「neuronal」の共起表現(1語右で並び替え)

「neuronal」の共起表現一覧(1語右で並び替え)

neuronal

1語右で並び替え

該当件数:169件

Neuronal acetylcholine receptor subunit alpha-7 is a p
Neuronal acetylcholine receptor subunit alpha-2 is a p
Neuronal acetylcholine receptor subunit alpha-3 is a p
Neuronal acetylcholine receptor subunit alpha-9 is a p
Neuronal acetylcholine receptor subunit beta-3 is a pr
Neuronal acetylcholine receptor subunit alpha-10 also
It is very similar to the neuronal acetylcholinesterase.
ess circuits, as opposed to producing diffuse neuronal activation.
ace proteins whose expression is regulated by neuronal activity early in an animal's life.
expression of c-fos as an indirect marker of neuronal activity because c-fos is often expressed whe
ter interfaces-electronic devices that sample neuronal activity in the brain, decode its meaning and
okyo Metropolitan Institute for Neuroscience) neuronal activity of the inferotemporal cortex in Maca
ith somatostatin, including the depression of neuronal activity.
, endothelial progenitor cells, glioblastoma, neuronal and glial stem cells, various pediatric brain
cals, protecting against oxidative stress and neuronal apoptosis.
f the hindbrain/midbrain border and aiding in neuronal axon guidance.
ncreased intracranial pressure, which damages neuronal axons.
ch as the effects of hormones on behavior and neuronal basis of behavior.
This gene is a member of the neuronal calcium channel gamma subunit gene subfamily
nel-interacting proteins, which belong to the neuronal calcium sensor family of proteins.
This gene is a member of the neuronal calcium channel gamma subunit gene subfamily
KA1 antibody protects against kainate-induced neuronal cell death.
However, neuronal cell bodies contain less APP as a function of
Notably, this is the second neuronal cell surface antigen (after anti-voltage-gate
For example, it is key in neuronal cell death in excitotoxicity, in which overac
se domain, GAK is 43% identical to auxilin, a neuronal cell uncoating clathrin cofactor, in its amin
other hand, TPH2 is exclusively expressed in neuronal cell types and is the predominant isoform in
Axotomy may cause neuronal cell death, espeically in embryonic or neonat
directly gate certain calcium ion channels in neuronal cell membranes.
nation of transcription factors that leads to neuronal cell fate differentiation.
otective effects on 6-hydroxydopamine-induced neuronal cell death.
GSK3B is involved in energy metabolism, neuronal cell development, and body pattern formation.
f NSE with antibodies can be used to identify neuronal cells and cells with neuroendocrine different
i-apoptotic activity has been demonstrated in neuronal cells, in vitro.
to be the most abundant microRNA expressed in neuronal cells.
st common form of a group of disorders called neuronal ceroid lipofuscinosis (or NCLs).
tations in this gene result in late-infantile neuronal ceroid lipofuscinosis, which is associated wi
ve disorder type called lipofuscinoses, e.g., neuronal ceroid lipofuscinosis, also known as Batten d
Defects in this gene are a cause of infantile neuronal ceroid lipofuscinosis 1 (CLN1, or INCL) and n
Neuronal ceroid lipofuscinoses (NCL) represent a group
l protein thioesterase gene causing infantile neuronal ceroid lipofuscinosis.
or behaviour; in particular, he has shown how neuronal circuits in the spine help control rhythmic m
nds on 'reverberating' electrical activity in neuronal circuits, and is very easily destroyed by int
play a role when nerve cells assemble to form neuronal circuits.
ptual bases to be respected in the process of neuronal classification.
This protein plays a role in the neuronal commitment and differentiation and in the gen
relationships are generally maintained in the neuronal connections between the nuclei and associated
ses which exhibit abnormal phosphorylation of neuronal cytoskeletal proteins by p25/Cdk5 such as tau
In addition to being a marker of neuronal damage in animal models of CNS damage, PK-111
blockade of excitotoxicity and attenuation of neuronal damage induced by cerebral ischemia/reperfusi
ered to be a useful tool in the assessment of neuronal damage.
visualize brain inflammation in patients with neuronal damage.
or targeted neuronal damaged in the entorhinal cortex or in the su
Death Receptor 6 (DR-6) refers to a neuronal Death Receptor which is physiologically activ
interestingly without producing any apparent neuronal death.
to a robust regenerative response without any neuronal death.
ructures that, by an unclear mechanism, cause neuronal death.
Autophagy could either clear the way for neuronal degeneration or it could be a medium for cell
ce several protective factors that will delay neuronal degeneration (Pallas etal., 2008).
