Symmetric Thiab Asymmetric Synapses Tsav Neurodegenerative Disorders Part 3
May 30, 2024
4.1. Symmetrical Synapses
Feem ntau ntawm cov nuclei yog inhibitory, yog li GABAergic innervations sawv cev rau lub hauv paus system los tswj cov firing tus nqi thiab cov qauv ntawm cov lus teb neuron nyob rau hauv lub BG, xws li hyperpolarizing lub membrane muaj peev xwm rov pib dua pacemaking kev ua ntawm neurons [145-147].
Kev sib raug zoo ntawm neural tswj thiab nco yog ze heev. Lub paj hlwb tswj hwm thiab tswj ntau qhov chaw ntawm lub cev los ntawm lub hlwb thiab qaum qaum. Kev nco yog ib lub hauv paus ntawm tib neeg kev txawj ntse. Nws lub zog ncaj qha cuam tshuam rau tus neeg lub peev xwm xav, kev txiav txim siab, kev muaj peev xwm kawm, thiab lub neej zoo. Yog li ntawd, muaj kev noj qab haus huv neural system tuaj yeem txhim kho kev nco zoo.
Tib neeg lub hlwb thiab lub paj hlwb yog cov rhiab heev thiab complex kab mob. Kev sib txuas thiab kev sib txuas lus ntawm cov neurons yog qhov nyuaj heev, thiab kev noj qab haus huv ntawm lub paj hlwb muaj txiaj ntsig zoo rau tib neeg kev noj qab haus huv. Piv txwv li, nyob rau hauv cov neeg mob uas muaj kab mob neurological, lawv lub peev xwm kev txawj ntse, kev nco, thiab kev muaj peev xwm xav tau tag nrho cov kev puas tsuaj loj.
Yog li, yuav ua li cas thiaj tswj tau qhov neural noj qab haus huv? Ua ntej tshaj plaws, nws yog ib qho tseem ceeb heev uas yuav tsum tau ua kom zoo. Kev tawm dag zog tuaj yeem ua kom cov pa oxygen, txhawb cov ntshav ncig, txhim kho kev ua haujlwm ntawm lub paj hlwb, thiab pab tswj kev noj qab haus huv ntawm lub cev thiab lub hlwb. Tsis tas li ntawd, kev noj haus kuj tseem ceeb heev. Qee cov khoom noj uas muaj antioxidants, xws li nqaij nruab deg, zaub, thiab txiv hmab txiv ntoo, tuaj yeem tiv thaiv cov paj hlwb los ntawm oxidants thiab yog li tiv thaiv kev ua haujlwm ntawm lub paj hlwb.
Nyob rau hauv luv luv, peb yuav tsum paub txog kev sib raug zoo ntawm neural tswj thiab nco, thiab ua active kev ntsuas los tiv thaiv kev noj qab haus huv ntawm lub paj hlwb. Tsuas yog los ntawm kev ua kom peb lub cev thiab lub hlwb noj qab haus huv tuaj yeem ua kom zoo dua qhov kev paub thiab kev txawj xav hauv lub neej thiab kev ua haujlwm thiab dhau los ua tus neeg muaj peev xwm thiab ua tiav. Nws pom tau tias peb yuav tsum txhim kho peb lub cim xeeb. Cistanche tuaj yeem txhim kho kev nco zoo vim tias nws tuaj yeem tswj hwm qhov sib npaug ntawm cov neurotransmitters, xws li nce qib ntawm acetylcholine thiab kev loj hlob, uas tseem ceeb heev rau kev nco thiab kev kawm. Tsis tas li ntawd, Cistanche tseem tuaj yeem txhim kho cov ntshav khiav thiab txhawb nqa cov pa oxygen, uas tuaj yeem ua kom lub hlwb tau txais cov khoom noj txaus thiab lub zog, yog li txhim kho lub hlwb tseem ceeb thiab kev ua siab ntev.
