Limits...
Ventromedial hypothalamic neurons control a defensive emotion state.

Kunwar PS, Zelikowsky M, Remedios R, Cai H, Yilmaz M, Meister M, Anderson DJ - Elife (2015)

Bottom Line: The hypothalamus plays a role in such behaviors, but prevailing textbook views depict it as an effector of upstream emotion centers, such as the amygdala, rather than as an emotion center itself.Importantly, these neurons can also condition learned defensive behavior, further refuting long-standing claims that the hypothalamus is unable to support emotional learning and therefore is not an emotion center.These data indicate that the hypothalamus plays an integral role to instantiate emotion states, and is not simply a passive effector of upstream emotion centers.

View Article: PubMed Central - PubMed

Affiliation: Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States.

ABSTRACT
Defensive behaviors reflect underlying emotion states, such as fear. The hypothalamus plays a role in such behaviors, but prevailing textbook views depict it as an effector of upstream emotion centers, such as the amygdala, rather than as an emotion center itself. We used optogenetic manipulations to probe the function of a specific hypothalamic cell type that mediates innate defensive responses. These neurons are sufficient to drive multiple defensive actions, and required for defensive behaviors in diverse contexts. The behavioral consequences of activating these neurons, moreover, exhibit properties characteristic of emotion states in general, including scalability, (negative) valence, generalization and persistence. Importantly, these neurons can also condition learned defensive behavior, further refuting long-standing claims that the hypothalamus is unable to support emotional learning and therefore is not an emotion center. These data indicate that the hypothalamus plays an integral role to instantiate emotion states, and is not simply a passive effector of upstream emotion centers.

Show MeSH
Activation of SF1+ neurons produces an increase in neuroendocrine responding.(A) Illustration of testing for stimulation induced changes in corticosterone. (B) Optogenetic stimulation of SF1+ neurons increases serum corticosterone levels in ChR2 mice compared to eYFP controls. n = 11–12 animals for each condition.DOI:http://dx.doi.org/10.7554/eLife.06633.015
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4379496&req=5

fig5s2: Activation of SF1+ neurons produces an increase in neuroendocrine responding.(A) Illustration of testing for stimulation induced changes in corticosterone. (B) Optogenetic stimulation of SF1+ neurons increases serum corticosterone levels in ChR2 mice compared to eYFP controls. n = 11–12 animals for each condition.DOI:http://dx.doi.org/10.7554/eLife.06633.015

Mentions: We also investigated whether transient activation of SF1+ neurons caused a persistent inhibitory influence on appetitive behavior, by testing whether it increased the latency to re-initiate mating, following its interruption (Figure 5J). We observed significantly longer latencies for ChR2 mice to re-initiate mating after SF1+ neurons were activated, compared to interleaved internal controls in which yellow rather than blue light was delivered (Figure 5K–M). Thus, activation of SF1+ neurons causes persistent defensive responses in a variety of behavioral assays, suggesting that it engenders an associated internal defensive state. Consistent with this idea, optogenetic stimulation of these neurons produced nearly a twofold elevation in serum corticosterone (Figure 5—figure supplement 2).


Ventromedial hypothalamic neurons control a defensive emotion state.

Kunwar PS, Zelikowsky M, Remedios R, Cai H, Yilmaz M, Meister M, Anderson DJ - Elife (2015)

Activation of SF1+ neurons produces an increase in neuroendocrine responding.(A) Illustration of testing for stimulation induced changes in corticosterone. (B) Optogenetic stimulation of SF1+ neurons increases serum corticosterone levels in ChR2 mice compared to eYFP controls. n = 11–12 animals for each condition.DOI:http://dx.doi.org/10.7554/eLife.06633.015
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4379496&req=5

fig5s2: Activation of SF1+ neurons produces an increase in neuroendocrine responding.(A) Illustration of testing for stimulation induced changes in corticosterone. (B) Optogenetic stimulation of SF1+ neurons increases serum corticosterone levels in ChR2 mice compared to eYFP controls. n = 11–12 animals for each condition.DOI:http://dx.doi.org/10.7554/eLife.06633.015
Mentions: We also investigated whether transient activation of SF1+ neurons caused a persistent inhibitory influence on appetitive behavior, by testing whether it increased the latency to re-initiate mating, following its interruption (Figure 5J). We observed significantly longer latencies for ChR2 mice to re-initiate mating after SF1+ neurons were activated, compared to interleaved internal controls in which yellow rather than blue light was delivered (Figure 5K–M). Thus, activation of SF1+ neurons causes persistent defensive responses in a variety of behavioral assays, suggesting that it engenders an associated internal defensive state. Consistent with this idea, optogenetic stimulation of these neurons produced nearly a twofold elevation in serum corticosterone (Figure 5—figure supplement 2).

Bottom Line: The hypothalamus plays a role in such behaviors, but prevailing textbook views depict it as an effector of upstream emotion centers, such as the amygdala, rather than as an emotion center itself.Importantly, these neurons can also condition learned defensive behavior, further refuting long-standing claims that the hypothalamus is unable to support emotional learning and therefore is not an emotion center.These data indicate that the hypothalamus plays an integral role to instantiate emotion states, and is not simply a passive effector of upstream emotion centers.

View Article: PubMed Central - PubMed

Affiliation: Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, United States.

ABSTRACT
Defensive behaviors reflect underlying emotion states, such as fear. The hypothalamus plays a role in such behaviors, but prevailing textbook views depict it as an effector of upstream emotion centers, such as the amygdala, rather than as an emotion center itself. We used optogenetic manipulations to probe the function of a specific hypothalamic cell type that mediates innate defensive responses. These neurons are sufficient to drive multiple defensive actions, and required for defensive behaviors in diverse contexts. The behavioral consequences of activating these neurons, moreover, exhibit properties characteristic of emotion states in general, including scalability, (negative) valence, generalization and persistence. Importantly, these neurons can also condition learned defensive behavior, further refuting long-standing claims that the hypothalamus is unable to support emotional learning and therefore is not an emotion center. These data indicate that the hypothalamus plays an integral role to instantiate emotion states, and is not simply a passive effector of upstream emotion centers.

Show MeSH