神经练习题

1、阐述神经元静息膜电位是如何产生的。

因为膜上钠钾泵的原因，导致神经元膜内钾离子多，而膜外钠离子多，但两边正负离子都处于平衡状态。在静息情况下，神经元膜上只有钾离子通道开放，导致钾离子顺浓度梯度流出，膜内有净负电荷。随着钾离子流出的增多，膜内侧有较多的负离子，而膜外侧有较多的正离子，从而产生内负外正的电压，此电压导致钾离子流入胞内，当浓度梯度导致的钾离子流出和电势梯度导致的钾离子流入相等时，此时的电压称之为静息膜电位。因为一般把胞外电压看做为零，所以静息膜电位一般为负值。神经胶质细胞静息时仅对钾通道开放，其膜电位一般为钾离子平衡电位，-80mV。神经元静息时还有一部分钠通道开放，其膜电位偏离钾离子平衡电位，一般为-65mV

2、试分别说明动作电位过程中下列现象形成的原因：阈值；上升相；超射；下降相；低射；绝对不应期；相对不应期；全或无。

阈值：钠通道需开放一定数目，抵制钾电流的外流，才能导致钠通道爆发性开放。 上升相：钠通道开放，钠离子内流。 超射：动作电位峰值接近于钠离子平衡电位。 下降相：钠通道失活，钾通道开放。 低射：接近于钾离子的平衡电位。

绝对不应期：钠通道失活，不能再次产生动作电位。

相对不应期：处于低射期，此时钠通道关闭，需要较大的刺激才能产生动作电位。

全和无：只要去极化电位超过动作电位的阈值，则会产生动作电位；如果去极化电位在阈值以下，则不会产生动作电位。

3、中枢神经突触传递的简要过程。 1）动作电位传导到突触前膜

2）突触前膜钙通道开放，钙离子流入突触前膜

3）突触前膜钙离子浓度升高，突触小泡与突触前膜融合，神经递质释放 4）释放到突触间隙的神经递质扩散到突触后膜，与后膜上的受体结合 5）受体自身通道或者通过G蛋白激活其它通道引起效应。

4、如果胞内Cl离子浓度是胞外的1.2倍，Cl离子通道开放，产生去极化还是超极化？为什么？什么条件下，开放GABAa受体可以产生EPSP，而不是IPSP。 一般情况下，神经元膜外氯离子浓度是膜内的10倍，而氯离子的平衡电位是-65mV。当膜内积聚的氯离子较正常值高时，其平衡电位绝对值将减小，趋向于去极化状态。也就是当氯离子通道开放时，氯离子外流，产生于类似正电荷内流的去极化状态（通过nerst方程也可以看出）。这种现象一般在胚胎发育初期或者出生不久，谷氨酸等兴奋性突触还没有完全发育的时候，神经元膜上的氯离子通道行使去极化突触传递的功能。而这种胞内氯离子增多的现象是有神经元膜上的氯离子转运体转运进神经元内的。随着发育的进行，胞内氯离子的浓度逐渐降低。

5、为什么开放钾通道可以产生抑制性，降低动作电位的发放？

钾通道开放，电位将向钾离子平衡电位转移，Ek=-80左右，远低于一般的神经元静息膜电位，故钾通道开放将产生抑制性效应。

6、试推测AMPA受体，NMDA受体和GABAa受体的反转电位。

通过电流电压（IV）曲线可知，AMPA受体的反转电位为0mV，其反转电位和nAChR的反转电位一致，其通道开放都允许钠离子和钾离子通过。

NMDA受体，通过IV曲线可以看出，其反转电位也是0mV，可能与流入的钙离子量比较少有关。

GABAa受体通道开放仅允许氯离子通过，其反转电位为氯离子平衡电位，即-65mV左右。

6、Glutamate activates a number of different metabotropic receptors. The consequence of activating one subtype is the inhibition of cAMP formation. A consequence of activating a second subtype is

activation of protein kinase C. Propose mechanisms for these different effects.

The subtype of glutamate metabotropic receptor that inhibits cAMP formation may

activate Gi. This is the mechanism used by the NE receptor subtype called

?2, which inhibits adenylyl cyclase and, consequently, inhibits cAMP

formation. The other subtype of glutamate metabotropic receptor might activate a G-protein that stimulates the enzyme phospholipase C (PLC). PLC splits the membrane phospholipids PIP2 into two parts: DAG and IP3. DAG stays in the plane of the membrane and activates the downstream enzyme protein kinase C (PKC). (IP3, on the other hand, diffuses away and causes organelles to discharge their calcium stores.)

7、Compare and contrast the properties of (a) AMPA and NMDA receptors, and (b) GABAA and GABAB receptors.

(a) AMPA and NMDA are glutamate receptor subtypes; both are activated by glutamate, but the drug AMPA acts only on the AMPA receptor and the drug NMDA acts only on the NMDA receptor. AMPA and NMDA are chemical agonists used to differentiate the glutamate receptor subtypes. Their antagonists can also distinguish receptor subtypes, for example, the antagonist for AMPA is CNQX and the antagonist for NMDA is AP5. The differences in the receptors are related to slight differences in the protein. An important property of the NMDA receptor is that it is only active in the presence of glutamate and sufficient depolarization in the postsynaptic neuron. (b) GABAA and GABAB are GABA receptor subtypes; both respond to GABA but muscimol is the agonist for the GABAA receptor, and the agonist for

GABAB is baclofen. The antagonist for GABAA is bicuculline whereas the antagonist for GABAB is phaclofen.

8、You apply ACh and activate nicotinic receptors on a muscle cell. Which way will current flow through the receptor channels when Vm = –60 mV? When Vm = 0 mV? When Vm = 60 mV? Why?

Nicotonic ACh receptors are permeable to both sodium and potassium. When Vm = –60 mV, net current flow through ACh-gated ion channels is inward, toward the equilibrium potential of sodium, causing depolarization. At Vm = 60 mV, the direction of net current flow through the ACh-gated ion channels is outward, toward the equilibrium potential of potassium, causing the membrane potential to become less positive. The critical value of membrane potential at which the direction of current flow reverses is called the reversal potential. In this case, the reversal potential is 0 mV because this is the value between the equilibrium potentials of sodium and potassium. At 0 mV, no current flows.

9、 We discussed a GABA-gated ion channel that is permeable to Cl–. GABA also activates a G-protein-coupled receptor called the GABAb receptor, which causes potassium-selective channels to open. What effect would GABAb receptor activation have on the membrane potential?

Activated GABA-gated Cl– ion channels bring the membrane toward the equilibrium

potential for Cl–, which is –65 mV. If the membrane potential was less negative than –65 mV when the transmitter was released, activation would cause hyperpolarization. The activation of GABAB receptors causes potassium-selective channels to open. As a result, GABAB activation brings membrane potential toward the equilibrium potential of potassium, which is –80 mV. If the membrane potential was less negative than –80 mV when the transmitter was released, activation would also cause hyperpolarization. This channel might also impact the neuron by shunting inhibition, allowing a depolarizing current from an excitatory synapse to leak out. This, in turn, decreases the likelihood of action potential. The action of a G-protein-coupled receptor is, however, slower than that of the GABA-gated Cl–ion channel or a typical excitatory synapse. Therefore, its effects would be slower to occur and would last longer.

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