Nyem paub ntxiv los txhim kho kev nco
4.1.1. Striatum-STR
STR suav nrog qhov sib xyaw ua ke loj tshaj plaws rau cortical thiab thalamic inputs (saib ntu ntu "asymmetric synapses" kom paub ntau ntxiv). Lub hauv paus tseem ceeb ntawm cov neeg nyob hauv STR yog GABAergic spiny projection neurons (SPNs), nrog ob peb chav kawm ntawm GABAergic thiab cholinergic interneurons [148,149].
SPNs txheej txheem cov ntaub ntawv afferent rauBG hauv ncaj (d) lossis tsis ncaj (i) txoj hauv kev, uas tau txhais los ntawm ob hom SPNs: dSPNs thiab iSPNs, raws li (Daim duab 4) [150,151]. dSPNs qhia D1 receptors thiab project ncaj qha rau SNr / GPi, whereas GPe thiab STN relay cov ntaub ntawv los ntawm iSPNsexpressing D2 receptors rau SNr / GPi (Daim duab 4) [150,151].
Raws li, cov kev sib txawv no ua rau muaj qhov sib txawv ntawm lub cev muaj zog, kev tso tawm ntawm GABA thiab kev txo qis hauv kev ua haujlwm ntawm SNr / GPi neurons los ntawm kev ua kom cov dSPNs uas txo cov kev tawm dag zog rau cov cheeb tsam hauv qab ntawm lub cev muaj zog thiab txhawb kev txav mus los; thiab kev ua haujlwm ntawm iSPNs uas ua rau muaj txiaj ntsig zoo ntawm SNr / GPi neurons los ntawm cov txheej txheem disinhibiting thiab ua rau inhibiting zog [152].
4.1.2. Sab nraud ntu ntawm Globus Pallidus-GPe
GPU yog tsim los ntawm ob lub ntsiab subtypes ntawm neurons, prototypic thiab arkypallidalneurons [153]. Thawj qhov dej ntws mus rau STN thiab SNr nuclei, thiab ntws mus rau STR; whereas tom kawg nkaus xwb tej yaam num rau STR, yog qhov tseem ceeb tshaj plaws ntawm GABA (Daim duab 4) [154].
Kev kwv yees los ntawm GPe neurons mus rau cortex thiab thalamushave kuj tau tshaj tawm [155]. Qhov inhibition muab los ntawm prototypic neurons yog qhov tseem ceeb rau kev rov ua haujlwm ntawm tus kheej ntawm STN neurons [156].
Ib yam li ntawd, GPe neurons yog qhov no tau txais ntawm GABAergic extrinsic innervations los ntawm iSPNs (feem ntau ntawm lawv) thiab dSPNs, innervations intrinsic los ntawm collaterals ntawm prototypic neurons rau lwm GPe neurons, thiab interconnections ntawm prototypic neurons (Daim duab 4 15) [157]
Ntxiv mus, arkypallidalneurons integrate signals los ntawm dSPNs, iSPNs, thiab STN [158]. Ob qhov kev pab cuam luv luv (STF) thiab kev nyuaj siab luv luv (STD) tuaj yeem pom ntawm extrinsic synapses, thaum intrinsicsynapses tam sim no STD [159,160].
4.1.3. Substantia Nigra Pars Reticulate-SNr
SNr ua haujlwm raws li kev sib koom ua ke ntawm nucleus, vim txhua SNr neuron tau txais kev pom zoo los ntawm ntau lub hauv paus chiv keeb xws li dSPNs, GP, thiab STN (Daim duab 4). Symmetric synapsesfrom STR thiab GPe tso saib cov txheej txheem sib txawv raws li STR-SNr inhibitory postsynapticcurrents (IPSCs) nthuav tawm STF, thaum GP-SNr IPSCs cuam tshuam los ntawm STD [161].