, behaviour changes, muscle degeneration, and neuronal degradation similar to Huntington's Disease.
Extracellular signaling to neuronal dendrites activates postsynaptic sites to inc
Cortistatin is a cortical neuropeptide with neuronal depressant and sleep-modulating properties.
r deafness might be related to some defect in neuronal development secondary to the absence of melan
n enters the brain and interferes with normal neuronal development.
urite outgrowth and process elongation during neuronal differentiation.
Chinese traditional medicine to treat several neuronal diseases, such as several types of paralysis,
brain glucose uptake, electrolyte imbalances, neuronal dysfunction or degeneration and inflammation.
to 7 seconds following an intense muscular or neuronal effort.
r, these findings suggest that CB1 influences neuronal excitability by a variety of mechanisms, and
, CB1 receptors, for the most part, influence neuronal excitability indirectly, by reducing the impa
Many of these mutations should lead to neuronal excitability, though others may lead to hypoe
They may regulate A-type currents, and hence neuronal excitability, in response to changes in intra
itter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transpor
that may regulate A-type currents, and hence neuronal excitability, in response to changes in intra
t delayed rectifier K+ current that regulates neuronal excitability, action potential duration, and
t transient current that may be important for neuronal excitability.
PNS: neuronal excitation (in autonomic, nociceptive neurons
001, Prof. Mahal did postdoctoral research on neuronal exocytosis in the laboratory of Prof. Jim Rot
the brain attempting to make sense of random neuronal firing in the cortex.
ved flavanoids might protect neurons, enhance neuronal function, and stimulate neuronal regeneration
ssenger systems and are responsible for other neuronal functions that are not typically controlled b
It has been demonstrated that several neuronal functions, including long term potentiation (
nuclein is involved in the functioning of the neuronal Golgi apparatus and vesicle trafficking.
Put another way, multiple neuronal groups can be used to sample a given stimulus
esearchers to determine if the same or unique neuronal groups are involved in processing two stimuli
D1 receptors regulate neuronal growth and development, mediate some behavior
covered functions and mechanisms of action of neuronal growth factors and axon guidance cues, and me
With neuronal heterogeneity (by Edelman called degeneracy),
More recently, the cardiovascular and neuronal importance of nitric oxide has been examined,
lmarks of genetic diseases, as in the case of Neuronal Inclusion bodies in disorders like Frontotemp
for release in signaling other neurons as the neuronal inclusions grow.
itory neurotransmitter in the brain, mediates neuronal inhibition by binding to GABA receptors.
r release at the presynaptic terminal, and in neuronal integration in many neuronal types.
in Chemistry for deciphering the structure of neuronal ion channel, his work was in part conducted a
ress following myocardial ischemia, cerebral ( neuronal) ischemia, traumatic brain injury and spinal
ine withdrawal episodes may result in similar neuronal kindling as that seen after repeated withdraw
c action of pentylenetetrazol at the cellular neuronal level is still unclear.
Increases in neuronal levels of DOPAC, a metabolic breakdown produc
was successfully used and enhanced to analyze neuronal lineages in larval Drosophila brains.
very few if any Pick bodies they show extreme neuronal loss that can, in some cases, be so severe as
o preventing cognitive impairment and loss of neuronal markers.
y synaptic stimulation of ion channels in the neuronal membrane causes osmotic swelling of cells as
PLP is highly related to GPM6A, a neuronal membrane glycoprotein.
d these appear to assemble as heterodimers in neuronal membranes by linking up by their intracellula
ence of binding sites for baclofen on central neuronal membranes.
glial cells, which help maintain and modulate neuronal metabolism.
to successfully test the hypothesis that the neuronal microtubular cytoskeleton is involved in memo
in playing important roles in corticogenesis, neuronal migration and plasticity.
trix protein which regulates the processes of neuronal migration and synaptic plasticity.
NDEL1/EOPA gene product) has been involved in neuronal migration during the cortex formation in huma
ing Neural development, there is an extensive Neuronal Migration.
Several simplified neuronal models have also been developed (such as Fitz
Main article: Cultured neuronal network
allosteric modulator for the α2β2 subtype of neuronal nicotinic acetylcholine receptor.
