scholarly journals On the regulator of spike activity in cortical neurons under hypothermic conditions

2016 ◽  
Author(s):  
Yulia S. Mednikova ◽  
Nadezda M. Zakharova ◽  
Natalia V. Pasikova ◽  
Inna V. Averina
Keyword(s):  
Guinea Pig ◽  
Spontaneous Activity ◽  
Functional Properties ◽  
Neuronal Activity ◽  
Spike Activity ◽  
Cortical Neurons ◽  
Ion Homeostasis ◽  
Iontophoretic Application ◽  
Dendritic Branches ◽  
Cortical Slices

In sensorimotor cortical slices of guinea pig in the course of cooling incubating fluid from 34 to 21-22°C it was shown that hypothermia exerted both increase and decrease of spontaneous activity in different neurons. On hypothermic increase of firing level spike responses of soma to iontophoretic application of glutamate to dendritic locus appeared with shorter latencies and with longer latencies on hypothermic decrease of spontaneous activity. At the same time hypothermia did not influence on the evoked spike reactions to iontophoretic application of glutamate straight to the soma. It means that hypothermic disorders of neuronal activity are not connected with changes in sensitivity to glutamate but determined by changes of amplitude of glutamatergic excitation while propagating along dendritic branches. The changes in spontaneous activity began at 30°C along with the decreased spike reactions to iontophoretic applications of acetylcholine and efficacy of dendro-somatic propagation. At the same temperature the fall of spike amplitude was initiated and increased with further hypothermia. It is proposed that the basis for hypothermic changes of neuronal activity is the decreased rate of M-cholinergic process at 27-29°C which leads both to attenuation of conductive function of dendrites and imbalance of K+ ion homeostasis. Peculiarities of hypothermic regulation of neuronal spike activity depend on individual functional properties of cortical neurons.

Responses of Neurons in Neonatal Cortex and Thalamus to Patterned Visual Stimulation Through the Naturally Closed Lids

2001 ◽  
Vol 85 (4) ◽  
pp. 1436-1443 ◽  
Author(s):  
Kristine Krug ◽  
Colin J. Akerman ◽  
Ian D. Thompson
Keyword(s):  
Visual Cortex ◽  
Spontaneous Activity ◽  
Neuronal Activity ◽  
Cortical Neurons ◽  
Visual Experience ◽  
Striate Cortex ◽  
Visual Stimulation ◽  
Self Organization ◽  
Visual Responses ◽  
Eye Opening

In studies of the developing mammalian visual system, it has been axiomatic that visual experience begins with eye-opening. Any role for neuronal activity earlier in development has been attributed to the patterned spontaneous activity found in retina and lateral geniculate nucleus (LGN). Here we show that, as early as 2 wk before eye-opening, visual stimuli presented through the closed eyelids can drive neuronal activity in LGN and striate cortex of the ferret. At this age, spontaneous activity in cortex is much lower than in LGN, and the visual responses of many cortical, but not geniculate, neurons depend on the orientation of a moving grating. Furthermore the selectivity of cortical neurons to the orientation of gratings presented through the closed eyelids improves with age. Thus neuronal activity patterned by visual experience, rather than by spontaneous retinal activity, is present in visual cortex much earlier than previously thought. This could have important implications for the self-organization of visual cortex.

ANG II modifies cardiomyocyte function via extracardiac and intracardiac neurons: in situ and in vitro studies

1997 ◽  
Vol 272 (3) ◽  
pp. R766-R775 ◽  
Author(s):  
M. Horackova ◽  
J. A. Armour
Keyword(s):  
Guinea Pig ◽  
Receptor Antagonist ◽  
Neuronal Activity ◽  
Ang Ii ◽  
Arterial Blood ◽  
Cardiac Ganglia ◽  
In Situ Experiments ◽  
Anesthetized Dogs

