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3. The Cerebellum as a Neuronal Machine > 3-4. Long-Term Depression

3-4. Long-Term Depression

In the late 1960s and early 1970s, many laboratories apparently tried to reveal such synaptic plasticity, but in vain. It is widely known that Eccles invited Marr to sit in front of a cathode ray oscilloscope with him while they tested the effects of conjunctive stimulation of climbing fibers and parallel fibers using stimulus parameters chosen by Marr. No sign of synaptic plasticity was then observed, however. At that time, experiments were conducted in vivo such that stable intracellular recording was not possible for a period sufficiently long to detect synaptic plasticity. Accordingly, transmission across parallel fiber-Purkinje cell synapses was examined only by extracellular recording of field potentials. However, as compared to field potentials recorded in the hippocampus to reveal long-term potentiation (Bliss and Lomo, 1973), those in the cerebellar cortex were ten times smaller. This meant that before the availability of high-performance electronic averagers, any potential long-term modification of synaptic transmission could not be detected. The observation was further impeded because several factors in in vivo experiments were later shown to interfere with the occurrence of the synaptic plasticity: postsynaptic inhibition caused by basket/stellate cells (Ekerot and Kano, 1985), local bleeding resulting in the release of hemoglobin that absorbs nitric oxide (Nagao and Ito, 1991), and general anesthesia (Vigot et al., 2002).


  

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