Mice were intraperitoneally injected with the hallucinogens DOI (2 mg/kg) and LSD (0.24 mg/kg), or vehicle.

I have a specific question that's been on my mind for a little while.

It has been established in most of psychedelic scientific literature (that i know of) that the 5ht2a receptor pathways are crucial in psychedelic effects.

From what i understand it is vital for Cerebrum and Cerebellum interaction. 5ht2a exceeds a lot of it's effects in the bridge of Varolius. It is also the main excitatory receptor subtype among the GPCRs for serotonin.

Now the "myth" i'm talking about is that 5ht2a activity is absolutely crucial for psychedelic hallucinations. AFAIK the only basis for this claim is that is has been tested on labaratory rats. In rats where 5ht2a receptors are removed and drugs are administered they do not show the "tell-tale" signs for being under the influence of a psychedelic.

I forgot what these signs are but i thought they consist (again AFAIK) of motor function and disorientation. Since the cerebellum is mostly used for motor function and the rat has no way of saying it is hallucinating like crazy isn't is so that this receptor plays a role in motor function. And these tests say nothing about actual hallucinations?

Sorry if i seem ignorant, cuz i really am ignorant. It's just that i want to be absolutely sure of the facts and don't get stuck at some point because my knowledge is of limited understanding and some of the things i thought i knew are simply not true.

Now the "myth" i'm talking about is that 5ht2a activity is absolutely crucial for psychedelic hallucinations. AFAIK the only basis for this claim is that is has been tested on labaratory rats.

Neuropsychopharmacology. 2005 Nov 2;
Hallucinogen-Induced UP States in the Brain Slice of Rat Prefrontal Cortex: Role of Glutamate Spillover and NR2B-NMDA Receptors.

Lambe EK, Aghajanian GK.

Department of Psychiatry, Yale School of Medicine, New Haven, CT, USA.

Psychedelic hallucinogens (eg LSD or DOI) induce disturbances of mood, perception, and cognition through stimulation of serotonin 5-HT(2A) receptors. While these drugs are not proconvulsant, they have been shown by microdialysis to increase extracellular glutamate in the prefrontal cortex. Electrophysiological studies in the rat prefrontal slice have shown that both LSD and DOI enhance a prolonged, late wave of glutamate release onto layer V pyramidal neurons after an electrical stimulus. Here, we hypothesize that the network activity underlying this UP state involves glutamate spillover from excitatory synapses. To test this hypothesis, we raised the viscosity of the extracellular solution by adding the inert macromolecule dextran ( approximately 1 mM) that is known to retard glutamate overflow into the extrasynaptic space. Dextran suppressed the UP state or late excitatory postsynaptic current (EPSC), but neither the fast EPSC, the traditional polysynaptic EPSC, nor a synaptic form of 5-HT(2A)-mediated transmission (serotonin-induced spontaneous EPSCs). Consistent with the previous work showing that extrasynaptic glutamate transmission in adult depends on NR2B-containing NMDA receptors, we found that NR2B-selective antagonists, ifenprodil and Ro25-6981, also suppressed the late EPSCs. The effect of psychedelic hallucinogens on UP states could be partially mimicked by inhibiting glutamate uptake but only after blocking inhibitory group II metabotropic glutamate receptors. This difference suggests that hallucinogens increase glutamate spillover in a phasic manner unlike glutamate uptake inhibitors. Increases in glutamate spillover have been suggested to recruit synapses not directly in the pathway activated by the electrical stimulus. Such recruitment could account for certain cognitive, affective, and sensory perturbations generated by psychedelic hallucinogens.Neuropsychopharmacology advance online publication, 2 November 2005; doi:10.1038/sj.npp.1300944.

I forgot what these signs are but i thought they consist (again AFAIK) of motor function and disorientation. Since the cerebellum is mostly used for motor function and the rat has no way of saying it is hallucinating like crazy isn't is so that this receptor plays a role in motor function. And these tests say nothing about actual hallucinations?

But i theorize that had they given the poor cat an mGluR2 antagonist before they spoonfed him a giant dose of LSD the cat woulden't be twitching it's muscles as much..

an ACh antagonist (ex. benztropine mesylate) would be more direct and effective.