 and 20 degrees C cells, a pHi difference consistent with alphastat regulation was maintained between 5 and 20 degrees C cells over the pHe range 7.8-8.3.


2021 ◽  
Author(s):  
Alexei M. Bygrave ◽  
Ayesha Sengupta ◽  
Ella P. Jackert ◽  
Mehroz Ahmed ◽  
Beloved Adenuga ◽  
...  

Synapses in the brain exhibit cell–type–specific differences in basal synaptic transmission and plasticity. Here, we evaluated cell–type–specific differences in the composition of glutamatergic synapses, identifying Btbd11, as an inhibitory interneuron–specific synapse–enriched protein. Btbd11 is highly conserved across species and binds to core postsynaptic proteins including Psd–95. Intriguingly, we show that Btbd11 can undergo liquid–liquid phase separation when expressed with Psd–95, supporting the idea that the glutamatergic post synaptic density in synapses in inhibitory and excitatory neurons exist in a phase separated state. Knockout of Btbd11 from inhibitory interneurons decreased glutamatergic signaling onto parvalbumin–positive interneurons. Further, both in vitro and in vivo, we find that Btbd11 knockout disrupts network activity. At the behavioral level, Btbd11 knockout from interneurons sensitizes mice to pharmacologically induced hyperactivity following NMDA receptor antagonist challenge. Our findings identify a cell–type–specific protein that supports glutamatergic synapse function in inhibitory interneurons–with implication for circuit function and animal behavior.


2019 ◽  
Author(s):  
Paloma P Maldonado ◽  
Alvaro Nuno-Perez ◽  
Jan Kirchner ◽  
Elizabeth Hammock ◽  
Julijana Gjorgjieva ◽  
...  

SummarySpontaneous network activity shapes emerging neuronal circuits during early brain development, however how neuromodulation influences this activity is not fully understood. Here, we report that the neuromodulator oxytocin powerfully shapes spontaneous activity patterns. In vivo, oxytocin strongly decreased the frequency and pairwise correlations of spontaneous activity events in visual cortex (V1), but not in somatosensory cortex (S1). This differential effect was a consequence of oxytocin only increasing inhibition in V1 and increasing both inhibition and excitation in S1. The increase in inhibition was mediated by the depolarization and increase in excitability of somatostatin+ (SST) interneurons specifically. Accordingly, silencing SST+ neurons pharmacogenetically fully blocked oxytocin’s effect on inhibition in vitro as well its effect on spontaneous activity patterns in vivo. Thus, oxytocin decreases the excitatory/inhibitory ratio and modulates specific features of V1 spontaneous activity patterns that are crucial for refining developing synaptic connections and sensory processing later in life.


2001 ◽  
Vol 39 ◽  
pp. 40-40
Author(s):  
J Loock ◽  
J Stange ◽  
S Mitzner ◽  
R Schmidt ◽  
E W Keefer ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document