SNrneurons tso saib cov theem tseem ceeb ntawm kev tua tus kheej uas tso cai rau cov tonic inhibition of downstream motor (Daim duab 4) [162,163]. Lawv nthuav tawm cov khoom lag luam siab thiab tau txais cov khoom lag luam inhibitory, ua los ntawm ob qho tib si ionotropic (GABAA) thiab metabotropic (GABAB) receptors, txawm tias thaum lub sijhawm ua kom muaj zog [164-166].
Plaub hom GABAergicneurons projecting rau cov hom phiaj sib txawv tuaj yeem pom hauv SNr, thalamus yog ib qho uas tau txais feem ntau ntawm SNr innervations [167,168].
4.1.4 ib. Noj qab nyob zoo thiab Pathological DA Modulation hauv Symmetric Synapses
STR yog lub hom phiaj tseem ceeb ntawm nigral DAergic innervation [144]. Raws li tau hais dhau los, dSPNs thiab iSPNs nthuav qhia D1 thiab D2 receptors, feem, uas ua rau muaj qhov sib txawv ntawm lub cev muaj zog tom qab DA tso tawm.
Thaum DA tso tawm, dSPNs nce lawv cov kev ua ub no los ntawm D1 receptor activation, whereas D2 receptors kho qhov txo qis ntawm iSPNs (Daim duab 4) [169,170]. Cov nyhuv yog qhov overactivation ntawm txoj kev ncaj qha piv rau qhov tsis ncaj, disinhibiting lub thalamus thiab pib txav. Yog li ntawd, DA modulates lub synaptic thiab intrinsic zog ntawm STR neurons los ntawm activating distinctDA receptors (Daim duab 4).
Tsis ntev los no, ib qho kev nthuav qhia tau nthuav tawm tias astrocytic GATs ua lub luag haujlwm tseem ceeb hauv kev tswj hwm ntawm striatal DA tso tawm los ntawm kev tshem tawm extrasynaptic GABAspillover, txo cov tonic inhibition, thiab yog li ntawd, txhawb DA tso tawm [171].
Qhov tseeb, muaj qhov txo qis hauv GATs uas ua rau muaj kev cuam tshuam ntxiv rau DA cov txiaj ntsig ntawm cov theem pib ntawm tus kab mob [171]. Tom qab tag nrho DA depletion, tag nrho cov haujlwm ntawm dSPNs txo qis thiab muaj qhov poob ntawm tus txha nraub qaum [152].
Yog li ntawd, qhov no disinhibits GABAergic projections los ntawm SNr / GPi neurons [172]. Nyob rau hauv sib piv, qhov tsis muaj DA tsub kom lub excitability ntawm iSPNsby tshem tawm cov inhibition los ntawm D2 receptors, txawm thaum tseem muaj ib tug txo nyob rau hauv tus txha nqaj qaum (Daim duab 4) [152,170]. Tsis tas li ntawd, qhov tsis muaj DA kuj tseem cuam tshuam nrog ntau dua GABA ntau lawm, raws li qhia los ntawm nuclear magnetic resonance spectroscopystudy hauv striatum ntawm tus qauv nas [173].
Ua ke, qhov no disinhibits STN kev ua uas ua rau muaj kev zoo siab dua ntawm SNr/GPi [170,174]. Cov txiaj ntsig tau tshwm sim yog qhov tsis txaus ntseeg ntawm txoj hauv kev ncaj qha thiab tsis ncaj qha qhia los ntawm kev txo qis hauv lub cev muaj zog (paucity thiab qeeb ntawm kev txav), nthuav tawm lub peev kev xav tau ntawm kev sib koom ua ke striatalactivity [175,176].
DA modulates qhov excitability ntawm GPe neurons, D2 receptor yog ib qho uas muaj nyob rau hauv tag nrho cov GPe neurons, txawm hais tias prototypical neurons qhia siab dua D2receptors tshaj arkypallidal neurons [177].
