Ensemble neural activity systematically changes across repeated encounters with an odorant.
(a)Schematic of the olfactory stimulation protocol. Each block consisted of twenty-five trials with a four seconds odor pulse delivered in each trial. The inter-trial interval was 56 s. Two datasets were collected. Each dataset consisted of five randomized blocks of four odorants (dataset 1: hex (H), hex (L), oct (H), oct (L), hex (H)-repeat; dataset 2: iaa (H), iaa (L), bza (H), bza (L), iaa (H)-repeat). A fifteen-minute no-odor stimulation period separated blocks of trials.
(b)Raster plots of eight representative projection neurons (PNs) in the locust antennal lobe are shown. Spiking activities are shown for twenty-five trials (rows) with earlier trials shown at the top and later trials at the bottom. The shaded region indicates the four seconds odor stimulation period, and the identity of the stimulus is indicated in each plot.
(c)Raster plots are shown for four representative PNs during two blocks of trials. The same odorant was presented in both blocks. Note that spiking activity changes are repeatable across the block of trials.
(d) Schematic showing how vesicular depletion and lateral inhibition facilitation models would change spiking activity in individual neurons. Y-axis represents the change in response over trials ((1st trial response – 25th trial response)/ (1st trial response + 25th trial response)). Positive numbers indicate that the first trial had a stronger response, hence response reduction. Negative numbers indicate that the last trial had a stronger response, hence response facilitation. Along the x-axis, the response in the 1st trial is shown. Vesicular depletion should impact the strongly activated neurons more, whereas lateral inhibition facilitation should progressively suppress weak responders.
(e)Following the schematic in panel d, response changes observed in PNs are shown. Only PNs with significant odor-evoked responses are included in this plot. Responsiveness of PN was determined based on whether their peak odor-evoked response in the first trial exceeded the mean + 6.5 SDs of spontaneous activity preceding odor stimulation in that first trial. In total hex (L/H), n = 26, 39 PNs; oct (L/H), n = 35, 28 PNs; iaa (L/H), n = 39, 35 PNs; bza (L/H), n = 33, 40 PNs were included in the plot. Different colors and symbols are used to denote the identity of the odorant and its intensity (low-intensity trials – triangles and high-intensity trials – circles). The dotted line shows the regression fit revealing a linear relationship, if any, between the activation strength in the first trial (x-axis) and the response reduction observed (y-axis). As can be noted the R2 values are low indicating that both vesicle depletion and lateral inhibition facilitation models fail to capture the adaptation trends in our datasets.
(f)Changes in PN spiking activity over trials during high-intensity odor exposures (y-axis) are plotted against response changes observed for the same PN during low-intensity exposures of the same odorant. The dotted line indicates the regression fit revealing a linear relationship between the response changes observed during high and low-intensity exposures of the same odorant (hex, R2=0.034; oct, R2=0.032; iaa R2=0.067; bza R2=0.0016). The poor linear regression fit here indicates that reductions in neural response amplitude for one odor intensity do not model reductions in response amplitude for another odor intensity.