Large Structural Change in Isolated Synaptic Vesicles upon Loading with Neurotransmitter

Budzinski, Kristi L.; Allen, Richard; Fujimoto, Bryant S.; Kensel-Hammes, Patricia; Belnap, David M.; Bajjalieh, Sandra M.; Chiu, Daniel T.

doi:10.1016/j.bpj.2009.08.032

Cited by 49 publications

(57 citation statements)

References 38 publications

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“…A complementary observation is that WD increases either vesicle number or vesicle content at IC-BLA synapses. The presence of multiple forms of vesicle fusion at central synapses (Zhang et al, 2009) and inconsistent reports about the prevalence of these different types of fusion mechanisms (Budzinski et al, 2009; Petukhov and Popov, 1986) complicate testing this hypothesis. Regardless, we show that WD increases levels of the vesicle associated proteins VAMP2 and VGlut2, but not VAMP1 or synaptotagmin (I/II).…”

Section: Discussionmentioning

confidence: 99%

Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

et al. 2013

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Amygdala glutamatergic neurotransmission regulates withdrawal induced anxiety-like behaviors following chronic ethanol exposure. The lateral/basolateral amygdala receives multiple glutamatergic projections that contribute to overall amygdala function. Our lab has previously shown that rat cortical (external capsule) afferents express postsynaptic alterations during chronic intermittent ethanol exposure and withdrawal. However, thalamic (internal capsule) afferents also provide crucial glutamatergic input during behavioral conditioning, and they have not been studied in the context of chronic drug exposure. We report here that these thalamic inputs express altered presynaptic function during withdrawal from chronic ethanol exposure. This is characterized by enhanced release probability, as exemplified by altered paired-pulse ratios and decreased failure rates of unitary events, and increased concentrations of synaptic glutamate. Quantal analysis further implicates a withdrawal-dependent enhancement of the readily-releasable pool of vesicles as a probable mechanism. These functional alterations are accompanied by increased expression of vesicle associated protein markers. These data demonstrate that chronic ethanol modulation of glutamate neurotransmission in the rat lateral/basolateral amygdala is afferent-specific. Further, presynaptic regulation of lateral/basolateral amygdala thalamic inputs by chronic ethanol may be a novel neurobiological mechanism contributing to the increased anxiety-like behaviors that characterize withdrawal.

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Section: Discussionmentioning

confidence: 99%

Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

et al. 2013

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“…SV2A −/− mice, on the other hand, exhibit early severe seizures and die within 2–3 weeks after birth (Kaminski et al, 2012). Other data from these transgenic mice demonstrated the role of SV2A in modulation of vesicular exocytosis (Xu and Bajjalieh, 2001; Budzinski et al, 2009; Chang and Sudhof, 2009; Wan et al, 2010; Yao et al, 2010; Joshi et al, 2013). Although LEV failed in classical seizure screening tests, this drug significantly inhibited the development of seizure kindling and displayed a potential antiepileptogenic effect in the chronic pilocarpine post-SE rat model (Kaminski et al, 2012).…”

Section: Introductionmentioning

confidence: 87%

Are vesicular neurotransmitter transporters potential treatment targets for temporal lobe epilepsy?

Liefferinge¹,

Massie²,

Portelli³

et al. 2013

Front. Cell. Neurosci.

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The vesicular neurotransmitter transporters (VNTs) are small proteins responsible for packing synaptic vesicles with neurotransmitters thereby determining the amount of neurotransmitter released per vesicle through fusion in both neurons and glial cells. Each transporter subtype was classically seen as a specific neuronal marker of the respective nerve cells containing that particular neurotransmitter or structurally related neurotransmitters. More recently, however, it has become apparent that common neurotransmitters can also act as co-transmitters, adding complexity to neurotransmitter release and suggesting intriguing roles for VNTs therein. We will first describe the current knowledge on vesicular glutamate transporters (VGLUT1/2/3), the vesicular excitatory amino acid transporter (VEAT), the vesicular nucleotide transporter (VNUT), vesicular monoamine transporters (VMAT1/2), the vesicular acetylcholine transporter (VAChT) and the vesicular γ-aminobutyric acid (GABA) transporter (VGAT) in the brain. We will focus on evidence regarding transgenic mice with disruptions in VNTs in different models of seizures and epilepsy. We will also describe the known alterations and reorganizations in the expression levels of these VNTs in rodent models for temporal lobe epilepsy (TLE) and in human tissue resected for epilepsy surgery. Finally, we will discuss perspectives on opportunities and challenges for VNTs as targets for possible future epilepsy therapies.

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“…The sugar moieties of SV2A define an important proportion of the vesicular proteoglycan matrix, which may hold and release transmitter by electrostatic interactions (Reigada et al ., ). This is consistent with the observation that wild‐type control SVs increased in size upon glutamate loading, whereas the size of isolated SVs from mice lacking SV2A remained the same (Budzinski et al ., ). However, SV size, number and location are similar between wild‐type mice and mice lacking SV2A (Crowder et al ., ; Janz et al ., ).…”

Section: Sv2a Functionmentioning

confidence: 97%

Synaptic vesicle protein 2A: basic facts and role in synaptic function

Mendoza-Torreblanca

Vanoye-Carlo

Phillips-Farfán

et al. 2013

Eur J of Neuroscience

103

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In recent years, there has been considerable interest in determining the function of synaptic vesicle protein 2A and its role as a target for antiepileptic drugs. Although it is known that synaptic vesicle protein 2A is involved in normal synaptic vesicle function, its participation in synaptic vesicle cycling and neurotransmitter release in normal and pathological conditions is unclear. However, the experimental evidence suggests that synaptic vesicle protein 2A could be a vesicular transporter, regulate synaptic exocytosis as a gel matrix, or modulate synaptotagmin-1 activity. This review describes and discusses the participation of synaptic vesicle protein 2A in synaptic modulation in normal and pathological conditions.

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Large Structural Change in Isolated Synaptic Vesicles upon Loading with Neurotransmitter

Cited by 49 publications

References 38 publications

Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol

Are vesicular neurotransmitter transporters potential treatment targets for temporal lobe epilepsy?

Synaptic vesicle protein 2A: basic facts and role in synaptic function

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