Raws li, ua kom cov presynaptic D2receptors txo GABAergic pallidosubthalamic innervations, txo lub zog ntawm qhov kev sib txuas no [178]. Nyob rau hauv lub xeev Parkinsonian, cov kev ua ntawm prototypic hlwb zoo li cuam tshuam los ntawm hyperactivity ntawm iSPNs, raws li tau hais yav dhau los (Daim duab 4) [179,180].Txawm li cas los xij, qhov no tsis yog ib qho teeb meem rau pom qhov nce GPe-STN GABAergic kis tau tus mob hauv anNMDA-mediated yam. [181, 182].
Ib yam li ntawd, GABAergic inhibition los ntawm arkypallidalneurons rau STR yog nce nyob rau hauv DA depletion, txawm tias thaum lawv excitability txo (Daim duab 4) [183,184].
Raws li tau hais dhau los, STF thiab STD tuaj yeem pom hauv striato-pallidaland pallido-pallidal synapses, feem [159,160]. Dhau li ntawm lawv lub luag haujlwm, STFand STD kuj muaj qhov sib txawv uas tsuas yog STF lub zog yog hloov kho los ntawm presynapticD2 receptors, uas ua rau txo qis GABA tso tawm [185]. Tsis tas li ntawd, GABAergictransmission tuaj yeem tswj hwm los ntawm kev txo qhov amplitude ntawm GABAA-mediated postsynapticcurrents los ntawm kev ua kom D4 receptors.
Ib yam li ntawd, kev sib txuas hauv nruab nrab kuj tuaj yeem txo qhov kev tua hluav taws tom qab [186]. Tsuas yog txoj kev tshawb fawb los ntawm Stefani thiab cov npoj yaig [187] tso lub teeb ntawm kev ua haujlwm hauv qab ntawm qhov txo qis excitability pom hauv GPe neurons.Qhov ntawd, cov kws sau ntawv tau pom tias kev ua kom D2 receptors inhibit GPe excitability hauv aprotein-kinase-C-dependent yam.
Kev ua haujlwm ntawm SNr kuj tau hloov kho los ntawm DA los ntawm kev qhia ntawm cov receptors sib txawv hauv SNr neurons (Daim duab 4). Txawm hais tias D1 receptors yog cov uas qhia ntau dua, muaj D4 thiab D5 receptors kuj tau tshaj tawm [188-190]. Txoj kev tshawb no los ntawm Zhou et al. [191] qhia tias qhov ua kom D1 receptors depolarizes SNr neurons, thiab yog li ntawd excites lawv.
Nyob rau hauv sib piv, lub pharmacological blockade ntawm D1 los yog D2 receptorsleads mus rau lub hyperpolarization ntawm SNr neurons, thiab qhov no yog zoo ib yam li qhov tau pom inrecordings los ntawm nas nrog DA depletion [192,193]. Rau STR-SNr synapses, muaj kev nce ntxiv hauv IPSCs amplitude uas yuav tau tsav los ntawm ob qho tib si tsis ua haujlwm GABAB receptors thiab txo qis presynaptic hauv GABA tso tawm [194].
Hais txog kev tswj hwm synaptic, presynaptic D4 receptor activation txo qhov kev sib kis hauv GPe-SNr kev sib txuas, whereaspresynaptic D1 receptors kho qhov nce hauv GABAergic signaling [195,196].
4.2. Asymmetric Synapses
4.2.1. Lub STR
Lub STR integrates cortical thiab thalamic excitatory cov ntaub ntawv, ua kev sib cuag nrog tus txha nraub qaum taub hau ntawm GABAergic SPNs (Daim duab 4) [149,197]. Nyob rau hauv STR, cortical andthalamic terminals tuaj yeem sib txawv los ntawm kev qhia txawv ntawm vesicular glutamatetransporter 1 (vGLUT1) thiab vesicular glutamate transporter 2 (vGLUT2), feem [198].
