Ilmuwan Indonesia Taruna Ikrar membuktikan terjadinya regenerasi sel otak, terutama di hipokampus. Penemuan ini menjadi dasar pengobatan penyakit degeneratif seperti Alzheimer dengan mengganti sel-sel otak yang rusak.
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D4 b. perkembangan otak dan metode penelitian syaraf kognitifRosida Marasabessy
bagaimana cara kerja otak manusia dalam memahami matematika ?? bagaimana para peneliti mengetahui bagian otak mana yang berfungsi ketika melakukan kerja matematika ?? benarkah bagian otak kiri mengendalikkan bagian tubuh kanan dan begitu juga sebaliknya ?? dalam file ini akan dijelaskan semuanya mengenai bagaimana perkembangan otak dan metode penelitian syaraf kogntif.
A disinhibitory microcircuit initiates critical period plasticity in the visu...Taruna Ikrar
Earlysensoryexperienceinstructsthematurationofneuralcircuitry in the cortex1,2. This has been studied extensively in the primary visualcortex,inwhichlossofvisiontooneeyepermanentlydegrades corticalresponsivenesstothateye3,4,aphenomenonknownasocular dominance plasticity (ODP). Cortical inhibition mediates this process4–6,butthepreciseroleofspecificclassesofinhibitoryneurons in ODP is controversial. Here we report that evoked firing rates of binocular excitatory neurons in the primary visual cortex immediatelydropbyhalfwhenvisionisrestrictedtooneeye,butgradually return to normal over the followingtwenty-four hours, despite the fact that vision remains restricted to one eye. This restoration of binocular-like excitatory firing rates after monocular deprivation resultsfromarapid,althoughtransient,reductioninthefiringrates of fast-spiking, parvalbumin-positive (PV) interneurons, which in turncanbeattributedtoadecreaseinlocalexcitatorycircuitinput onto PV interneurons.This reduction in PV-cell-evoked responses after monocular lid suture is restricted to the critical period for ODPandappearstobenecessaryforsubsequentshiftsinexcitatory ODP. Pharmacologically enhancing inhibition at the time of sight deprivation blocks ODP and, conversely, pharmacogenetic reduction of PV cell firing rates can extend the critical period for ODP. Thesefindingsdefinethemicrocircuitchangesinitiatingcompetitive
plasticityduringcriticalperiodsofcorticaldevelopment.Moreover, they show that the restoration of evoked firing rates of layer 2/3 pyramidal neurons by PV-specific disinhibition is a key step in the progression of ODP.
An inhibitory pull–push circuit in frontal cortexTaruna Ikrar
Push–pull is a canonical computation of excitatory cortical circuits. By contrast, we identify a pull–push inhibitory circuit in frontal cortex that originates in vasoactive intestinal polypeptide (VIP)-expressing interneurons. During arousal, VIP cells rapidly and directly inhibit pyramidal neurons; VIP cells also indirectly excite these pyramidal neurons via parallel disinhibition. Thus, arousal exerts a feedback pull–push influence on excitatory neurons—an inversion of the canonical push–pull of feedforward input.
D4 b. perkembangan otak dan metode penelitian syaraf kognitifRosida Marasabessy
bagaimana cara kerja otak manusia dalam memahami matematika ?? bagaimana para peneliti mengetahui bagian otak mana yang berfungsi ketika melakukan kerja matematika ?? benarkah bagian otak kiri mengendalikkan bagian tubuh kanan dan begitu juga sebaliknya ?? dalam file ini akan dijelaskan semuanya mengenai bagaimana perkembangan otak dan metode penelitian syaraf kogntif.
A disinhibitory microcircuit initiates critical period plasticity in the visu...Taruna Ikrar
Earlysensoryexperienceinstructsthematurationofneuralcircuitry in the cortex1,2. This has been studied extensively in the primary visualcortex,inwhichlossofvisiontooneeyepermanentlydegrades corticalresponsivenesstothateye3,4,aphenomenonknownasocular dominance plasticity (ODP). Cortical inhibition mediates this process4–6,butthepreciseroleofspecificclassesofinhibitoryneurons in ODP is controversial. Here we report that evoked firing rates of binocular excitatory neurons in the primary visual cortex immediatelydropbyhalfwhenvisionisrestrictedtooneeye,butgradually return to normal over the followingtwenty-four hours, despite the fact that vision remains restricted to one eye. This restoration of binocular-like excitatory firing rates after monocular deprivation resultsfromarapid,althoughtransient,reductioninthefiringrates of fast-spiking, parvalbumin-positive (PV) interneurons, which in turncanbeattributedtoadecreaseinlocalexcitatorycircuitinput onto PV interneurons.This reduction in PV-cell-evoked responses after monocular lid suture is restricted to the critical period for ODPandappearstobenecessaryforsubsequentshiftsinexcitatory ODP. Pharmacologically enhancing inhibition at the time of sight deprivation blocks ODP and, conversely, pharmacogenetic reduction of PV cell firing rates can extend the critical period for ODP. Thesefindingsdefinethemicrocircuitchangesinitiatingcompetitive
plasticityduringcriticalperiodsofcorticaldevelopment.Moreover, they show that the restoration of evoked firing rates of layer 2/3 pyramidal neurons by PV-specific disinhibition is a key step in the progression of ODP.
