Genetic Modifications of Seizure Susceptibility and Expression by Altered Excitability in Drosophila Na+ and K+ Channel Mutants

2006 ◽  
Vol 96 (5) ◽  
pp. 2465-2478 ◽  
Author(s):  
Jisue Lee ◽  
Chun-Fang Wu

A seizure-paralysis repertoire characteristic of Drosophila “bang-sensitive” mutants can be evoked electroconvulsively in tethered flies, in which behavioral episodes are associated with synchronized spike discharges in different body parts. Flight muscle DLMs (dorsal longitudinal muscles) display a stereotypic sequence of initial and delayed bouts of discharges (ID and DD), interposed with giant fiber (GF) pathway failure and followed by a refractory period. We examined how seizure susceptibility and discharge patterns are modified in various K+ and Na+ channel mutants. Decreased numbers of Na+ channels in nap ts flies drastically reduced susceptibility to seizure induction, eliminated ID, and depressed DD spike generation. Mutations of different K+ channels led to differential modifications of the various components in the repertoire. Altered transient K+ currents in Sh 133 and Hk mutants promoted ID induction. However, only Sh 133 but not Hk mutations increased DD seizure and GF pathway failure durations. Surprisingly, modifications in sustained K+ currents in eag and Shab mutants increased thresholds for DD induction and GF pathway failure. Nevertheless, both eag and Shab, like Sh 133, increased DD spike generation and recovery time from GF pathway failure. Interactions between channel mutations with the bang-sensitive mutation bss demonstrated the role of membrane excitability in stress-induced seizure-paralysis behavior. Seizure induction and discharges were suppressed by nap ts in bss nap double mutants, whereas Sh heightened seizure susceptibility in bss Sh 133 and bss Sh M double mutants. Our results suggest that individual seizure repertoire components reflect different neural network activities that could be differentially altered by mutations of specific ion channel subunits.

2019 ◽  
Vol 14 (7) ◽  
pp. 598-606
Author(s):  
Sarah Albogami

Background:: Regeneration is the process by which body parts lost as a result of injury are replaced, as observed in certain animal species. The root of regenerative differences between organisms is still not very well understood; if regeneration merely recycles developmental pathways in the adult form, why can some animals regrow organs whereas others cannot? In the regulation of the regeneration process as well as other biological phenomena, epigenetics plays an essential role. Objective:: This review aims to demonstrate the role of epigenetic regulators in determining regenerative capacity. Results:: In this review, we discuss the basis of regenerative differences between organisms. In addition, we present the current knowledge on the role of epigenetic regulation in regeneration, including DNA methylation, histone modification, lysine methylation, lysine methyltransferases, and the SET1 family. Conclusion:: An improved understanding of the regeneration process and the epigenetic regulation thereof through the study of regeneration in highly regenerative species will help in the field of regenerative medicine in future.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Mingzhao Su ◽  
Junhua Liu ◽  
Baocong Yu ◽  
Kaixing Zhou ◽  
Congli Sun ◽  
...  

AbstractThe rodent whisker-barrel cortex system has been established as an ideal model for studying sensory information integration. The barrel cortex consists of barrel and septa columns that receive information input from the lemniscal and paralemniscal pathways, respectively. Layer 5a is involved in both barrel and septa circuits and play a key role in information integration. However, the role of layer 5a in the development of the barrel cortex remains unclear. Previously, we found that calretinin is dynamically expressed in layer 5a. In this study, we analyzed calretinin KO mice and found that the dendritic complexity and length of layer 5a pyramidal neurons were significantly decreased after calretinin ablation. The membrane excitability and excitatory synaptic transmission of layer 5a neurons were increased. Consequently, the organization of the barrels was impaired. Moreover, layer 4 spiny stellate cells were not able to properly gather, leading to abnormal formation of barrel walls as the ratio of barrel/septum size obviously decreased. Calretinin KO mice exhibited deficits in exploratory and whisker-associated tactile behaviors as well as social novelty preference. Our study expands our knowledge of layer 5a pyramidal neurons in the formation of barrel walls and deepens the understanding of the development of the whisker-barrel cortex system.


2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Stuart A Collins ◽  
Ipe Ninan

Abstract The onset of several neuropsychiatric disorders including anxiety disorders coincides with adolescence. Consistently, threat extinction, which plays a key role in the regulation of anxiety-related behaviors, is diminished during adolescence. Furthermore, this attenuated threat extinction during adolescence is associated with an altered synaptic plasticity in the infralimbic medial prefrontal cortex (IL-mPFC), a brain region critical for threat extinction. However, the mechanism underlying the altered plasticity in the IL-mPFC during adolescence is unclear. Given the purported role of vasoactive intestinal polypeptide expressing interneurons (VIPINs) in disinhibition and hence their potential to affect cortical plasticity, we examined whether VIPINs exhibit an adolescence-specific plasticity in the IL-mPFC. We observed an increase in GABAergic transmission and a decrease in excitability in VIPINs during adolescence. Male mice show a significantly higher VIPIN-pyramidal neuron GABAergic transmission compared with female mice. The observed increase in GABAergic transmission and a decrease in membrane excitability in VIPINs during adolescence could play a role in the altered plasticity in the adolescent IL-mPFC. Furthermore, the suppression of VIPIN-mediated GABAergic transmission in females might be relevant to sex differences in anxiety disorders.


