Changes

**Optogenetics can control the activity of a genetically defined set of neurons to see if they are important for your topic of interest. e.g. express anion-conducting channelrhodopsins (ACRs, an inhibitory type of ChR) in α1β2γ2 GABA-R expressing neurons.

**Optogenetics can control the activity of a genetically defined set of neurons to see if they are important for your topic of interest. e.g. express anion-conducting channelrhodopsins (ACRs, an inhibitory type of ChR) in α1β2γ2 GABA-R expressing neurons.

***Could we use optogenetics to clarify whether certain non-canonical propofol targets receptors (e.g. α4β2 nAChR, HCN1) are necessary or sufficient for its effects?

***Could we use optogenetics to clarify whether certain non-canonical propofol targets receptors (e.g. α4β2 nAChR, HCN1) are necessary or sufficient for its effects?

***Assuming that α1β2γ2 GABA_AR is the critical receptor, can we demonstrate which circuits play a critical role?

***Assuming that α1β2γ2 GABA_AR is the critical receptor, can we demonstrate which circuits play a critical role? As a starting point (from Brown's Part I):

## Excitatory cortical pyramidal neurons

## Excitatory cortical pyramidal neurons

## Galan-/GABA-ergic hypothalamic POA projections to monoaminergic brainstem nuclei: LC (NE), DR (5HT), vPAG (DA), TMN (His)

## Galan-/GABA-ergic hypothalamic POA projections to monoaminergic brainstem nuclei: LC (NE), DR (5HT), vPAG (DA), TMN (His)