An inhibitory pull–push circuit in frontal cortexTaruna Ikrar
Push–pull is a canonical computation of excitatory cortical circuits. By contrast, we identify a pull–push inhibitory circuit in frontal cortex that originates in vasoactive intestinal polypeptide (VIP)-expressing interneurons. During arousal, VIP cells rapidly and directly inhibit pyramidal neurons; VIP cells also indirectly excite these pyramidal neurons via parallel disinhibition. Thus, arousal exerts a feedback pull–push influence on excitatory neurons—an inversion of the canonical push–pull of feedforward input.
Pten and eph b4 regulate the establishment of perisomatic inhibition in mouse...Taruna Ikrar
Perisomatic inhibition of pyramidal neurons is established by fast-spiking, parvalbuminexpressing interneurons (PV cells). Failure to assemble adequate perisomatic inhibition is thought to underlie the aetiology of neurological dysfunction in seizures, autism spectrum disorders and schizophrenia. Here we show that in mouse visual cortex, strong perisomatic inhibition does not develop if PV cells lack a single copy of Pten. PTEN signalling appears to drive the assembly of perisomatic inhibition in an experience-dependent manner by suppressing the expression of EphB4; PVcells hemizygous for Pten show an B2-fold increase in expression of EphB4, and over-expression of EphB4 in adult PV cells causes a dismantling of perisomatic inhibition. These findings implicate a molecular disinhibitory mechanism driving the establishment of perisomatic inhibition whereby visual experience enhances Pten signalling, resulting in the suppression of EphB4 expression; this relieves a native synaptic repulsion between PV cells and pyramidal neurons, thereby promoting the assembly of perisomatic inhibition.
Abstract In the mammalian neocortex, excitatory neurons provide excitation in both columnar and laminar dimensions, which is modulated further by inhibitory neurons. However, our understanding of intracortical excitatory and inhibitory synaptic inputs in relation to principal excitatory neurons remains incomplete, and it is unclear how local excitatory and inhibitory synaptic connections to excitatory neurons are spatially organized on a layer-by-layer basis. In the present study, we combined whole cell recordings with laser scanning photostimulation via glutamate uncaging to map excitatory and inhibitory synaptic inputs to single excitatory neurons throughout cortical layers 2/3–6 in the mouse primary visual cortex (V1). We find that synaptic input sources of excitatory neurons span the radial columns of laminar microcircuits, and excitatory neurons in different V1 laminae exhibit distinct patterns of layer-specific organizationofexcitatoryinputs.Remarkably,thespatialextentofinhibitoryinputsofexcitatory neurons for a given layer closely mirrors that of their excitatory input sources, indicating that excitatory and inhibitory synaptic connectivity is spatially balanced across excitatory neuronal networks. Strong interlaminar inhibitory inputs are found, particularly for excitatory neurons in layers 2/3 and 5. This differs from earlier studies reporting that inhibitory cortical connections to excitatory neurons are generally localized within the same cortical layer. On the basis of the functional mapping assays, we conducted a quantitative assessment of both excitatory and inhibitory synaptic laminar connections to excitatory cells at single cell resolution, establishing precise layer-by-layer synaptic wiring diagrams of excitatory neurons in the visual cortex.
