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Neural circuits containing olfactory neurons are involved in the prepulse inhibition of the startle reflex in rats.

Niu H, He X, Zhou T, Shi X, Zhang Q, Zhang Z, Qiao Y, Xu F, Hu M - Front Behav Neurosci (2015)

Bottom Line: Our results demonstrated that blockage of olfactory sensory input could disturb olfactory behavior.In the function studies, we demonstrated that blockage of olfactory sensory input could impair the pre-pulse inhibition of the startle response following decreased c-Fos expression in relevant brain regions during the PPI responses.Thus, these data suggest that the olfactory system participates in the PPI regulating fields and plays a role in the pre-pulse inhibition of the startle response in rats.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, Xuzhou Medical College Xuzhou, China ; The Institute of Audiology and Speech Science, Xuzhou Medical Collage Xuzhou, China.

ABSTRACT
Many neuropsychiatric disorders, such as schizophrenia, have been associated with olfactory dysfunction and abnormalities in the prepulse inhibition (PPI) response to a startle reflex. However, whether these two abnormalities could be related is unclear. The present investigations were designed to determine whether theblockage of olfactory sensory input by zinc sulfate infusion in the olfactory naris (0.5 ml, 0.17 M, ZnE) can disturb the PPI response. Furthermore, a bilateral microinjection of lidocaine/MK801 in the olfactory bulb (OB) was administered to examine whether the blockage of olfactory sensory input could impair the PPI response. To identify the neural projection between olfaction and PPI-related areas, trans-synaptic retrograde tracing with the recombinant pseudorabies virus (PRV) was used. Our results demonstrated that blockage of olfactory sensory input could disturb olfactory behavior. In the function studies, we demonstrated that blockage of olfactory sensory input could impair the pre-pulse inhibition of the startle response following decreased c-Fos expression in relevant brain regions during the PPI responses. Furthermore, similar and more robust findings indicated that blockage of olfactory sensory input by microinjection of lidocaine/MK801 in the OB could impair the PPI response. In the circuit-level studies, we demonstrated that trans-synaptic retrograde tracing with PRV exhibited a large portion of labeled neurons in several regions of the olfactory cortices from the pedunculopontine tegmental nucleus (PPTg). Thus, these data suggest that the olfactory system participates in the PPI regulating fields and plays a role in the pre-pulse inhibition of the startle response in rats.

No MeSH data available.


Related in: MedlinePlus

The effects of ZnE on the startle magnitude and PPI response. (A) The effect of ZnE treatment on the startle response magnitude. An independent sample t test identified a significant difference between the groups (F(1,21) = 10.044, p > 0.05). (B) The effect of ZnE on the percentage change induced by a prepulse prior to an ASR PPI. A two-way ANOVA identified a main treatment effect (F(2,42) = 4.836, p < 0.05), but there was no significant interaction (intensity × treatment) (F(4,42) = 1.689, p > 0.05). A post hoc (LSD) test indicated that the ZnE treatment significantly altered the PPI response (naïve control vs. ZnE, p < 0.05). The data are presented as the mean ± SD. * indicates a significant difference compared with the naïve control group (p < 0.05).
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Figure 2: The effects of ZnE on the startle magnitude and PPI response. (A) The effect of ZnE treatment on the startle response magnitude. An independent sample t test identified a significant difference between the groups (F(1,21) = 10.044, p > 0.05). (B) The effect of ZnE on the percentage change induced by a prepulse prior to an ASR PPI. A two-way ANOVA identified a main treatment effect (F(2,42) = 4.836, p < 0.05), but there was no significant interaction (intensity × treatment) (F(4,42) = 1.689, p > 0.05). A post hoc (LSD) test indicated that the ZnE treatment significantly altered the PPI response (naïve control vs. ZnE, p < 0.05). The data are presented as the mean ± SD. * indicates a significant difference compared with the naïve control group (p < 0.05).

Mentions: Figure 2 shows the effect of a prepulse on the acoustic startle reflex in the ZnE and naïve control rats. The animals treated with ZnE were evaluated for their ASR and their prepulse inhibition to determine if olfaction has an impact on PPI and ASR. ZnE treatment caused significant changes in the animal’s PPI, but the ASR was unclear. The effects of ZnE treatments on the PPI and ASR are illustrated in Figure 2. An independent samples t-test of the ASR indicated that there was no significant difference between the groups (Figure 2A; p > 0.05). A two-way ANOVA of the PPI test identified a main treatment effect (F(2,42) = 4.836, p < 0.05), but there was no significant interaction between the groups and stimulus intensities (Figure 2B; F(4,42) = 1.689, p > 0.05). A post hoc analysis (LSD) indicated that ZnE treatment decreased the PPI (p < 0.05: naïve control vs. ZnE). These results indicated that ZnE treatment significantly reduced the PPI at all auditory intensities tested. Further analysis of the relationship between ZnE treatment and prepulse intensity was used to examine and differentiate the main effects caused by increasing the auditory intensity of the prepulse. Significant differences between the ZnE treatment and naïve control groups were identified at 70, 75 and 80 dB (Figure 2B). ZnE treatment disrupted the PPI expression in the 75 and 80 dB tests and may have led to a decrease in the startle response after an acoustic prepulse compared with the naïve control group (one way ANOVA, F(2,21) = 5.379, p < 0.05; F(2,21) = 4.820, p < 0.05).


