Faculty Opinions recommendation of A single vesicular glutamate transporter is sufficient to fill a synaptic vesicle.

2006 ◽  
Author(s):  
Volker Haucke
Keyword(s):  
Synaptic Vesicle ◽  
Glutamate Transporter ◽  
Vesicular Glutamate Transporter

scholarly journals A Single Vesicular Glutamate Transporter Is Sufficient to Fill a Synaptic Vesicle

Neuron ◽  
2006 ◽  
Vol 49 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Richard W. Daniels ◽  
Catherine A. Collins ◽  
Kaiyun Chen ◽  
Maria V. Gelfand ◽  
David E. Featherstone ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Glutamate Transporter ◽  
Vesicular Glutamate Transporter

A role for vesicular glutamate transporter 1 in synaptic vesicle clustering and mobility

2013 ◽  
Vol 37 (10) ◽  
pp. 1631-1642 ◽  
Author(s):  
Léa Siksou ◽  
Kätlin Silm ◽  
Christoph Biesemann ◽  
Ralf B. Nehring ◽  
Sonja M. Wojcik ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Glutamate Transporter ◽  
Vesicular Glutamate Transporter ◽  
Glutamate Transporter 1

scholarly journals Synaptic Vesicle Protein 2A Expression in Glutamatergic Terminals Is Associated with the Response to Levetiracetam Treatment

2021 ◽  
Vol 11 (5) ◽  
pp. 531
Author(s):  
Itzel Jatziri Contreras-García ◽  
Gisela Gómez-Lira ◽  
Bryan Víctor Phillips-Farfán ◽  
Luz Adriana Pichardo-Macías ◽  
Mercedes Edna García-Cruz ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Glutamate Transporter ◽  
Critical Factor ◽  
Saline Control ◽  
Vesicular Glutamate Transporter ◽  
Seizure Reduction ◽  
Synaptic Vesicle Protein ◽  
Vesicle Protein ◽  
Animal Models Of Epilepsy ◽  
Synaptic Vesicle Protein 2A

Synaptic vesicle protein 2A (SV2A), the target of the antiepileptic drug levetiracetam (LEV), is expressed ubiquitously in all synaptic terminals. Its levels decrease in patients and animal models of epilepsy. Thus, changes in SV2A expression could be a critical factor in the response to LEV. Epilepsy is characterized by an imbalance between excitation and inhibition, hence SV2A levels in particular terminals could also influence the LEV response. SV2A expression was analyzed in the epileptic hippocampus of rats which responded or not to LEV, to clarify if changes in SV2A alone or together with glutamatergic or GABAergic markers may predict LEV resistance. Wistar rats were administered saline (control) or pilocarpine to induce epilepsy. These groups were subdivided into untreated or LEV-treated groups. All epileptic rats were video-monitored to assess their number of seizures. Epileptic rats with an important seizure reduction (>50%) were classified as responders. SV2A, vesicular γ-aminobutyric acid transporter and vesicular glutamate transporter (VGLUT) expression were assessed by immunostaining. SV2A expression was not modified during epilepsy. However, responders showed ≈55% SV2A-VGLUT co-expression in comparison with the non-responder group (≈40%). Thus, SV2A expression in glutamatergic terminals may be important for the response to LEV treatment.

scholarly journals Activity-Dependent Modulation of Neurotransmitter Innervation to Vasopressin Neurons of the Supraoptic Nucleus

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 348-354 ◽  
Author(s):  
Nancy K. Mueller ◽  
Shi Di ◽  
Charles M. Paden ◽  
James P. Herman
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Supraoptic Nucleus ◽  
Glutamate Transporter ◽  
Acid Decarboxylase ◽  
Vesicular Glutamate Transporter ◽  
Salt Loading ◽  
Synaptic Boutons ◽  
Vasopressin Neurons ◽  
Activity Dependent

Confocal microscopy was used to assess activity-dependent neuroplasticity in neurotransmitter innervation of vasopressin immunoreactive magnocellular neurons in the supraoptic nucleus (SON). Vesicular glutamate transporter 2, glutamic acid decarboxylase, and dopamine β-hydroxylase (DBH) synaptic boutons were visualized in apposition to vasopressin neurons in the SON. A decrease in DBH synaptic boutons per cell was seen upon salt loading, indicating diminished noradrenergic/adrenergic innervation. Loss of DBH appositions to vasopressin neurons was associated with a general loss of DBH immunoreactivity in the SON. In contrast, the number of vesicular glutamate transporter 2 synaptic boutons per neuron increased with salt loading, consistent with increased glutamatergic drive of magnocellular SON neurons. Salt loading also caused an increase in the total number of glutamic acid decarboxylase synaptic boutons on vasopressinergic neurons, suggesting enhanced inhibitory innervation as well. These studies indicate that synaptic plasticity compensates for increased secretory demand and may indeed underlie increased secretion, perhaps via neurotransmitter-specific, activity-related changes in synaptic contacts on vasopressinergic magnocellular neurons in the SON.

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