Cov kev nkag siab zoo no yog qhov tseem ceeb rau hyperpolarizing SPN neurons, uas tom qab tso cai rau kev tua ntawm lawv qhov kev ua tau zoo (APs) [199,200]. Ob leeg dSPNs thiab iSPNs expressAMPA thiab NMDA receptors, nrog rau cov metabotropic glutamate receptors (mGluRs) uas nruab nrab synaptic kis tau tus mob thiab LTP / LTD [201].
Hauv dSPNs, kev ua kom NMDAand D1 receptors yog lub luag haujlwm rau LTP induction, whereas LTD induction yog kho los ntawm muscarinic acetylcholine M4 thiab mGluR5 receptors [202,203].
Ntawm qhov tod tes, LTPinduction hauv iSPNs yog kho los ntawm kev ua kom NMDA thiab A2A receptors, whereasLTD raug ntxias los ntawm postsynaptic D2 receptors thiab mGluR5 receptors [202].
4.2.2. Subthalamic Nucleus-STN
Ib yam li STR, STN tau txais cov khoom siv monosynaptic los ntawm cerebral cortexthrough txoj kev hyperdirect (Daim duab 4) [197]. Tom qab AMPAR/NMDA-mediatedpostsynaptic excitatory currents (EPSC), nrog rau GPe inhibition, tswj lub peev xwm ntawm STN neurons los tua APs spontaneously [182].
Cov antagonistic inputs tswj cov firingrate thiab qauv ntawm STN kis tau tus mob, thiab cov kev hloov nyob rau hauv lub firing qauv yog xam tau tias yog ahallmark ntawm PD [204,205].
Nyob rau hauv sib piv rau inhibitory STR, STN neurons yog glutamatergicand project ib txhij rau GPe thiab SNr / GPi (Daim duab 4). Concretely, activation ntawm STN muab ob qho kev tshwm sim sib txawv: muaj zog thiab txhawb nqa excitation ntawm prototypic cell ua rau cov disinhibition ntawm SPNs, thiab luv luv, excitation ntawm arkypallidal, implying ib tug luv luv-lub sij hawm inhibition rau SPNs (Daim duab 4) [158,206].
Hais txog SNr, STN innervations sawv cev rau lub ntsiab excitatory inputs, ua rau monosynaptic EPSCs thiab nce GABAergicsignaling nyob rau hauv downstream motors [162,207].
4.2.3. Noj qab nyob zoo thiab Pathological DA Modulation hauv Asymmetric Synapses
DAergic innervation hauv STR yog koom nrog hauv ob lub peev txheej: tswj LTPof cortiostriatal synapses thiab tseem tswj hwm qhov ua haujlwm tshwj xeeb ntawm STR neuronsin teb rau cortical thiab thalamic afferents [208].
Raws li, DAergic denervation txhawb kev poob ntawm cortico- thiab thalamo-striatal terminals, ua rau muaj kev cuam tshuam ntawm kev ua haujlwm ntawm txoj hauv kev ncaj thiab tsis ncaj, nrog rau kev hloov pauv tseem ceeb hauv LTP thiab LTD (Daim duab 4) [151,208,209].
Tseeb tiag, kev tuag ntawm nigral DAergic neurons thim rov qab lub zog ntawm thalamic inputs rau dSPNs thiab iSPNs los ntawm kev txhim kho thalamostriatal inputs nkaus xwb rau iSPNs, yog li tsav tsheb asymmetric activation ntawm basal ganglia (Daim duab 4) [210].
Raws li tau hais dhau los, LTP thiab LTD muaj nyob rau hauv striatal SPNs, thiab qhov bidirectionalsynaptic plasticity no tau hloov pauv hauv xeev Parkinsonian [209,211]. Yog tsis muaj DA, dSPNs poob LTP vim tsis muaj D1 receptor ua kom, zoo ib yam li qhov tsis muaj LTD hauv iSPNs vim tias tsis muaj D2 receptor activation [202].