otinine binds to, activates, and desensitizes neuronal nicotinic acetylcholine receptors, though at
by Abbott, which acts as a partial agonist at neuronal nicotinic acetylcholine receptors, binding to
d as a novel positive allosteric modulator of neuronal nicotinic acetylcholine receptor with sub-typ
hannels, a superfamily that also includes the neuronal nicotinic acetylcholine receptors (nAChRs), a
CHRNA7, coding the neuronal nicotinic acetylcholine receptor alpha7 subun
It also acts as a potent, noncompetitive α3β4 neuronal nicotinic acetylcholine receptor antagonist.
L-arginine (NPA), is a selective inhibitor of neuronal nitric oxide synthase (nNOS).
Its known actions include: inhibition of neuronal nitric oxide synthase, nNOS, assisting the in
Inhibits neuronal nitric oxide synthase (nNOS)
nd/or stored in memory, but by an increase in neuronal noise in stimulus representations as complexi
etely clear whether its location is primarily neuronal or glial.
imer, is found in mature neurons and cells of neuronal origin.
maker activity, low-threshold calcium spikes, neuronal oscillations and resonance, and rebound burst
understood, the relationship between NgR and neuronal outgrowth has been fleshed out.
NPAS3 or Neuronal PAS domain protein 3 is a brain-enriched tran
tion is often used in experimental studies on neuronal physiology and neuronal death or survival as
one known for its important role in learning, neuronal plasticity and myelination.
spoken or signed, a striking demonstration of neuronal plasticity.
If Stimulus 1 (S1) excites a certain neuronal population, repeated exposure to S1 will resu
In neuronal precursors both are expressed at comparable l
medicine for many centuries to treat various neuronal problems, such as chronic pain, paralysis, ap
Autopsychognosia is a neuronal process which gives rise to emotional-intelle
ial sections accurately enough to reconstruct neuronal processes and microvasculature.
In neuroscience, synaptic pruning, neuronal pruning or neuro-structural re-assembly refer
, there is some evidence tying this effect to neuronal rather than endothelial reactions.
eatment of neurodegenerative disorders or for neuronal regeneration in the brain.
restorative function, neural transplantation, neuronal regeneration after stroke, cerebrovascular su
claims involving protection from strokes, and neuronal regeneration.
odorant molecules in the nose, to initiate a neuronal response that triggers the perception of a sm
ore, some research indicated that it inhibits neuronal responses in a neuropathic pain model, so it
demonstrate that duloxetine potently inhibits neuronal serotonin and norepinephrine reuptake, and it
D-serine acts as a neuronal signaling molecule by activating NMDA recepto
gnificant rise occurs, it will interfere with neuronal signaling by depolarizing neurons.
dietary phytochemicals interact with several neuronal signaling cascade pathways that are responsib
its active function meant to calm or mitigate neuronal signaling (barbiturates, etc) can additionall
Unlike the main olfactory bulb that sends neuronal signals to the olfactory cortex, the VNO send
The blocking of neuronal sodium channels which occurs in PSP produces
it refers specifically to the arrangement of neuronal soma (biology) (cell bodies) in the brain.
f appropriate speed and magnitude to activate neuronal spike firing.
uning is believed to be to remove unnecessary neuronal structures from the brain; as the human brain
ely to be re-used, but rather replaced by new neuronal structures or synaptic structures, and have b
e intracellular NAD+ levels are essential for neuronal survival.
nal by removal (uptake) of glutamate from the neuronal synapse into Glia cells.
n to be involved in cellular adhesion in some neuronal synapses.
of GABAergic, cholinergic, and monoaminergic neuronal systems that give antiamnesia effects to the
4. Mental disorders and neuronal systems Work in this area includes applicatio
subunit, which is predominantly expressed in neuronal tissue.
us coeruleus, which then reduces or increases neuronal tone to the iris sphincter muscle by modulati
nce that this metabolite may be the source of neuronal toxicity following the administration of MDA
ly used by researchers interested in studying neuronal transmission with a high-affinity, subtype sp
In 1989, Olney et al. discovered that neuronal vacuolation and other cytotoxic changes ("les
MK-801 leads to the development of neuronal vacuolization in the posterior cingulate/retr
Acid-sensing ion channels (ASICs) are neuronal voltage-insensitive cationic channels activat
rmation of testable hypotheses in how precise neuronal wiring diagram is established in the brain, b