Q2. What are the contributions in "Altered medial temporal activation related to local glutamate levels in subjects with prodromal signs of psychosis" ?
This study provides the first evidence that links medial temporal dysfunction with the central glutamate system in humans and is consistent with evidence that drugs that modulate glutamatergic transmission might be useful in the treatment of psychosis.
Q3. What are the two fundamental pathophysiological features of psychosis?
Background: Both medial temporal cortical dysfunction and perturbed glutamatergic neurotransmission are regarded as fundamental pathophysiological features of psychosis.
Q4. What tests were used to assess the effect of potential outliers and influential cases?
Cook’s distance test and leverage plot were used to assess the effect of potential outliers and influential cases (details of imaging procedures and data analysis in online supplementary Methods).
Q5. What is the link between the medial temporal cortex and local glutamate levels?
N-methyl-D-aspartate glutamate (NMDA) receptor antagonists, such as ketamine, induce acute psychotic symptoms and impair memory performance (4), and psychotic disorders are associated with increased glutamine in the anterior cingulate cortex and thalamus (5), and a reduction in activated hippocampal NMDA receptor density (6) and NMDA receptor subunit mRNA (7).
Q6. What is the main reason why the present study included glutamine?
Due to the partial overlap of glutamate and glutamine resonances at 3T, glutamate levels in the present study may thus include a contribution from glutamine.
Q7. What was the correlation between the ARMS and the IQ?
In controls, activation in this cluster during encoding was positively correlated with left medial temporal glutamate levels (r=0.592, df=12, p=0.026) (Fig 1), whereas there was a negative correlation in the ARMS subjects (r=-0.447, df=20, p=0.037).
Q8. How did the authors study the relationship between medial temporal activation and local glutamate levels?
The authors used a combination of functional MRI (fMRI) and MR spectroscopy (MRS) to investigate the relationship between medial temporal activation during an episodic memory task and local glutamate levels in 22 individuals with an At Risk Mental State for psychosis and 14 healthy volunteers.
Q9. What is the relationship between glutamate levels and the thalamus?
These results suggest that medial temporal dysfunction in people with prodromal symptoms of psychosis is related to a loss of the normal relationship between function in this region and local glutamate levels.
Q10. What is the first evidence that links medial temporal dysfunction with the central glutamate system?
This study provides the first evidence that links medial temporal dysfunction with the central glutamate system in humans, and is consistent with evidence that drugs that modulate glutamatergic transmission may be useful in the treatment of psychosis.
Q11. What is the NMDA receptor hypofunction in schizophrenia?
4. Newcomer JW, Farber NB, Jevtovic-Todorovic V, Selke G, Melson AK, Hershey T, et al. (1999): Ketamine-induced NMDA receptor hypofunction as a model of memory impairment and psychosis.
Q12. What is the link between the medial temporal cortex and the local glutamate levels?
Animal models of psychosis and circuit analyses suggest that glutamatergic and medial temporal abnormalities are inter-related, with medial temporal cortex considered critical for the memory impairments observed after NMDA antagonists administration and in psychosis (8).
Q13. Why were two of the control subjects excluded?
However two of the control subjects were subsequently excluded, due to the poor quality of their MRS data in the hippocampal region.