A characteristic of the developing mammalian visual system is a brief interval of plasticity, termed the “critical period,” when the circuitry of
primary visual cortex is most sensitive to perturbation of visual experience. Depriving one eye of vision (monocular deprivation [MD]) during
the critical period alters ocular dominance (OD) by shifting the responsiveness of neurons in visual cortex to favor the nondeprived eye. A
disinhibitory microcircuit involving parvalbumin-expressing (PV) interneurons initiates this OD plasticity. The gene encoding the neuronal
nogo-66-receptor1(ngr1/rtn4r) is required to close the critical period.Herewecombinedmousegenetics, electrophysiology,andcircuitmapping
with laser-scanning photostimulation to investigate whether disinhibition is confined to the critical period by ngr1.We demonstrate that ngr1
mutant mice retain plasticity characteristic of the critical period as adults, and that ngr1 operates within PV interneurons to restrict the loss of
intracortical excitatory synaptic input following MD in adult mice, and this disinhibition induces a “lower PV network configuration” in both
critical-period wild-type miceandadult ngr1/mice.Wepropose that ngr1 limits disinhibition to close the critical period forODplasticityand
that a decrease in PV expression levels reports the diminished recent cumulative activity of these interneurons.
A disinhibitory microcircuit initiates critical period plasticity in the visu...Taruna Ikrar
Early sensory experience instructs the maturation of neural circuitry in the cortex1, 2. This has been studied extensively in the primary visual cortex, in which loss of vision to one eye permanently degrades cortical responsiveness to that eye3, 4, a phenomenon known as ocular dominance plasticity (ODP). Cortical inhibition mediates this process4, 5, 6, but the precise role of specific classes of inhibitory neurons in ODP is controversial. Here we report that evoked firing rates of binocular excitatory neurons in the primary visual cortex immediately drop by half when vision is restricted to one eye, but gradually return to normal over the following twenty-four hours, despite the fact that vision remains restricted to one eye. This restoration of binocular-like excitatory firing rates after monocular deprivation results from a rapid, although transient, reduction in the firing rates of fast-spiking, parvalbumin-positive (PV) interneurons, which in turn can be attributed to a decrease in local excitatory circuit input onto PV interneurons. This reduction in PV-cell-evoked responses after monocular lid suture is restricted to the critical period for ODP and appears to be necessary for subsequent shifts in excitatory ODP. Pharmacologically enhancing inhibition at the time of sight deprivation blocks ODP and, conversely, pharmacogenetic reduction of PV cell firing rates can extend the critical period for ODP. These findings define the microcircuit changes initiating competitive plasticity during critical periods of cortical development. Moreover, they show that the restoration of evoked firing rates of layer 2/3 pyramidal neurons by PV-specific disinhibition is a key step in the progression of ODP.
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Ilmuwan Indonesia Berhasil Buktikan Proses Regenerasi
Sel Otak
Sabtu, 1 4 Desember 201 3 , 1 4:50:00 WIB
Laporan: Widian Vebriyanto
16
Desember
2013
Indeks
ISTIMEWA
RMOL. Ilmuwan Indonesia y ang
bertugas sebagai staf akademik dan
dokter spesialis di School of
Medicine, Univ ersity of California,
Irv ine, AS, berhasil membuktikan
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Irv ine, AS, berhasil membuktikan
terjadiny a regenerasi (proses
perbaharuan) sel-sel otak y ang
menjadi prinsip dasar pengobatan
alzheimer dan peny akit degeneratif
otak lainny a.
Penemuan Dr. Taruna Ikrar, PhD
tersebut juga telah dipublikasikan di
jurnal Frontiers of Neural Circuit
y ang terbit pada 1 0 Desember 201 3
dengan judul "Adult Neurogenesis
Modifies Ex citability of The Dentate
Gy rus. Penelitian itu juga bisa dibaca
secara online di
Gairahkan Pertanian, BRI Salurkan
Kredit Perkebunan Rp 26,4 T riliun
http://w w w .frontiersin.org/Neural_Circuits/1 0.3389/fncir.201 3.00204/abstract.
Dalam surat elektronik kepada Raky at Merdeka Online (Sabtu, 1 4/1 2), Dr. Taruna Ikrar
menjelaskan bahwa setiap orang dalam hidupny a, pernah lupa akan sesuatu, apalagi jika
kejadian itu telah berlangsung lama. Semua orang juga pernah merasakan emosi dan marah,
y ang mungkin disebabkan harapan tidak kesampaian. Itu merupakan sifat dasar manusia.
Namun kalau terlalu sering lupa, misalny a lupa meletakkan kunci mobil, lupa nomor telepon,
lupa mencampurkan gula dalam minuman, atau bahkan disorientasi waktu, maka itu
merupakan hal y ang tidak normal, bahkan ini bisa menjadi tanda khas peny akit alzheimer.