Cov kev hloov pauv uas cuam tshuam nrog PD no ua rau muaj qhov xwm txheej uas dSPNs tsuas yog nthuav tawm LTD thiab iSPNs tsuas yog nthuav tawm LTP, ua rau muaj kev cuam tshuam ntawm dSPNs thiab iSPNs kev ua haujlwm [211].DA tso tawm muaj lub luag haujlwm tseem ceeb hauv kev ua haujlwm ntawm STN neurons los ntawm kev tswj cov synaptictransmission thiab. lub zog ntawm cortico-subthalamic inputs, yog li ntawd, tsis muaj DAmodulation muaj qhov tshwm sim loj heev hauv locomotion [204,212].
D2 thiab D5 receptors yog cov uas muaj kev qhia siab ntawm STN neuron daim nyias nyias, thiab kev ua kom txhua tus muaj qhov sib txawv rau lawv qhov kev tua hluav taws (Daim duab 4) [15,213]. Cov txiaj ntsig yav dhau los tau tshaj tawm tias D2 ua kom nce qhov tso tawm ntawm STN neurons los ntawm depolarizing lub peev xwm membrane [214].
Kev ua kom D5 receptors, txawm li cas los xij, ua rau muaj qhov sib txawv nyob ntawm seb hom kev tawm ntawm STN neurons [215]. Hyperpolarized STN neurons hluav taws kub hnyiab ntawm APs thiab D5 ua kom ncua sij hawm tawg [216].Nyob rau hauv depolarized STN neurons, D5 activation tsub kom firing tus nqi ntawm ib leeg thiab tonic APs [217].
Tsis ntev los no, nws tau pom tias qhov ua kom D5 receptors hauv STNneurons tuaj yeem hloov kho cortical inputs los ntawm kev nyuaj siab AMPAR-mediated EPSC [214] .Tom qab DAergic denervation, STN neurons poob lawv txoj kev tswj hwm pacemaking vim ob qho tib si nce inputs los ntawm iSPNs rau GPs. STN neurons, thiab kev ua kom ntau dhau ntawm NMDARs [218] txawm tias thaum lub cortical glutamatergic innervations raug txo qis (Daim duab 4) [219–221].
Qhov tseeb no, thiab tej zaum yuav muaj kev hloov pauv hauv lwm txoj hauv kev xws li cov poov tshuaj / sodium hyperpolarization-activated cyclic nucleotide-gated ion channel 2 (HCN2) [222], tso cai rau lub xeev pathological hyperactive rau STN neurons nrog lub suab thiab synchronous tawg ntawm APs [223]. Nyob rau hauv lub xeev no, kuj tseem muaj kev sib txuas ntawm GPe thiab STN uas tau kho los ntawm kev ua kom ntau dhau ntawm NMDARs hauv STN [176,181].
Txawm hais tias qhov no tuaj yeem yog qhov tsis sib xws, nws tuaj yeem piav qhia txij li STN neuron kev ua haujlwm tsis ua haujlwm rau GPe kev ua haujlwm thiab hauv-theem rau cortical kev ua haujlwm [224] yog li nws xav tias GPe-STN inhibitory inputs tsis tshua muaj txiaj ntsig hauv kev tawm tsam corticalexcitation [225].
Hais txog SNr, dopamine receptors D1 thiab D2 muaj lub luag haujlwm tsis sib xws hauv kev hloov pauv EPSCamplitude: D1 receptor ua raws li kev txhim kho, thaum D2 receptor txo nws [226].
Lub xub ntiag ntawm LTD ntawm STN-SNr synapses, tshwm sim los ntawm kev ua kom cov postsynaptic D1receptors, kuj tau tshaj tawm. Thaum lub sij hawm LTD no, endocytosis ntawm AMPARs kho los ntawm NMDARs depresses EPSC amplitude [214]. Thaum tsis muaj dopamine, STN-SNrLTD yog tag nrho depleted ua rau muaj kev sib kis ntawm synaptic hauv STN-SNrcircuitry [227,228].
