Table 1.
Neural cell population | Pharmacological treatment effects | ||||
---|---|---|---|---|---|
Marker | Region | t6 BMS493 | t24 BMS493 | t6 RA | t24 RA |
GLU-/AT-ir | Anterior | 0 | 0 | + | + |
GLU-/AT-ir | Middle | 0 | + | + | + |
GLU-/AT-ir | Posterior | 0 | + | − | + |
hu/elav | Anterior | 0 | 0 | + | + |
hu/elav | Middle | 0 | 0 | + | +/0 |
hu/elav | Posterior | 0 | + | 0 | + |
tlx | Anterior | 0 | 0 | 0 | 0 |
tlx | Middle | 0 | 0 | 0 | 0 |
tlx | Posterior | 0 | 0 | − | 0 |
soxb1c | Anterior | 0 | 0 | + | +/0 |
soxb1c | Middle | − | 0 | + | + |
soxb1c | Posterior | + | + | 0 | + |
Sensory functions | Mildly impaired | Strongly impaired | Impaired | Impaired |
Results were obtained from immunohistochemical and gene expression analyses of ectodermal sensory neurons (ESNs) and ESN progenitors (ESNPs) following pharmacological treatments of developing amphioxus with the retinoic acid receptor (RAR) antagonist BMS493 or all-trans retinoic acid (RA). The developmental time point (t) of the treatments, at either 6 or 24 hpf (hours post fertilization), is given together with the compound. The observed effects on the formation of selected neural cell populations and on sensory functions are indicated. Treatment outcomes for the different neural cell populations are depicted as follows: 0 = no effect, + = gain of cells, − = loss of cells. Minor effects are indicated with a “/0”
GLU-/AT-ir glutamate/acetylated tubulin immunoreactivity