simple exam 2 essay

cochlea（蝸牛）の仕組み

👉 音 → 振動 → 膜が動く → 毛が曲がる → 電気信号 → 脳

👉 Sound → membrane → hair bend → K⁺ → depolarize → brain

① Basilar membrane（基底膜）

② Sound vibration（音の振動）

③ Basilar membrane moves（基底膜が動く）

④ Hair cells bend（有毛細胞）👉 イオンチャネルが開く　👉 K⁺（カリウム）が入る

⑤ Receptor potential（受容器電位）　Positive charge enters → depolarization

⑥ Signal to brain（脳へ）　Neurotransmitter → action potential → brain

ストローク

👉 血が止まる → エネルギー不足 → 暴走 → Ca²⁺ → 細胞死

👉 Clot → pump fail → fire → glutamate ↑ → Ca²⁺ ↑ → death

① Blood clot

② Energy failure　No oxygen & glucose → Na⁺/K⁺ pump fails、depolarize

③ Overfiring

④ Glutamate release

⑤ Glutamate buildup

⑥ Ca²⁺ influx　Postsynaptic neurons overactivated　→ Ca²⁺ & Zn²⁺ enter

⑦ Cell death　Excess Ca²⁺

Beer attack 副交感神経（parasympathetic）の流れ

👉 Relax → ACh → Heart rate ↓

① Interpret as relaxation

② Preganglionic neuron

③ Signal to ganglion

④ ACh release (first synapse) ACh → nicotinic receptors

⑤ Postganglionic neuron → releases ACh again

⑥ Target organ (heart) 👉 cAMP ↓

⑦ Effect

👉 Parasympathetic = ACh → muscarinic (Gi) → ↓HR

Bear Attack 交感神経（sympathetic）の流れ

👉 Danger → NE → Heart rate ↑ 👉 危険 → ノルエピ → 心拍アップ

① See a bear

② Brain response

③ Preganglionic neuron → releases ACh

④ Ganglion ACh → nicotinic receptors

👉 神経節ではニコチン受容体

⑤ Postganglionic neuron Releases norepinephrine (NE)

⑥ Target organ (heart) Heart has adrenergic receptors (β1, Gs) → ↑ cAMP

⑦ Effect

👉 Sympathetic = ACh → NE → β1 → ↑HR

交感神経＋副腎髄質（adrenal medulla）ルート

👉 Sympathetic + Adrenal Medulla → Hormone release (Epi/NE)

⑦ Skip postganglionic neuron

⑧ ACh release

⑨ Adrenal medulla activation

Adrenal medulla has nicotinic receptors

👉 ニコチン受容体で受け取る

→ releases epinephrine & norepinephrine into blood

👉 エピネフリン＆ノルエピネフリンを血中へ

嗅覚（olfactory transduction）の流れ

👉 Odor → G protein → cAMP → Na⁺/Ca²⁺ → AP

① Odor binds receptor

② GDP → GTP

③ G protein activated

④ cAMP produced

⑤ Ion channels open

⑥ Ca²⁺ effect Ca²⁺ opens Cl⁻ channels

⑦ Cl⁻ leaves → more depolarization

⑧ Receptor potential → AP

⑨ Synapse Releases neurotransmitter to mitral cell

⑩ Brain

視覚（phototransduction）*の流れ

👉 Light → ↓cGMP → channels close → hyperpolarization

① Light hits rhodopsin

② G protein activation

③ GDP → GTP

④ Alpha subunit activates PDE

⑤ PDE action PDE converts cGMP → GMP

⑥ cGMP decreases Na⁺ channels close → cell becomes more negative

⑦ Hyperpolarization

👉 視覚 = cGMP減少 → 過分極

暗いとき（dark）の視覚

👉 Dark → cGMP high → channels open → depolarization

① No light

② Rhodopsin inactive

③ G protein inactive

④ PDE inactive No breakdown of cGMP

⑤ cGMP stays high

⑥ Channels open cGMP keeps Na⁺ channels open

⑦ Ions enter

⑧ Depolarization

⑨ Neurotransmitter release Lots of glutamate released

⑩ Signal to bipolar cells

光のとき（LIGHT）の視覚

👉 Light → ↓cGMP → channels close → hyperpolarization → ↓glutamate

① Light hits rhodopsin

② Retinal changes shape

③ Rhodopsin activated

④ G protein activation Activates transducin

⑤ PDE activation

⑥ cGMP breakdown PDE: cGMP → GMP

⑦ cGMP decreases

⑧ Channels close cGMP-gated Na⁺ channels close

⑨ Hyperpolarization

⑩ Less glutamate

⑪ Signal to brain Bipolar → ganglion → brain

てんかん（epilepsy）の仕組み

👉 Cl⁻ control fails → inhibition ↓ → neurons overfire → seizure

① Chloride regulation problem Neurons cannot properly regulate Cl⁻ (often via GABA system)

② GABA inhibition fails Normally: Cl⁻ enters → hyperpolarization BUT Now: Cl⁻ gradient is messed up

③ IPSP becomes weak

④ Neurons become too excitable Less inhibition → easier to fire

⑤ Excess firing

⑥ Seizure