Interestingly, animals that had been conditioned and returned to

Interestingly, animals that had been conditioned and returned to their normal rearing environment for 7–9 hr had thresholds at higher spatial frequencies (13.1 ± 1.14 cycles cm-1) than nonconditioned controls (10.3 ± 0.8 cycles cm-1, p < 0.05, Figures 6E and 6F). To determine if

the enhanced BDNF signaling resulting from visual conditioning played a role in this change, we injected K252a twice into the tectal ventricle at 3.5 and 4.5 hr after conditioning, corresponding to the period when we found facilitation of synaptic plasticity. Animals were then tested at 7–9 hr after conditioning. TrkB inhibition (n = 16), but not control vehicle injection (n = 12), prevented the improvement in spatial sensitivity produced by conditioning (K252a: 9.2 ± AZD2281 datasheet 1.0 cycles cm-1; vehicle: 9.8 ± 1.11 cycles Z-VAD-FMK solubility dmso cm-1) (Figure 6F). The fact that only about half the tadpoles responded to three or more of the counterphasing gratings most likely

reflects independent modulation of the behavioral output rather than low-order visual system differences between animals as the fall-off of visually evoked responses measured electrophysiologically in tectal neurons correlated well with spatial frequency in nearly all animals tested (Figure 5). Thus, the data show that the observed increase in tectal cell sensitivity to finer gratings can affect the visually-evoked behavior of the awake unrestrained animal in a BDNF-dependent manner. However, for the reasons mentioned above, this behavioral assay provides an estimate of the visual sensitivity of the animals rather than a measurement of absolute acuity. To confirm that the observed change in swimming acceleration in response to visual stimuli involved retinotectal transmission, we thermally lesioned the optic tract just anterior Bay 11-7085 to the optic

tectum using the two-photon microscope with the infrared laser set at high intensity (∼200 mW on the stage at 810 nm) (Figure S5). At 5 hr after lesioning, we performed the behavioral test. Although animals that had undergone optic tract lesions still exhibited normal startle responses to full-screen ON stimuli, their response to counterphasing gratings was dramatically impaired. This finding is in agreement with previous studies attributing the visual acuity of behavioral responses to sensory processing in the optic tectum (Yolen and Hodos, 1976). Taken together, our data demonstrate that BDNF signaling induced by visual conditioning is able to facilitate bidirectional retinotectal synaptic plasticity, resulting in a behaviorally significant improvement in the response thresholds of tectal neurons to visual stimuli. We previously reported that a repeating visual stimulus was able to upregulate plasticity-related gene transcription in the Xenopus optic tectum ( Schwartz et al., 2009).

Leave a Reply

Your email address will not be published. Required fields are marked *

*

You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <strike> <strong>