Last time I looked at four early papers from Laurent's lab, which described the basics of how insect olfaction works. They showed that when you present a locust with an odor, their olfactory centers' LFPs oscillate at 20Hz, and antennal lobe (AL) neurons fire action potentials in sync with the LFP. Macleod and Laurent further showed that blocking GABAA transmission abolishes the LFP oscillations, presumably via local neurons (LN) in the AL.
Today I'm going to cover three papers by Mark Stopfer, a post-doc in the Laurent lab around the turn of the millenium.
And bees do it too!
Laurent started investigating insect olfaction in locusts, which do not have well-defined, manipulable behaviours. To start doing behaviour, Stopfer and Laurent repeated all of the locust experiments in honeybees, which extend their proboscis in response to sugars (proboscis extension reflex, PER). And when I say repeated, I mean almost literally repeated: they showed that the honeybee MB LFP oscillates at 30Hz, that GABAAinhibitors abolish the oscillations, that projection neurons respond to subsets of odors, etc.
Carlson lab, when investigating odorant receptor responses used dozens of odors, and characterized their similarity. Perhaps Stopfer got tired of bees after using 1000(!) of them.
In the discussion, Stopfer claims that these experiments show how important the LFP is in shaping responses to similar odors, but do not provide any explanation of how. My guess is that since PNs fire APs in the presence of PCT, the effect of the LFP desynchronization is not in the AL, but downstream in the mushroom body (MB). I believe the paper that investigated this in Perez-Orive, 2002.
Two years later, Stopfer and Laurent published a paper using a protocol near to my heart: they simply manipulated the stimulus and saw what happened. They returned to locusts, and recorded intracellularly from PNs, LNs and the LFP in the MB. They then presented odors to naive locusts ten times (1s odor pulse, 0.1Hz), and found that all the responses evolved over the ten presentations. During the first trial, the PNs and LNs had strong EPSPs, and PNs fired many action potentials. On subsequent trials, however, the EPSP amplitudes and action potential number both shrunk (see below). However, while the amplitudes had decreased, the precision had increased: the LN EPSPs and PN action potentials both became synchronized with the LFP. In contrast to the decreased strength of the AL neurons' responses, the LFP in the MB increased in strength over the trials.
blocked the nostril of a mouse, I would love to see that experimental setup).
the odor representation changes with each sniff in mice. However, the time scales are very different. In mice, each sniff is separate by 250ms, not 2.5s; and the adaptation resets in the 10s between trials, not the 2 min. shown here.
Furthermore, the increase in precision may not be important for mammals. Mice have been shown to perceive odor identity in a single sniff.
In 2003, Stopfer published another paper that used a simple protocol to examine the olfactory system. This time, he presented locusts with odors ranging in concentration over three orders of magnitude. They found that the MB LFP, and LN EPSPs both increased in magnitude with increasing concentration. In contrast, PN firing rate was flat across all concentrations, although there was an increase in LFP phase precision. This increase in precision could explain how the LFP amplitude increased, despite the flat firing rate.
They then focused on individual PNs, and found that PNs could respond completely differently to the same odor at different concentrations. There was no clear trend in these changes.
|Four example neurons' response to odors at different concentrations. I leave finding the changes as an exercise for the reader.|
|Different concentrations of the same odor cluster together. Dendrogram of similarity for three odors (red, blue, and green), at five concentrations (numbers at right). Different concentrations of the same odor generally cluster together.|
In the final figure of the paper, they took a peek at the decoder by recording Kenyon cells in the MB. Kenyon cells could be split into two groups: some cells responded to an odor at all concentrations (30%), while others responded to odors only at a specific concentration (15%).
To date, I believe this is the most complete exploration of how concentration is coded in the mitral cells/antennal lobe. Some work has been done in anesthetized rodents, but the standard now is to record in awake animals. There have also been a large number of imaging studies in glomeruli that show that more glomeruli (and thus ORNs) are active as concentration increases. Whether this would translate into more neurons being active at higher concentrations, a shift to earlier spike times, or some other phenomenon is unclear. How this would be decoded downstream in cortex is also unclear.
That's it for today. Only a dozen or so more papers to go! I like this post-doc centered format, so next time I'll take a look at Rainer Friedrich or Rachel Wilson's work.
Stopfer M, Bhagavan S, Smith BH, & Laurent G (1997). Impaired odour discrimination on desynchronization of odour-encoding neural assemblies. Nature, 390 (6655), 70-4 PMID: 9363891
Stopfer M, & Laurent G (1999). Short-term memory in olfactory network dynamics. Nature, 402 (6762), 664-8 PMID: 10604472
Stopfer M, Jayaraman V, & Laurent G (2003). Intensity versus identity coding in an olfactory system. Neuron, 39 (6), 991-1004 PMID: 12971898
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