Schmidt J T
J Neurophysiol. 1985 Jan;53(1):237-51. doi: 10.1152/jn.1985.53.1.237.
In goldfish tectum, alpha-bungarotoxin (alpha BTX) blocks postsynaptically generated field potentials elicited by either photic or electrical stimulation, but leaves presynaptic activity unaffected. To assess the chronic effects of blocking transmission on synaptic stability, small restricted areas of synaptic block were created by slow, low-pressure microinjection of toxin-Ringer's solution from a micropipette. Local transmission was blocked, but field potentials outside the injected region were unchanged. Radioautography of 125I-alpha BTX demonstrated that 6 days postinjection it was still highly localized and concentrated in discrete synaptic laminae of the tectal neuropil, in agreement with its known tight binding in goldfish brain (18). Electrophysiological maps made 6-8 days postinjection showed that few if any optic terminals could be recorded in the toxin-blocked zone, but there was no scotoma in the visual field. Terminals with receptive fields that would normally have corresponded to the region of injection were instead recorded from surrounding tectal areas. Since the normal units were also recorded there, this produced very large multiunit receptive fields. Apparently the optic terminals within the toxin-blocked area moved outward and innervated neighboring areas. In a minority of cases, no silent areas were noted and only the enlarged multiunit receptive fields were seen in the injection zone. All tecta injected with alpha BTX, but none injected with Ringer's, showed these disturbances in the map at the treated area at 6-8 days postinjection. By 2-3 wk, the maps in the alpha BTX-injected tecta had returned to normal. There were no silent areas and no enlarged receptive fields. The movement of the optic arbors was shown to be dependent on activity in the optic fibers. In fish receiving intraocular injections of tetrodotoxin (TTX) for the first 4-6 days, no changes were seen in the retinotectal maps recorded after the effects of the TTX wore off. When the entire surface of the tectum was blocked with multiple injections of alpha BTX, normal maps were recorded at 6-8 days postinjection. Thus in order to produce movements in optic terminals, the fibers require activity and an opportunity to make effective synapses in a nearby zone.
在金鱼视顶盖中,α-银环蛇毒素(αBTX)能阻断光刺激或电刺激引起的突触后产生的场电位,但不影响突触前活动。为了评估阻断传递对突触稳定性的慢性影响,通过用微量移液器缓慢、低压微量注射毒素-林格氏液,在小范围内造成突触阻断。局部传递被阻断,但注射区域外的场电位未改变。125I-αBTX放射自显影显示,注射后6天,它仍高度定位并集中在视顶盖神经毡的离散突触层中,这与其在金鱼脑中已知的紧密结合情况相符(18)。注射后6 - 8天制作的电生理图谱显示,在毒素阻断区几乎记录不到视终端,但视野中没有暗点。具有通常对应于注射区域感受野的终端反而从周围视顶盖区域记录到。由于在那里也记录到了正常的神经元,这就产生了非常大的多单位感受野。显然,毒素阻断区内的视终端向外移动并支配了邻近区域。在少数情况下,未观察到静区,仅在注射区看到扩大的多单位感受野。所有注射αBTX的视顶盖,但未注射林格氏液的视顶盖,在注射后6 - 8天在处理区域的图谱中都显示出这些干扰。到2 - 3周时,注射αBTX的视顶盖中的图谱已恢复正常。没有静区,也没有扩大的感受野。视轴突的移动被证明依赖于视纤维的活动。在最初注射河豚毒素(TTX)4 - 6天的鱼中,在TTX作用消失后记录的视网膜-视顶盖图谱中未观察到变化。当通过多次注射αBTX阻断视顶盖的整个表面时,在注射后6 - 8天记录到正常图谱。因此,为了使视终端发生移动,纤维需要活动以及在附近区域形成有效突触的机会。