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Habituation of glomerular responses in the olfactory bulb following prolonged odor stimulation reflects reduced peripheral input.

Ogg MC, Bendahamane M, Fletcher ML - Front Mol Neurosci (2015)

Bottom Line: Currently, it is unclear if this decrease is a function of adaptation of peripheral olfactory sensory neuron (OSN) responses or reflects depression of bulb circuits.To test whether depression of OSN terminals contributed to this habituation, olfactory nerve layer (ON) stimulation was used to drive glomerular layer responses in the absence of peripheral odor activation of the OSNs.The difference in response between odor and electrical stimulation following odor habituation provides evidence that odor response reductions measured in the glomerular layer of the OB are most likely the result of OSN adaptation processes taking place in the periphery.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Neurobiology, University of Tennessee Health Science Center Memphis, TN, USA.

ABSTRACT
Following prolonged odor stimulation, output from olfactory bulb (OB) mitral/tufted (M/T) cells is decreased in response to subsequent olfactory stimulation. Currently, it is unclear if this decrease is a function of adaptation of peripheral olfactory sensory neuron (OSN) responses or reflects depression of bulb circuits. We used wide-field calcium imaging in anesthetized transgenic GCaMP2 mice to compare excitatory glomerular layer odor responses before and after a 30-s odor stimulation. Significant habituation of subsequent glomerular odor responses to both the same and structurally similar odorants was detected with our protocol. To test whether depression of OSN terminals contributed to this habituation, olfactory nerve layer (ON) stimulation was used to drive glomerular layer responses in the absence of peripheral odor activation of the OSNs. Following odor habituation, in contrast to odor-evoked glomerular responses, ON stimulation-evoked glomerular responses were not habituated. The difference in response between odor and electrical stimulation following odor habituation provides evidence that odor response reductions measured in the glomerular layer of the OB are most likely the result of OSN adaptation processes taking place in the periphery.

No MeSH data available.


Related in: MedlinePlus

Thirty seconds odor exposure decreases subsequent glomerular responses to odors, but not to ON electrical stimulation. (A) Baseline glomerular responses to an odor presentation and ON electrical stimulation (ONS) in the same animal displayed in different color channels (2-heptanone, 0.5% s.v.: green; ONS, 100 μA: red) at 10× magnification. (B) Overlay of the baseline glomerular responses to odor and ONS shown in (A), highlighting glomeruli (yellow) that respond to both stimuli. White arrows indicate some examples of these shared glomeruli. (C) Pseudo-color glomerular responses to odor and ONS before (Pre Odor Hab) and after (Post Odor Hab) a 30-s exposure to 2-heptanone. Thirty seconds after a habituating odor exposure (bottom panel), glomerular responses to 2-heptanone are significantly decreased compared to control. However, 1 min after the habituating odor exposure, glomerular responses to ON stimulation are unchanged. (D) Example fluorescence traces taken from an overlapping glomerulus (A–C: middle white arrow) responding to both 2-heptanone (top panel) and ONS (bottom panel) before (black trace) and after (blue trace) odor habituation. The gray trace in the bottom panel shows the response to ONS following bulbar lidocaine application. Black arrows indicate stimulus onset. (E) Population data show glomerular responses to the odor were significantly reduced following odor habituation, while pre and post ONS responses in the same glomeruli were unchanged. Error bars indicate SEM. *p < 0.05.
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Figure 4: Thirty seconds odor exposure decreases subsequent glomerular responses to odors, but not to ON electrical stimulation. (A) Baseline glomerular responses to an odor presentation and ON electrical stimulation (ONS) in the same animal displayed in different color channels (2-heptanone, 0.5% s.v.: green; ONS, 100 μA: red) at 10× magnification. (B) Overlay of the baseline glomerular responses to odor and ONS shown in (A), highlighting glomeruli (yellow) that respond to both stimuli. White arrows indicate some examples of these shared glomeruli. (C) Pseudo-color glomerular responses to odor and ONS before (Pre Odor Hab) and after (Post Odor Hab) a 30-s exposure to 2-heptanone. Thirty seconds after a habituating odor exposure (bottom panel), glomerular responses to 2-heptanone are significantly decreased compared to control. However, 1 min after the habituating odor exposure, glomerular responses to ON stimulation are unchanged. (D) Example fluorescence traces taken from an overlapping glomerulus (A–C: middle white arrow) responding to both 2-heptanone (top panel) and ONS (bottom panel) before (black trace) and after (blue trace) odor habituation. The gray trace in the bottom panel shows the response to ONS following bulbar lidocaine application. Black arrows indicate stimulus onset. (E) Population data show glomerular responses to the odor were significantly reduced following odor habituation, while pre and post ONS responses in the same glomeruli were unchanged. Error bars indicate SEM. *p < 0.05.