Neural circuits containing olfactory neurons are involved in the prepulse inhibition of the startle reflex in rats.

Niu H, He X, Zhou T, Shi X, Zhang Q, Zhang Z, Qiao Y, Xu F, Hu M - Front Behav Neurosci (2015)

The effects of ZnE on the startle magnitude and PPI response. (A) The effect of ZnE treatment on the startle response magnitude. An independent sample t test identified a significant difference between the groups (F(1,21) = 10.044, p > 0.05). (B) The effect of ZnE on the percentage change induced by a prepulse prior to an ASR PPI. A two-way ANOVA identified a main treatment effect (F(2,42) = 4.836, p < 0.05), but there was no significant interaction (intensity × treatment) (F(4,42) = 1.689, p > 0.05). A post hoc (LSD) test indicated that the ZnE treatment significantly altered the PPI response (naïve control vs. ZnE, p < 0.05). The data are presented as the mean ± SD. * indicates a significant difference compared with the naïve control group (p < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4373374&req=5

Figure 2: The effects of ZnE on the startle magnitude and PPI response. (A) The effect of ZnE treatment on the startle response magnitude. An independent sample t test identified a significant difference between the groups (F(1,21) = 10.044, p > 0.05). (B) The effect of ZnE on the percentage change induced by a prepulse prior to an ASR PPI. A two-way ANOVA identified a main treatment effect (F(2,42) = 4.836, p < 0.05), but there was no significant interaction (intensity × treatment) (F(4,42) = 1.689, p > 0.05). A post hoc (LSD) test indicated that the ZnE treatment significantly altered the PPI response (naïve control vs. ZnE, p < 0.05). The data are presented as the mean ± SD. * indicates a significant difference compared with the naïve control group (p < 0.05).
Mentions: Figure 2 shows the effect of a prepulse on the acoustic startle reflex in the ZnE and naïve control rats. The animals treated with ZnE were evaluated for their ASR and their prepulse inhibition to determine if olfaction has an impact on PPI and ASR. ZnE treatment caused significant changes in the animal’s PPI, but the ASR was unclear. The effects of ZnE treatments on the PPI and ASR are illustrated in Figure 2. An independent samples t-test of the ASR indicated that there was no significant difference between the groups (Figure 2A; p > 0.05). A two-way ANOVA of the PPI test identified a main treatment effect (F(2,42) = 4.836, p < 0.05), but there was no significant interaction between the groups and stimulus intensities (Figure 2B; F(4,42) = 1.689, p > 0.05). A post hoc analysis (LSD) indicated that ZnE treatment decreased the PPI (p < 0.05: naïve control vs. ZnE). These results indicated that ZnE treatment significantly reduced the PPI at all auditory intensities tested. Further analysis of the relationship between ZnE treatment and prepulse intensity was used to examine and differentiate the main effects caused by increasing the auditory intensity of the prepulse. Significant differences between the ZnE treatment and naïve control groups were identified at 70, 75 and 80 dB (Figure 2B). ZnE treatment disrupted the PPI expression in the 75 and 80 dB tests and may have led to a decrease in the startle response after an acoustic prepulse compared with the naïve control group (one way ANOVA, F(2,21) = 5.379, p < 0.05; F(2,21) = 4.820, p < 0.05).

Bottom Line: Our results demonstrated that blockage of olfactory sensory input could disturb olfactory behavior.In the function studies, we demonstrated that blockage of olfactory sensory input could impair the pre-pulse inhibition of the startle response following decreased c-Fos expression in relevant brain regions during the PPI responses.Thus, these data suggest that the olfactory system participates in the PPI regulating fields and plays a role in the pre-pulse inhibition of the startle response in rats.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, Xuzhou Medical College Xuzhou, China ; The Institute of Audiology and Speech Science, Xuzhou Medical Collage Xuzhou, China.

ABSTRACT
Many neuropsychiatric disorders, such as schizophrenia, have been associated with olfactory dysfunction and abnormalities in the prepulse inhibition (PPI) response to a startle reflex. However, whether these two abnormalities could be related is unclear. The present investigations were designed to determine whether theblockage of olfactory sensory input by zinc sulfate infusion in the olfactory naris (0.5 ml, 0.17 M, ZnE) can disturb the PPI response. Furthermore, a bilateral microinjection of lidocaine/MK801 in the olfactory bulb (OB) was administered to examine whether the blockage of olfactory sensory input could impair the PPI response. To identify the neural projection between olfaction and PPI-related areas, trans-synaptic retrograde tracing with the recombinant pseudorabies virus (PRV) was used. Our results demonstrated that blockage of olfactory sensory input could disturb olfactory behavior. In the function studies, we demonstrated that blockage of olfactory sensory input could impair the pre-pulse inhibition of the startle response following decreased c-Fos expression in relevant brain regions during the PPI responses. Furthermore, similar and more robust findings indicated that blockage of olfactory sensory input by microinjection of lidocaine/MK801 in the OB could impair the PPI response. In the circuit-level studies, we demonstrated that trans-synaptic retrograde tracing with PRV exhibited a large portion of labeled neurons in several regions of the olfactory cortices from the pedunculopontine tegmental nucleus (PPTg). Thus, these data suggest that the olfactory system participates in the PPI regulating fields and plays a role in the pre-pulse inhibition of the startle response in rats.

No MeSH data available.


Related in: MedlinePlus