You can provoke intense FEAR responses in animals by artificially stimulating the PAG, anterior-medial hypothalamus, or anterior-medial amygdala. Low-intensity stimulation causes freezing; high-intensity stimulation causes fleeing. We know that stimulating animals in the PAG is causing them subjective distress and not just motor responses because they will strenuously avoid returning to places where they were once PAG-stimulated.
I think this is a bit misleading. Maybe this wasn’t understood when Panksepp was writing in 2004, but I think it’s clear today that we should think of PAG as kind of a “switchboard”—lots of little side-by-side cell groups that each triggers a different innate motor and/or autonomic behavior. If you stimulate one little PAG cell group, the animal will laugh; move a microscopic amount over to the next little PAG cell group, and it makes the animal flinch; move another microscopic amount over and the animal will flee, etc. [those are slightly-made-up examples, not literal, because I’m too lazy to look it up right now].
So then these old experiments where someone “stimulates PAG” would amount to basically mashing all the buttons on the switchboard at the same time. It creates some complicated mix of simultaneous reactions, depending on mutual inhibition etc. The net result for PAG turns out to be basically a fear reaction, I guess. But that’s not particularly indicative of how we should think about PAG.
Ditto for much or all of the hypothalamus, amygdala, septum, VTA, and more. Each of them has lots of little nearby cell groups that are quite different. Gross stimulation studies (as opposed to narrowly-targeted optogenetic studies) are interesting data-points, but they shouldn’t be interpreted as indicating broadly what that part of the brain does.
I think this is a bit misleading. Maybe this wasn’t understood when Panksepp was writing in 2004, but I think it’s clear today that we should think of PAG as kind of a “switchboard”—lots of little side-by-side cell groups that each triggers a different innate motor and/or autonomic behavior. If you stimulate one little PAG cell group, the animal will laugh; move a microscopic amount over to the next little PAG cell group, and it makes the animal flinch; move another microscopic amount over and the animal will flee, etc. [those are slightly-made-up examples, not literal, because I’m too lazy to look it up right now].
So then these old experiments where someone “stimulates PAG” would amount to basically mashing all the buttons on the switchboard at the same time. It creates some complicated mix of simultaneous reactions, depending on mutual inhibition etc. The net result for PAG turns out to be basically a fear reaction, I guess. But that’s not particularly indicative of how we should think about PAG.
Ditto for much or all of the hypothalamus, amygdala, septum, VTA, and more. Each of them has lots of little nearby cell groups that are quite different. Gross stimulation studies (as opposed to narrowly-targeted optogenetic studies) are interesting data-points, but they shouldn’t be interpreted as indicating broadly what that part of the brain does.