To determine whether angiotensin II (ANG II) affects cardiac performance via neurons in intrathoracic cardiac ganglia, studies were performed on anesthetized dogs. To exclude possible vascular regulatory effects of ANG II, experiments were also performed using long-term cultures of adult guinea pig ventricular cardiomyocytes with or without intrathoracic neurons. 1) In in situ experiments in 10 anesthetized dogs, cardiac augmentation occurred when ANG II (10 microl or 0.1 ml; 10-100 microM) was administered into limited loci within acutely decentralized stellate or middle cervical ganglia that were neurally connected to, but not those disconnected from, the heart. In another 18 dogs, ANG II increased intrinsic cardiac neuronal activity when administered adjacent to such neurons or into their local arterial blood supply. Ventricular ionotropic effects elicited by ANG II were eliminated by timolol, whereas increases in intrinsic cardiac neuronal activity were not affected. Effects elicited by ANG II were eliminated by administration of a selective AT1 receptor antagonist (losartan) but not by a selective AT2 receptor antagonist (PD-123319). 2) In in vitro experiments, ANG II (100 nM) induced positive chronotropic effects on cultured adult guinea pig cardiomyocytes innervated with adult extrinsic or intrinsic cardiac neurons, but not those cultured without neurons. The frequency of calcium inward current (Ca(i)) transients (recorded by fura 2 fluorescence) increased in innervated cocultures but not in the noninnervated cardiomyocyte cultures; however, the amplitude of Ca(i) transients was not affected by ANG II in cultures or in freshly isolated adult guinea pig cardiomyocytes. ANG II-induced effects in cocultures were blocked by losartan but not PD-123319 or timolol. Thus 1) ANG II-sensitive neurons exist in intrathoracic extracardiac and intrinsic cardiac ganglia; 2) these neurons possess AT1 receptors; and 3) these neurons appear to act directly and indirectly via adrenergic neurons to enhance cardiomyocyte function.

1812 Optical imaging of neuronal activity with a voltage-sensitive dye in guinea pig piriform cortex in vitro

1993 ◽  
Vol 18 ◽  
pp. S199
Author(s):  
Michio Sugitani ◽  
Tokio Sugai ◽  
Manabu Tanifuji ◽  
Kazuyuki Murase ◽  
Norihiko Onoda
Keyword(s):  
Guinea Pig ◽  
Optical Imaging ◽  
Neuronal Activity ◽  
Piriform Cortex ◽  
Voltage Sensitive Dye

scholarly journals Effect of Membrane Depolarization by High K+ on Carbachol-Stimulated Phosphoinositides Hydrolysis in Guinea Pig Cerebral Cortical Slices

1990 ◽  
Vol 53 (2) ◽  
pp. 229-234 ◽  
Author(s):  
Xiao-Ming ZHOU ◽  
Shuji UCHIDA ◽  
Atsushi MIZUSHIMA ◽  
Hiroshi YOSHIDA
Keyword(s):  
Guinea Pig ◽  
Membrane Depolarization ◽  
High K ◽  
Cortical Slices

scholarly journals Neuronal activity enhances aryl hydrocarbon receptor-mediated gene expression and dioxin neurotoxicity in cortical neurons

2008 ◽  
Vol 104 (5) ◽  
pp. 1415-1429 ◽  
Author(s):  
Chun-Hua Lin ◽  
Shu-Hui Juan ◽  
Chen Yu Wang ◽  
Yu-Yo Sun ◽  
Chih-Ming Chou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Aryl Hydrocarbon Receptor ◽  
Neuronal Activity ◽  
Cortical Neurons ◽  
Aryl Hydrocarbon

scholarly journals Neuronal activity disrupts myelinated axon integrity in the absence of NKCC1b

2020 ◽  
Vol 219 (7) ◽  
Author(s):  
Katy L.H. Marshall-Phelps ◽  
Linde Kegel ◽  
Marion Baraban ◽  
Torben Ruhwedel ◽  
Rafael G. Almeida ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Ion Homeostasis ◽  
Myelinated Axon ◽  
Cell Type ◽  
Myelinated Axons ◽  
Specific Loss ◽  
Uncharacterized Gene ◽  
Interface Cell ◽  
Cell Type Specific ◽  
Periaxonal Space

Through a genetic screen in zebrafish, we identified a mutant with disruption to myelin in both the CNS and PNS caused by a mutation in a previously uncharacterized gene, slc12a2b, predicted to encode a Na+, K+, and Cl− (NKCC) cotransporter, NKCC1b. slc12a2b/NKCC1b mutants exhibited a severe and progressive pathology in the PNS, characterized by dysmyelination and swelling of the periaxonal space at the axon–myelin interface. Cell-type–specific loss of slc12a2b/NKCC1b in either neurons or myelinating Schwann cells recapitulated these pathologies. Given that NKCC1 is critical for ion homeostasis, we asked whether the disruption to myelinated axons in slc12a2b/NKCC1b mutants is affected by neuronal activity. Strikingly, we found that blocking neuronal activity completely prevented and could even rescue the pathology in slc12a2b/NKCC1b mutants. Together, our data indicate that NKCC1b is required to maintain neuronal activity–related solute homeostasis at the axon–myelin interface, and the integrity of myelinated axons.

