ffrench-Mullen J M, Hori N, Nakanishi H, Slater N T, Carpenter D O
Cell Mol Neurobiol. 1983 Jun;3(2):163-81. doi: 10.1007/BF00735280.
The responses of pyramidal neurons of rat prepyriform cortex to ionophoretic application of acetylcholine (ACh) were studied in a submerged, perfused brain slice. ACh excited some neurons but only if applied to an area near to the cut surface of the slice. This area contained the basal dendrites of the pyramidal cells and some cell bodies. No excitation was seen if ACh was applied at depths of 250 microns or more from the cut surface, an area which contained only apical dendrites, although the apical dendrites were very sensitive to excitatory amino acids such as aspartate (Asp) and glutamate (Glu). On all neurons which did not discharge to ionophoretic application of ACh, ACh potentiated the response to Glu and Asp. No potentiation of amino acid responses was obtained on apical dendrites. The potentiation had a time course similar to that of the discharge of neurons which fired to ACh. This observation suggests that pyramidal neurons have receptors for ACh on basal but not apical dendrites. The ACh response in the basal dendrite-soma region was elicted by pilocarpine and blocked by atropine but not curare. This was true whether the response studied was direct excitation or potentiation of the response to an amino acid. The ACh response was associated with a voltage-dependent increase in membrane resistance which had a slow time course and appeared to be due to a turning off of an M current, as described by Brown and Adams (1980) in sympathetic ganglion cells. The effects of ACh were minimal at the resting potential but increased with depolartization. ACh had no effect on the current-voltage relation of the cell, except at depolarized potentials of less than -60 mV. Ionophoretic application of Ba2+ to the basal dendritic region resulted in potentiation of the amino acid responses and sometimes induced a discharge similar to that of ACh. Since Ba2+ mimics the ACh response, presumably by a direct blockade of the M channel, the effects of Ba2+ on apical dendrites were tested to determine whether these dendrites contain M channels associated with a transmitter receptor other than ACh. However, Ba2+ did not induce potentiation in apical dendrites, suggesting that M channels are also restricted to the basal dendrites or cell bodies.(ABSTRACT TRUNCATED AT 400 WORDS)
在浸没于灌流液中的大鼠梨状前皮质脑片中，研究了锥体神经元对离子导入乙酰胆碱（ACh）的反应。ACh能兴奋一些神经元，但前提是将其施加于靠近脑片切面的区域。该区域包含锥体细胞的基底树突和一些细胞体。如果将ACh施加于距切面250微米或更深的区域（该区域仅包含顶端树突），则未见兴奋现象，尽管顶端树突对兴奋性氨基酸如天冬氨酸（Asp）和谷氨酸（Glu）非常敏感。在所有对离子导入ACh不产生放电反应的神经元上，ACh增强了对Glu和Asp的反应。在顶端树突上未观察到对氨基酸反应的增强作用。这种增强作用的时间进程与对ACh产生放电反应的神经元的放电时间进程相似。这一观察结果表明，锥体神经元在基底树突而非顶端树突上具有ACh受体。在基底树突-胞体区域，毛果芸香碱可引发ACh反应，阿托品可阻断该反应，但箭毒则不能。无论所研究的反应是直接兴奋还是对氨基酸反应的增强，情况均如此。ACh反应与膜电阻的电压依赖性增加有关，其时间进程缓慢，似乎是由于M电流的关闭所致，正如Brown和Adams（1980年）在交感神经节细胞中所描述的那样。ACh在静息电位时作用最小，但随着去极化而增强。除了在去极化电位小于-60 mV时，ACh对细胞的电流-电压关系没有影响。向基底树突区域离子导入Ba2+会增强氨基酸反应，有时还会诱发类似于ACh的放电。由于Ba2+模拟ACh反应，推测是通过直接阻断M通道，因此测试了Ba2+对顶端树突的作用，以确定这些树突是否含有与ACh以外的递质受体相关的M通道。然而，Ba2+并未在顶端树突中诱导增强作用，这表明M通道也仅限于基底树突或细胞体。（摘要截短于400字）
