Within a block click here of 24 trials, the amount of reward was always large (0.25 or 0.3 ml) for the saccades to one direction and small (0 or 0.03 ml) for the saccades to the other direction. Even in the small-reward trials, the monkeys had to make a correct saccade; otherwise, the same trial was repeated. The reward-position contingency was reversed for the next block of trials without external instructions. We used a pseudorandom reward schedule in which each block was divided into six “subblocks,” each consisting of two large-reward and two small-reward trials presented in a random order. In the following inactivation study, we used a reward-biased visually guided saccade task (Lauwereyns et al., 2002).
After the central fixation (600 or 1,000 ms), the fixation point turned off and simultaneously the target appeared either to the selleck inhibitor right or left 20° from the fixation point. The monkeys had to immediately make a saccade to the visible target. There was no cue during the fixation period. The reward schedule was the same
as the memory-guided saccade task. We followed Haber et al. (1993) for the anatomical localization of the VP which is located ventral to the AC and anterior to the GPe-GPi. Thus defined location of the VP was estimated on the basis of magnetic resonance (MR) images (4.7 T, Bruker). Single-unit recordings of VP neurons were performed with an epoxy-coated or a glass-coated Tungsten microelectrode (0.8–1.5 MΩ at 1 kHz). The electrode was inserted obliquely Carnitine palmitoyltransferase II (36° from vertical in the frontal plane) into the pallidum (Figure 1C) using an oil-driven micromanipulator (MO-97A, Narishige). The recording sites were determined using a grid system, which allowed recordings
at every 1 mm between penetrations. The unitary activity recorded from the microelectrode was amplified, filtered (200 Hz to 5 kHz), converted into digital data with an online window discriminator, and stored in a computer at the sampling rate of 1 kHz. During recording, the VP is located below the AC, which was identified on the basis of axonal signals such as high-frequency background noises and initially positive spikes. Only stable and well-isolated neurons were included in the present data. After the electrophysiological recording (mapping) of VP neurons in monkey H, we performed inactivation experiments to test a causal relationship between the VP activity and the reward modulation of saccadic performance. To accurately inactivate the brain structure, we used an electrode assembly (injectrode) consisting of an epoxy-coated Tungsten microelectrode for unit recording and a silica tube for drug delivery as described previously (Tachibana et al., 2008). After the precise identification of the aimed structures by unit recording, we injected a GABAA receptor agonist, muscimol (Sigma; 0.88–44 mM; 1–2 μl), into the target structure of each hemisphere.