scholarly journals ApoE4 attenuates cortical neuronal activity and impairs memory in young apoE4 rats

2021 ◽  
Author(s):  
Ilona Har-Paz ◽  
Elor Arieli ◽  
Anan Moran
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Neuronal Activity ◽  
Genetic Risk ◽  
Cortical Neurons ◽  
Late Onset ◽  
Genetic Risk Factor ◽  
Normal Brain ◽  
Brain Functions

AbstractThe E4 allele of apolipoprotein E (apoE4) is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD). However, apoE4 may cause innate brain abnormalities before the appearance of AD related neuropathology. Understanding these primary dysfunctions is vital for early detection of AD and the development of therapeutic strategies for it. Recently we have shown impaired extra-hippocampal memory in young apoE4 mice – a deficit that was correlated with attenuated structural pre-synaptic plasticity in cortical and subcortical regions. Here we test the hypothesis that these early structural deficits impact learning via changes in basal and stimuli evoked neuronal activity. We recorded extracellular neuronal activity from the gustatory cortex (GC) of three-month-old humanized apoE4 and wildtype rats, before and after conditioned taste aversion (CTA) training. Despite normal sucrose drinking behavior before CTA, young apoE4 rats showed impaired CTA learning, consistent with our previous results in apoE4 mice. This behavioral deficit was correlated with decreased basal and taste-evoked firing rates in both putative excitatory and inhibitory GC neurons. Single neuron and ensemble analyses of taste coding demonstrated that apoE4 neurons could be used to correctly classify tastes, but were unable to undergo plasticity to support learning. Our results suggest that apoE4 impacts brain excitability and plasticity early in life and may act as an initiator for later AD pathologies.Significant statementThe ApoE4 allele is the strongest genetic risk-factor for late-onset Alzheimer’s disease (AD), yet the link between apoE4 and AD is still unclear. Recent molecular and in-vitro studies suggest that apoE4 interferes with normal brain functions decades before the development of its related AD neuropathology. Here we recorded the activity of cortical neurons from young apoE4 rats during extra-hippocampal learning to study early apoE4 neuronal activity abnormalities, and their effects over coding capacities. We show that apoE4 drastically reduces basal and stimuli-evoked cortical activity in both excitatory and inhibitory neurons. The apoE4-induced activity attenuation did not prevent coding of stimuli identity and valence, but impaired capacity to undergo activity changes to support learning. Our findings support the hypothesis that apoE4 interfere with normal neuronal plasticity early in life; a deficit that may lead to late-onset AD development.

scholarly journals A MICROCALORIMETRIC STUDY OF TURTLE CORTICAL SLICES: INSIGHTS INTO BRAIN METABOLIC DEPRESSION

1994 ◽  
Vol 191 (1) ◽  
pp. 141-153 ◽  
Author(s):  
C Doll ◽  
P Hochachka ◽  
S Hand
Keyword(s):  
Cortical Neurons ◽  
Heat Dissipation ◽  
Energy Charge ◽  
Utilization Rate ◽  
Rapid Decline ◽  
Metabolic Depression ◽  
Slice Preparation ◽  
Cortical Slices

In previous papers, we have examined turtle cortical neurons in vitro for mechanisms of anoxic metabolic depression ('channel arrest' and changes in electrical parameters). Negative results prompted the current study with the aim of examining more closely the energy profile and metabolism of turtle cortical slices. Calorimetry is used to measure heat dissipation during normoxia and nitrogen perfusion (120 min) and the results are converted into an ATP utilization rate. These indicate that the control rate of ATP utilization (1.72 µmol ATP g-1 min-1) agrees closely with in vivo whole-brain metabolic measurements. Both nitrogen perfusion and pharmacologically induced anoxic (cyanide+N2) groups depressed heat dissipation considerably compared with the control value (nitrogen 37 %; pharmacological anoxia 49 %). The resulting ATP utilization estimates indicate metabolic depressions of 30 % (nitrogen) and 42 % (pharmacological anoxia). The slice preparation did not exhibit a change in any measured adenylate parameter for up to 120 min of anoxia or pharmacological anoxia. Significant changes did occur in [ADP], ATP/ADP ratio and energy charge after 240 min of exposure to anoxic conditions. These results support the idea that the turtle cortical slice preparation has a profound resistance to anoxia, with both nitrogen perfusion and pharmacological anoxia causing a rapid decline in heat dissipation and metabolism.

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