Our human consciousness is a 'Controlled Hallucination' and AI can never achieve it.

I want to suggest that readers have a look at an engaging popular article by Darren Orf that summarizes the ideas of Anil Seth. Seth is a neuroscientist at the University of Sussex whose writing was on of the sources I used in preparing my most recent lecture, New Perspectives on how our Minds Work.  On the 'singularity' or point at which the intelligence of artificial minds might surpass that of human minds, Seth makes the simple point that intelligence is not the same thing as consciousness, which depends on our biological bodies (something AI simply doesn't have)  - bodies that use a bunch of controlled hallucinations to run our show. 

How ketamine breaks through anhedonia - reigniting desire

When chronic depression has not been relieved by behavioral therapies such as meditation or cognitive therapy ketamine is sometimes found to provide relief. Lucan at all probe brain changes in mice given a single expose to ketamine that rescues then from chronic stress inducted anhedonia.  Here is their summary of the paper:

Ketamine is recognized as a rapid and sustained antidepressant, particularly for major depression unresponsive to conventional treatments. Anhedonia is a common symptom of depression for which ketamine is highly efficacious, but the underlying circuits and synaptic changes are not well understood. Here, we show that the nucleus accumbens (NAc) is essential for ketamine’s effect in rescuing anhedonia in mice subjected to chronic stress. Specifically, a single exposure to ketamine rescues stress-induced decreased strength of excitatory synapses on NAc-D1 dopamine receptor-expressing medium spiny neurons (D1-MSNs). Using a cell-specific pharmacology method, we establish the necessity of this synaptic restoration for the sustained therapeutic effects of ketamine on anhedonia. Examining causal sufficiency, artificially increasing excitatory synaptic strength onto D1-MSNs recapitulates the behavioral amelioration induced by ketamine. Finally, we used opto- and chemogenetic approaches to determine the presynaptic origin of the relevant synapses, implicating monosynaptic inputs from the medial prefrontal cortex and ventral hippocampus.