Peny akit Alzheimer, lanjutny a, didasarkan pada penurunan kemampuan mengingat y ang
progresif. Serangan peny akit Alzheimer ditandai dengan kehilangan day a pikir secara bertahap
dan akhirny a dapat menjadi cacat mental total. Gejala awal alzheimer adalah mudah lupa pada
hal-hal y ang sering dilakukan dan hal-hal baru. Penderita juga mengalami disorientasi waktu
dan mengalami kesulitan berpikir y ang kompleks seperti matematika atau aktiv itas organisasi.
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dan mengalami kesulitan berpikir y ang kompleks seperti matematika atau aktiv itas organisasi.
"Alzheimer berat ditandai dengan kehilangan day a ingat y ang progresif sampai mengganggu
aktiv itas sehari-hari, disorientasi tempat, orang dan waktu, serta mengalami masalah dalam
perawatan diri, seperti lupa mengganti pakaian," kata dia.
Dr. Ikrar juga menjelaskan bahwa proses degeneratif menjadi peny ebab utama alzheimer.
Alzheimer bukan peny akit menular, melainkan merupakan sejenis kumpulan gejala dengan
gambaran sel-sel otak mengalami degradasi, sehingga otak tampak mengerut dan mengecil.
Resiko alzheimer meningkat seiring dengan pertambahan usia. Dalam gambaran otak,
ditemukan perubahan struktur dimana otak terlihat mengerut, y ang dipenuhi dengan sedimen
protein y ang disebut amiloid dan serat-serat neuro fibrillary .
"Berdasarkan gejala, ditemukan fakta bahwa alzheimer disebabkan oleh kerusakan v ascular,
peradangan otak, aterosklerosis, penurunan atau hipoperfusi otak akibat stroke," tambahny a.
Dalam ilmu peny akit saraf, sebelum hingga fase 20 tahun terakhir, para ahli masih berpikir
bahwa semua sy stem tubuh kita dapat mengalami regenerasi, kecuali sel-sel otak, atau neuron.
Namun postulat tersebut berubah, dengan penemuan Dr. Taruna Ikrar di Univ ersity of
California, Irv ine, y ang dipublikasi di Journal Frontiers of Neural Circuit menjelaskan bahwa
ada proses regenerasi y ang berlanjut secara kontiny u di otak, y ang terjadi dalam fase
kehidupan seseorang. Penemuan ini y ang dilakukan pada mamalia hidup, dengan
menggunakan metode: focal x -irradiation of hippocampus, V oltage Sensitiv e Dy e Imaging
(V SDI) of ev oked neural activ ity , v oltage sensitiv e dy e imaging of ev oked neural activ ity ,
retrov iral v ectors, v irus preparation and injections, immunohistochemistry , imaging
phy siology .
"Penemuan ini menjadi dasar peny akit alzheimer dan kelainan degeneratif otak lainny a. Selama
ini dalam pengobatan alzheimer hany a dilakukan secara simptomatik (atau menghilangkan
gejala) berupa peruban pola hidup, serta diperkuat oleh beberapa obat-obatan kimia, seperti;
Donepezil dan Riv astigmine. Namun belum bisa mengobati peny akit alzheimer secara kausal
dan mendasar. Sebab, alzheimer merupakan peny akit degeratif, sehingga pengobatanny a
seharusny a secara kausal dalam upay a merangsang tumbuhny a atau proses perbaharuan selsel otak y ang mengalami kerusakan," lanjut Ikrar.
Dia juga menjelaskan bahwa harapan masa depan pengobatan alzheimer, harus dilakukan
secara mendasar, y aitu berupa neuroreplacement (penggantian sel-sel saraf y ang rusak),
sehingga kerusakan akibat degenerasi sel-sel saraf dapat dicegah bahkan diperbaiki. Teknik ini
dimungkinkan, atas prinsip temuan Dr. Taruna Ikrar berupa pembuktian proses regenrasi
otak, khususny a di daerah otak tengah dipusat Hipocampus y ang dalam istilah ilmu saraf
disebut Dentate Gy rus.
Sehingga kedepan, pada daerah ini terjadi proses regenerasi sel-sel otak secara terus menerus.
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Sehingga kedepan, pada daerah ini terjadi proses regenerasi sel-sel otak secara terus menerus.
Jika proses teknik isolasi dan pemeliharaan serta pengembangbiakan Neural Stem cells (NSCs).
Bisa dilanjutkan transplantasikan kedalam otak manusia y ang menderita peny akit Alzheimer.
Maka, teknik replacement atau penggantian sel-sel otak dapat dicegah dan digantikan. Maka,
tidak mustahil dalam waktu y ang tidak terlalu lama lagi berbagai kelaianan otak akibat proses
kerusakan (degeneratif) sel-sel otak akan bisa diobati. [ian]
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