Glutamate and its role in psychiatric illness

Belsham, Brendan

doi:10.1002/hup.279.abs

Cited by 3 publications

(4 citation statements)

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“…Nöronlara ek olarak, astrositler glutamat prekürsörü olan glutamin için ana kaynaklardır (Dwivedi ve Pandey 2011). Sentezlenen glutamat vesiküler glutamat taşıyıcı ailesi (VGLUT1-3) tarafından sinaptik aralığa salınmak için veziküllere alınmaktadır (Belsham 2001, Dwivedi ve Pandey 2011, Shan ve ark. 2013, Hammond ve ark.…”

Section: Glutamat Nörotransmisyonu (İletimi)unclassified

“…Uyarıcı aminoasit sistemleri çeşitli dokularda nöronal gelişimi uyarma veya inhibe etme potansiyeline sahiptir. Bu nedenle, gelişim aşamalarında bu sistemler nöronal plastisite oluşumunda yeterli nöronal bağlantıların oluşumunda önemlidir (Belsham 2001, Tamminga ve ark. 2012.…”

Section: Glutamat Ve Fonksiyonlarıunclassified

“…Şizofrenide glutamat hipotezi beyin omirilik sıvısında glutamat düzeylerinin azalmasına, ve şizofreni hastalarında hipokampus ve talamusta NMDA, AMPA reseptör expresyonlarının azalmasına dayanır (Fatemi 2008). Bu hipotez başlangıçta yazarlar tarafından çok destek görmese de daha sonra bu teoriyi destekleyen birçok kanıt ortaya çıkmıştır (Ceylan ve Taşçı 1999, Belsham 2001, Gargiula ve Landa De Gargiulo 2014, Howes ve ark. 2015.…”

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Glutamat Sistemi ve Şizofreni

Özdemir¹,

Özdemir²

2016

Psikiyatride Guncel Yaklasimlar - Current Approaches in Psychiatry

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ÖzGlutamat santral sinir sisteminin ana uyarıcı nörotransmitteridir. Glutamat öğrenme, bellek ve algı gibi birçok bilişsel fonksiyonlarda görev alır. Glutamat beyin gelişiminde, nöronal göçte, nöronal farklılaşmada, akson oluşumunda ve nöronal yaşamında önemli görev almaktadır. Glutamat birçok nörodejeneratif hastalıkta görülen eksitotoksisite ile ilişkilendirilmektedir. Şizofreni patogenezinde glutamat disfonksiyonun katkısı olduğunu düşündüren birçok kanıt bulunmaktadır. Fensiklidin ve ketamin gibi NMDA reseptör antagonistleri sağlıklı gönüllülerde hem pozitif hem de negatif belirtilere neden olabilmektedir. Ayrıca bu moleküller şizofreni hastalarında belirtileri arttırmaktadır. Bu nedenle şizofreninin N-metil-D-aspartat (NMDA) reseptör hipofonksiyonu ile ilişkili olduğu öne sürülmüştür. Bu hipoteze göre NMDA reseptör hipofonksiyonu glutamat nöronları üzerindeki inhibisyonun azalmasına ve aşırı glutamat salınımına yol açmaktadır. Sonuçta, şizofreni hastaların-da birçok beyin bölgesinde görülen hacim azalmasının NMDA reseptör aracılı glutamat nörotoksisi-tesi ile ilişkili olduğu düşünülmektedir. AbstractGlutamate is the major excitatory neurotransmitter in the brain. It has a role several cognitive functions including learning, memory and perception. Glutamatergic neurotransmission is also involved in regulating neuronal migration, synaptogenesis, and the pruning neurons. Glutamatergic excitotoxicity has been implicated in various neuropsychiatric disorders. Accumulating evidence suggests that glutamatergic dysfunction may contribute to the pathogenesis of schizophrenia. The N-methyl-D-aspartic acid (NMDA) receptor antagonists such as phencyclidine and ketamine can cause both the positive and negative symptoms psychotic symptoms in normal humans, and worsen these symptoms in persons with schizophrenia. Hence, it has been hypotesized that schizophrenia may be associated with decreased NMDA-receptor activity. According to the hypothesis, NMDA reseptor hypofunction can lead to decreased inhibition of glutamatergic neurons and excessive glutamate release. Finally, the reduction of gray matter in several brain regions seen in patients with schizophrenia has been suggested to be the result of neurotoxicity mediated by NMDA receptors.

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Section: Glutamat Nörotransmisyonu (İletimi)unclassified

Section: Glutamat Ve Fonksiyonlarıunclassified

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Glutamat Sistemi ve Şizofreni

Özdemir¹,

Özdemir²

2016

Psikiyatride Guncel Yaklasimlar - Current Approaches in Psychiatry

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“…Also, glutamate plays a vital role in neuronal differentiation and migration. So, theoretically, anxiety is also biologically linked to essential parts of life (Belsham, 2001).…”

Section: Adjustment Versus Death Anxietymentioning

confidence: 99%

Concepts of Death: A Key to Our Adjustment

Hossain¹,

Gilbert

2010

Illness, Crisis & Loss

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Although death is the inevitable end of life, historical, sociological, and psychological analyses converge to demonstrate that human beings struggle to integrate it as a personal reality. In this article we attempt to bring to bear recent theoretical work on the linkage between our conceptions of death, and our difficulty adjusting to it as a species, by first surveying historical and philosophic perspectives on the meaning of death, and then sampling some of the broad field of psychological research on death attitudes in a variety of cultures and subcultures. Finally, we advance an argument that a fuller understanding of death as a phenomenon could mitigate the pervasive contemporary tendency toward its denial, and promote better adjustment to this ultimate reality, on both personal and societal levels.

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SYNGAP1: Mind the Gap

Jeyabalan

Clement

2016

Front. Cell. Neurosci.

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A cardinal feature of early stages of human brain development centers on the sensory, cognitive, and emotional experiences that shape neuronal-circuit formation and refinement. Consequently, alterations in these processes account for many psychiatric and neurodevelopmental disorders. Neurodevelopment disorders affect 3–4% of the world population. The impact of these disorders presents a major challenge to clinicians, geneticists, and neuroscientists. Mutations that cause neurodevelopmental disorders are commonly found in genes encoding proteins that regulate synaptic function. Investigation of the underlying mechanisms using gain or loss of function approaches has revealed alterations in dendritic spine structure, function, and plasticity, consequently modulating the neuronal circuit formation and thereby raising the possibility of neurodevelopmental disorders resulting from synaptopathies. One such gene, SYNGAP1 (Synaptic Ras-GTPase-activating protein) has been shown to cause Intellectual Disability (ID) with comorbid Autism Spectrum Disorder (ASD) and epilepsy in children. SYNGAP1 is a negative regulator of Ras, Rap and of AMPA receptor trafficking to the postsynaptic membrane, thereby regulating not only synaptic plasticity, but also neuronal homeostasis. Recent studies on the neurophysiology of SYNGAP1, using Syngap1 mouse models, have provided deeper insights into how downstream signaling proteins and synaptic plasticity are regulated by SYNGAP1. This knowledge has led to a better understanding of the function of SYNGAP1 and suggests a potential target during critical period of development when the brain is more susceptible to therapeutic intervention.

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Glutamate and its role in psychiatric illness

Cited by 3 publications

References 0 publications

Glutamat Sistemi ve Şizofreni

Glutamat Sistemi ve Şizofreni

Concepts of Death: A Key to Our Adjustment

SYNGAP1: Mind the Gap

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