Mentions: We used olfactory nerve-stimulation (ONS) to assess whether reduced glomerular responses following prolonged odor stimulation reflect synaptic depression of OSN input. To accomplish this, we stimulated the axons of the OSNs within the OB to generate glomerular responses without odorant activation. In two animals, responses to ONS were compared before and after OB lidocaine application to verify that ONS was not directly activating glomeruli (Figure 4D; gray trace). Following bulbar lidocaine application, glomerular responses to ONS were completely blocked (Pre: 7.0 ± 0.3% ΔF/F; Post: 0.3 ± 0.2% ΔF/F; one sample t-test: t(21) = 1.85, p = 0.09, n = 22 glomeruli). In four animals, pre-habituation baseline responses to one of the odors and to electrical ONS were established (Figure 4A). Analysis was performed on overlapping glomeruli that were activated by both the odor and the ON stimulation (n = 28; Figure 4B). Glomerular responses changed within 1 min following the odor habituation trial (ANOVA: F(3,81) = 21.25, p < 0.0001). Post hoc tests showed significant reduction of the mean glomerular response to odor (Pre: 11.4 ± 0.6% ΔF/F; Post: 8.3 ± 0.5% ΔF/F; Figures 4C–E). However, in the same glomeruli, the mean glomerular response to ONS was not significantly reduced following odor habituation (Pre: 8.2 ± 0.4% ΔF/F; Post: 7.7 ± 0.4% ΔF/F), demonstrating that postsynaptic responses independent of odor input were not depressed.


Habituation of glomerular responses in the olfactory bulb following prolonged odor stimulation reflects reduced peripheral input.

Ogg MC, Bendahamane M, Fletcher ML - Front Mol Neurosci (2015)