1995 ◽  
Vol 269 (3) ◽  
pp. H805-H811 ◽  
Author(s):  
S. Najibi ◽  
R. A. Cohen

Endothelium-dependent relaxations to acetylcholine remain normal in the carotid artery of hypercholesterolemic rabbits, but unlike endothelium-dependent relaxations of normal rabbits, they are inhibited by charybdotoxin, a specific blocker of Ca(2+)-dependent K+ channels. Because nitric oxide (NO) is the mediator of endothelium-dependent relaxation and can activate Ca(2+)-dependent K+ channels directly or via guanosine 3',5'-cyclic monophosphate, the present study investigated the role of Ca(2+)-dependent K+ channels in relaxations caused by NO, sodium nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-Brc-GMP) in hypercholesterolemic rabbit carotid artery. Isometric tension was measured in rabbit carotid artery denuded of endothelium from normal and hypercholesterolemic rabbits which were fed 0.5% cholesterol for 12 wk. Under control conditions, relaxations to all agents were similar in normal and hypercholesterolemic rabbit arteries. Charybdotoxin had no significant effect on relaxations of normal arteries to NO, sodium nitroprusside, or 8-BrcGMP, but the Ca(2+)-dependent K+ channel blocker significantly inhibited the relaxations caused by each of these agents in the arteries from hypercholesterolemic rabbits. By contrast, relaxations to the calcium channel blocker nifedipine were potentiated to a similar extent by charybdotoxin in both groups. In addition, arteries from hypercholesterolemic rabbits relaxed less than normal to sodium nitroprusside when contracted with depolarizing potassium solution. These results indicate that although nitrovasodilator relaxations are normal in the hypercholesterolemic rabbit carotid artery, they are mediated differently, and to a greater extent, by Ca(2+)-dependent K+ channels. These data also suggest that K+ channel-independent mechanism(s) are impaired in hypercholesterolemia.


Perception ◽  
10.1068/p5853 ◽  
2007 ◽  
Vol 36 (10) ◽  
pp. 1547-1554 ◽  
Author(s):  
Francesco Pavani ◽  
Massimiliano Zampini

When a hand (either real or fake) is stimulated in synchrony with our own hand concealed from view, the felt position of our own hand can be biased toward the location of the seen hand. This intriguing phenomenon relies on the brain's ability to detect statistical correlations in the multisensory inputs (ie visual, tactile, and proprioceptive), but it is also modulated by the pre-existing representation of one's own body. Nonetheless, researchers appear to have accepted the assumption that the size of the seen hand does not matter for this illusion to occur. Here we used a real-time video image of the participant's own hand to elicit the illusion, but we varied the hand size in the video image so that the seen hand was either reduced, veridical, or enlarged in comparison to the participant's own hand. The results showed that visible-hand size modulated the illusion, which was present for veridical and enlarged images of the hand, but absent when the visible hand was reduced. These findings indicate that very specific aspects of our own body image (ie hand size) can constrain the multisensory modulation of the body schema highlighted by the fake-hand illusion paradigm. In addition, they suggest an asymmetric tendency to acknowledge enlarged (but not reduced) images of body parts within our body representation.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Daisuke Kase ◽  
Keiji Imoto

Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels were first reported in heart cells and are recently known to be involved in a variety of neural functions in healthy and diseased brains. HCN channels generate inward currents when the membrane potential is hyperpolarized. Voltage dependence of HCN channels is regulated by intracellular signaling cascades, which contain cyclic AMP, PIP2, and TRIP8b. In addition, voltage-gated potassium channels have a strong influence on HCN channel activity. Because of these funny features, HCN channel currents, previously called funny currents, can have a wide range of functions that are determined by a delicate balance of modulatory factors. These multifaceted features also make it difficult to predict and elucidate the functional role of HCN channels in actual neurons. In this paper, we focus on the impacts of HCN channels on neural activity. The functions of HCN channels reported previously will be summarized, and their mechanisms will be explained by using numerical simulation of simplified model neurons.


2012 ◽  
Vol 4 (2) ◽  
pp. 157-165
Author(s):  
Sally Gardner

Drawing on experiences that have entailed watching and learning forms of so-called ‘Indian dance’ (Bharata Natyam and Odissi), and watching Odissi dancers performing in various locations in Orissa’s ‘sacred triangle’ (Puri, Konark, Bhubaneswar), and against my own background in contemporary dance, I propose that the difference of the Odissi body is that the dancer dances with his or her feet in more than one kingdom – that is, he or she maintains a link between human bodies and the bodies of plants. Such a perception can help to displace questions of the dancer’s spatiality and representations, challenging western or westernized visions of the industrial or mechanical body, assumed hierarchies of body parts and their signifying powers, and assumptions about the role of the joints. The sense of a botanical imaginary or specific cultural body-schema at work in Odissi dance is supported by discussion of historical and ethnographic literature pertaining to the (former) female dancers of the Jagannath Temple in Puri; the temple’s links with Oriyan tribal cultures; the dancers’ traditional importance according to an axis of social auspiciousness/inauspiciousness as opposed to social purity/impurity; and the particular processes of the reconstruction of Odissi dance (separate from that of Bharata natyam) after independence.


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