関連する実験動画
Updated: May 5, 2026

13:06
Viral Tracing of Genetically Defined Neural Circuitry
Published on: October 17, 2012
19.2K
自己無効化狂犬病ウイルスによる神経回路への生涯に渡る遺伝的および機能的アクセス
Ernesto Ciabatti1, Ana González-Rueda1, Letizia Mariotti1
1Division of Neurobiology, MRC Laboratory of Molecular Biology, Cambridge, UK.
Cell
|July 11, 2017
まとめ
研究者は神経回路を研究するために自己不活性化狂犬病ウイルス (SiR) を開発しました. この新しいツールは 脳のネットワークの 長期的な機能的および遺伝的操作を 有害な影響なしに可能にします
科学分野:
- 神経科学
- 分子生物学
- 遺伝学
背景:
- 神経ネットワークの機能不全が 精神病や神経変性障害の根底にあるのです
- 神経回路をターゲットにする現在の方法は,特に長期の研究では限られています.
- 狂犬病ウイルスは神経回路を追跡するのに有用ですが,細胞毒性であり,機能的および遺伝的操作を妨げます.
研究 の 目的:
- 長期的な安全で効果的な神経回路操作のための 新しい狂犬病ウイルスシステムを開発する
- 細胞毒性と時間的な制約を含む伝統的な狂犬病ウイルスの限界を克服する.
主な方法:
- 自己無効化する ΔG 狂犬病ウイルス (SiR) の発現
- 感染したニューロンからの SiRの転写消失の実証.
- 追跡されたニューラルネットワークへの永久的な遺伝的アクセスを検証する.
- ニューロン生理と回路機能に対するSiRの影響の評価
主要な成果:
- SiRは ニューラル回路のトランスクリプション・サイレント・トラッキングを可能にします
- ネットワークのダイナミクスを研究するために 仮想的に無制限の時間窓を提供します.
- SiRは神経回路の遺伝的および機能的操作を in vivoで可能にします.
- SiRは神経生理学や回路機能に悪影響を及ぼさない.
結論:
- 自己無効化狂犬病ウイルス (SiR) は,神経科学の研究のための強力な新しいツールです.
- SiRは従来の狂犬病ウイルスの限界を克服し,長期的な神経回路の研究を行います.
- この技術は,神経回路の深い調査と操作を in vivo 容易にします.
さらに関連する動画
関連する概念動画
Long-term Potentiation
51.6K
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
51.6K
Long-term Potentiation
2.7K
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when...
Hebbian LTP
LTP can occur when...
2.7K
Disorders of the Nervous Tissue
3.0K
Nervous tissue is a vital component of the human body's communication system, enabling us to perceive and respond to stimuli. However, like all other tissues, it is vulnerable to disorders and diseases that can significantly impact our neurological functioning.
Homeostatic Imbalances:
Alzheimer's disease manifests as a gradual decline in memory and cognitive abilities, attributed to the buildup of amyloid plaques and neurofibrillary tangles in the brain.
Parkinson's disease arises from the...
Homeostatic Imbalances:
Alzheimer's disease manifests as a gradual decline in memory and cognitive abilities, attributed to the buildup of amyloid plaques and neurofibrillary tangles in the brain.
Parkinson's disease arises from the...
3.0K
Encephalitis ll: Pathophysiology
22
Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
22
Alzheimer Disease ll: Pathophysiology
35
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
35
Parkinson Disease ll: Pathophysiology
28
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
28

