Why Shrooms Vs Acid Will Make You Question Everything
Two explanations were given for the increase in cortical glutamate after the use of the 5-HT2A agonist. The first was that glutamate was released from terminals from the central thalamus (Aghajanian and Marek, 1997; Marek and Aghajanian, 1998a; Scruggs et al., 2000).
Further evidence of such a machine was provided by Marek et al. (2001), which found that thalamus lesions in mice in rats led to a significant decrease in the frequency of 5-HT-induced EPSCs recorded from a layer of V pyramidal cells.
Autoradiographic studies
Have shown that moderate thalamic lesions lead to a significant decrease in the concentration of Shrooms Vs Acid II mGlu2 / 3 receptors in mPFC, which is associated with a loss of presynaptic glutamate terminals. Unexpectedly, however, these lesions led to an increase in the concentration of cortical 5-HT2A receptors.
- The findings
- Of which
- Would not be
- Fully consistent with
- Presynaptic 5-HT2A
- Receptor localization
A major problem with the presynaptic glutamate release hypothesis was that immunocytochemistry thegaiavoice.com revealed that most (73%) of 5-HT2A protective profiles were postsynaptic processes, particularly proximal and distal dendritic shafts, with only 24% profiles. identifies immunoreactive on.
Presynaptic properties
These latter structures do not normally form synaptic contacts in a single phase, and the 5-HT2A receptor label was not detected in the hypothetical glutamate axon terminals, found with other studies that failed to identify large numbers of 5-HT2A immunoreactive axon terminals. feature of glutamate profiles.
Interestingly, the
Remaining labeled profiles (4%) were glial processes, suggesting that perhaps activation of 5-HT2A The Gaia Voice in glial processes may also trigger the release of glutamate. These results were not in line with the hypothesis that 5-HT2A receptors may act as presynaptic heteroreceptors in the central thalamic glutamate terminals in central PFCs.
Evidence against the hypothesis
Of the release of presynaptic glutamate from thalamic glutamate terminals was provided by Puig et al. (2003), who evaluated the effect of DOI on the concentration of concentrated doses of DOI on pyramidal cells in vivo in mPFC control animals and compared the responses with those observed in electrolytic lesions of the mid- and mid-thalamus nuclei, which is a dense project in mPFC, and and a Shrooms Vs Acid other nuclei also work in mPFC.
- They found that
- DOI caused a
- Dramatic increase
- In the shooting
- Rate of
- Subpopulation of
- mPFC pyramidal
Neurons that was not affected by the previous release of the project thalamic nuclei in mPFC, and the authors concluded that DOI did not affect pyramidal cell shooting by acting on presynaptic. 5-HT2A mushroom are regulated by thalamocortical afferents in mPFC.