Thirty seconds odor exposure decreases subsequent glomerular responses to odors, but not to ON electrical stimulation. (A) Baseline glomerular responses to an odor presentation and ON electrical stimulation (ONS) in the same animal displayed in different color channels (2-heptanone, 0.5% s.v.: green; ONS, 100 μA: red) at 10× magnification. (B) Overlay of the baseline glomerular responses to odor and ONS shown in (A), highlighting glomeruli (yellow) that respond to both stimuli. White arrows indicate some examples of these shared glomeruli. (C) Pseudo-color glomerular responses to odor and ONS before (Pre Odor Hab) and after (Post Odor Hab) a 30-s exposure to 2-heptanone. Thirty seconds after a habituating odor exposure (bottom panel), glomerular responses to 2-heptanone are significantly decreased compared to control. However, 1 min after the habituating odor exposure, glomerular responses to ON stimulation are unchanged. (D) Example fluorescence traces taken from an overlapping glomerulus (A–C: middle white arrow) responding to both 2-heptanone (top panel) and ONS (bottom panel) before (black trace) and after (blue trace) odor habituation. The gray trace in the bottom panel shows the response to ONS following bulbar lidocaine application. Black arrows indicate stimulus onset. (E) Population data show glomerular responses to the odor were significantly reduced following odor habituation, while pre and post ONS responses in the same glomeruli were unchanged. Error bars indicate SEM. *p < 0.05.
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Figure 4: Thirty seconds odor exposure decreases subsequent glomerular responses to odors, but not to ON electrical stimulation. (A) Baseline glomerular responses to an odor presentation and ON electrical stimulation (ONS) in the same animal displayed in different color channels (2-heptanone, 0.5% s.v.: green; ONS, 100 μA: red) at 10× magnification. (B) Overlay of the baseline glomerular responses to odor and ONS shown in (A), highlighting glomeruli (yellow) that respond to both stimuli. White arrows indicate some examples of these shared glomeruli. (C) Pseudo-color glomerular responses to odor and ONS before (Pre Odor Hab) and after (Post Odor Hab) a 30-s exposure to 2-heptanone. Thirty seconds after a habituating odor exposure (bottom panel), glomerular responses to 2-heptanone are significantly decreased compared to control. However, 1 min after the habituating odor exposure, glomerular responses to ON stimulation are unchanged. (D) Example fluorescence traces taken from an overlapping glomerulus (A–C: middle white arrow) responding to both 2-heptanone (top panel) and ONS (bottom panel) before (black trace) and after (blue trace) odor habituation. The gray trace in the bottom panel shows the response to ONS following bulbar lidocaine application. Black arrows indicate stimulus onset. (E) Population data show glomerular responses to the odor were significantly reduced following odor habituation, while pre and post ONS responses in the same glomeruli were unchanged. Error bars indicate SEM. *p < 0.05.
Mentions: We used olfactory nerve-stimulation (ONS) to assess whether reduced glomerular responses following prolonged odor stimulation reflect synaptic depression of OSN input. To accomplish this, we stimulated the axons of the OSNs within the OB to generate glomerular responses without odorant activation. In two animals, responses to ONS were compared before and after OB lidocaine application to verify that ONS was not directly activating glomeruli (Figure 4D; gray trace). Following bulbar lidocaine application, glomerular responses to ONS were completely blocked (Pre: 7.0 ± 0.3% ΔF/F; Post: 0.3 ± 0.2% ΔF/F; one sample t-test: t(21) = 1.85, p = 0.09, n = 22 glomeruli). In four animals, pre-habituation baseline responses to one of the odors and to electrical ONS were established (Figure 4A). Analysis was performed on overlapping glomeruli that were activated by both the odor and the ON stimulation (n = 28; Figure 4B). Glomerular responses changed within 1 min following the odor habituation trial (ANOVA: F(3,81) = 21.25, p < 0.0001). Post hoc tests showed significant reduction of the mean glomerular response to odor (Pre: 11.4 ± 0.6% ΔF/F; Post: 8.3 ± 0.5% ΔF/F; Figures 4C–E). However, in the same glomeruli, the mean glomerular response to ONS was not significantly reduced following odor habituation (Pre: 8.2 ± 0.4% ΔF/F; Post: 7.7 ± 0.4% ΔF/F), demonstrating that postsynaptic responses independent of odor input were not depressed.

Bottom Line: Currently, it is unclear if this decrease is a function of adaptation of peripheral olfactory sensory neuron (OSN) responses or reflects depression of bulb circuits.To test whether depression of OSN terminals contributed to this habituation, olfactory nerve layer (ON) stimulation was used to drive glomerular layer responses in the absence of peripheral odor activation of the OSNs.The difference in response between odor and electrical stimulation following odor habituation provides evidence that odor response reductions measured in the glomerular layer of the OB are most likely the result of OSN adaptation processes taking place in the periphery.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Neurobiology, University of Tennessee Health Science Center Memphis, TN, USA.

ABSTRACT
Following prolonged odor stimulation, output from olfactory bulb (OB) mitral/tufted (M/T) cells is decreased in response to subsequent olfactory stimulation. Currently, it is unclear if this decrease is a function of adaptation of peripheral olfactory sensory neuron (OSN) responses or reflects depression of bulb circuits. We used wide-field calcium imaging in anesthetized transgenic GCaMP2 mice to compare excitatory glomerular layer odor responses before and after a 30-s odor stimulation. Significant habituation of subsequent glomerular odor responses to both the same and structurally similar odorants was detected with our protocol. To test whether depression of OSN terminals contributed to this habituation, olfactory nerve layer (ON) stimulation was used to drive glomerular layer responses in the absence of peripheral odor activation of the OSNs. Following odor habituation, in contrast to odor-evoked glomerular responses, ON stimulation-evoked glomerular responses were not habituated. The difference in response between odor and electrical stimulation following odor habituation provides evidence that odor response reductions measured in the glomerular layer of the OB are most likely the result of OSN adaptation processes taking place in the periphery.

No MeSH data available.


Related in: MedlinePlus