Assignments got your hair on fire?

Douse the flames with our full-range writing service!

Experienced academic writing professionals are at your fingertips. Use this handy tool to get a price estimate for your project.

Schizophrenia Biology and Genetics

The glutamate hypothesis of schizophrenia has been developed based on the observation that psychotic symptoms induced by phencyclidine and related agents, which are antagonists at the N-methyl-D-aspartate (NMDA) glutamate receptor, closely resemble both the positive and negative symptoms of schizophrenia. In contrast to the dopamine hypothesis, which explains primarily with positive schizophrenic symptoms, the glutamate hypothesis may provide a more comprehensive view of the illness.

The original dopamine hypothesis of schizophrenia posits that psychosis is associated with a hyperactive dopamine transmission. This hypothesis has been revised through the years to account for the cognitive and negative symptoms that are increasingly recognized as the core features of schizophrenia. The critical support for this hypothesis stems from the fact that until recently it was assumed that all antipsychotic drugs block dopamine receptors; however, decades of research have failed to provide solid evidence for a primary dopaminergic disruption in schizophrenia. An alternative hypothesis, based on glutamate transmission, was developed after discovering that the psychotomimetic agent phencyclidine is an antagonist of glutamate NMDA receptors. Further clinical and basic research has provided support for the notion that various genetic and cellular susceptibility factors in schizophrenia may converge at the level of NMDA receptor dysfunction. This hypothesis predicts that a disrupted glutamatergic transmission causes the core cognitive deficits of schizophrenia and may lead to a secondary disruption in dopamine transmission that in turn causes psychosis. This hypothesis has provided novel therapeutic targets for schizophrenia that modulate glutamatergic transmission through a number of mechanisms including metabotropic and AMPA receptors and glycine modulatory site on NMDA receptors.

29/05/2012 · References

Complementary Schizophrenia Treatments

29-4-2012 · International Scholarly Research Notices Table the glutamate hypothesis of schizophrenia “NMDA receptor hypofunction model of schizophrenia.

Results from studies using NMDA antagonists have led to the development of the glutamate hypothesis of schizophrenia schizophrenia; NMDA receptor hypofunction.

Complementary Treatments, Natural Treatments Schizophrenia ..

Support for the N-methyl-d-aspartate receptor (NMDAR) hypofunction hypothesis of schizophrenia has led to increasing focus on restoring proper glutamatergic signaling.

Versatile Services that Make Studying Easy
We write effective, thought-provoking essays from scratch
We create erudite academic research papers
We champion seasoned experts for dissertations
We make it our business to construct successful business papers
What if the quality isn’t so great?
Our writers are sourced from experts, and complete an obstacle course of testing to join our brigade. Ours is a top service in the English-speaking world.
How do I know the professor won’t find out?
Everything is confidential. So you know your student paper is wholly yours, we use CopyScape and WriteCheck to guarantee originality (never TurnItIn, which professors patrol).
What if it doesn’t meet my expectations?
Unchanged instructions afford you 10 days to request edits after our agreed due date. With 94% satisfaction, we work until your hair is comfortably cool.
Clients enjoy the breezy experience of working with us
Click to learn our proven method

Causes of schizophrenia - Wikipedia


89%
of clients claim significantly improved grades thanks to our work.
98%
of students agree they have more time for other things thanks to us.
Clients Speak
“I didn’t expect I’d be thanking you for actually improving my own writing, but I am. You’re like a second professor!”