5. Cov lus xaus
Ob leeg asymmetric thiab symmetric synapses muaj lub luag haujlwm tseem ceeb hauv kev tsim cov qauv thiab kev ua haujlwm ntawm lub hlwb. Yog li ntawd, qhov sib npaug ntawm excitation thiab inhibition yog peev rau lub hlwb muaj nuj nqi.
Tsis tas li ntawd, txawm tias tom qab ib qho kev puas tsuaj, kev loj hlob ntawm tus kab mob txhais tau hais tias cov lus teb ntawm circuitries; tej yam txiaj ntsig thaum pib yuav tsis zoo tom qab.
Hauv qhov no, nws tau raug piav qhia tias kev txhawb nqa kev taw qhia ua kom pom tseeb tom qab lub paj hlwb ischemia tau txais txiaj ntsig tsuas yog thaum lub sijhawm mob hnyav; tom qab ntawd, nws ntxiv qhov kev puas tsuaj rau thawj zaug. Synapses tuaj yeem hloov pauv los ntawm cov neeg ua si tsis ncaj qha ntsig txog lawv; Hauv Alzheimer's Disease, qhov mob ntev thiab ntev neurodegeneration mediated los ntawm tau lub hom phiaj tseem ceeb asymmetric synapses, txo qis neuronalplasticity thiab functionality.
Tseeb tiag, kev tuag ntawm midbrain dopaminergic neurons impairslocomotion, nyob rau hauv tus kab mob Parkinson. Txij li thaum symmetric thiab asymmetric synapses ua lub luag haujlwm tseem ceeb hauv pathophysiology ntawm ntau cov kab mob hauv lub paj hlwb, xws li mob hlab ntsha tawg, Alzheimer's, lossis Parkinson's Disease, xav tau kev tshawb fawb ntxiv los qhia txog cov txheej txheem molecular uas tuaj yeem ua rau kev txhim kho cov tshuaj kho tshiab rau cov kab mob phem no.
Sau Kev Koom Tes: Conceptualization, DR-S., JMA, AO, thiab TS; Resources, TS; sau-original draft npaj, DR-S., AO, and TS; sau-review and editing, DR-S., AC, MA-N., AP-F., LV-V., JC-C., YL, JMP-P., JMA, AO and TS; saib xyuas, TS; kev nrhiav nyiaj txiag, DR-S., AC, thiab TS Txhua tus kws sau ntawv tau nyeem thiab pom zoo rau cov ntawv luam tawm ntawm cov ntawv sau.
Cov Nyiaj Txiag: Txoj kev kawm no tau txais kev txhawb nqa ib nrab los ntawm cov nyiaj pab los ntawm Xunta de Galicia (TS: IN607A2018/3, TS: IN607D 2020/09, AC: IN606A-2021/015 & DRS: IN606B-2021/010) , thiab Science Ministry of Spain(TS: RTI2018-102165-BI00, TS: RTC2019-007373-1). Tsis tas li ntawd, txoj kev tshawb no kuj tau txais kev txhawb nqa los ntawm INTERREG Atlantic Area (TS: EAPA_791/2018_ EURO ATLANTIC project), INTER-REG VA España Portugal (POCTEP) (TS: 0624_2 IQBIONEURO_6_E), thiab EuropeanRegional Development Fund (ERDF).
Ntxiv mus, MAN (IFI18/00008) yog tus tau txais daim ntawv cog lus iPFIS, thiab TS (CPII17/00027) yog tus tau txais daim ntawv cog lus tshawb fawb los ntawm Miguel Servet Program los ntawm Instituto de Salud Carlos III. Cov peev nyiaj tsis muaj lub luag haujlwm hauv kev tsim qauv, sau cov ntaub ntawv thiab kev tshuaj xyuas, kev txiav txim siab tshaj tawm, lossis kev npaj cov ntawv sau.
Kev tsis sib haum xeeb ntawm kev txaus siab: Cov neeg sau ntawv tshaj tawm tsis muaj teeb meem ntawm kev txaus siab.
Cov ntaub ntawv
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