Differential expression of SNAP-25a and SNAP-25b RNA transcripts in cranial nerve nuclei

Jacobsson, Gunilla; Bark, Christina; Meister, Björn

doi:10.1002/(sici)1096-9861(19990906)411:4<591::aid-cne5>3.0.co;2-0

Cited by 12 publications

(9 citation statements)

References 40 publications

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“…While our results demonstrating the predominant expression of SNAP-25b isoform transcripts among neuronal populations of the adult mouse brain agree with a general shift in alternative splicing accompanying neuronal maturation [ 15 ], we were surprised to find no evidence for the differential expression of the two isoforms that has been observed previously between other regions of the CNS [ 15 , 16 , 19 - 21 ]. Among the brain regions we sampled, the prevalence of SNAP-25a transcripts was remarkably consistent (averaging 9.8% ± 1.7%, S.D.…”

Section: Discussionsupporting

confidence: 68%

The role of the t-SNARE SNAP-25 in action potential-dependent calcium signaling and expression in GABAergic and glutamatergic neurons

et al. 2008

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Background: The soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex, comprised of SNAP-25, syntaxin 1A, and VAMP-2, has been shown to be responsible for action potential (AP)-dependent, calcium-triggered release of several neurotransmitters. However, this basic fusogenic protein complex may be further specialized to suit the requirements for different neurotransmitter systems, as exemplified by neurons and neuroendocrine cells. In this study, we investigate the effects of SNAP-25 ablation on spontaneous neuronal activity and the expression of functionally distinct isoforms of this t-SNARE in GABAergic and glutamatergic neurons of the adult brain.

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Section: Discussionsupporting

confidence: 68%

The role of the t-SNARE SNAP-25 in action potential-dependent calcium signaling and expression in GABAergic and glutamatergic neurons

et al. 2008

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“…Certain brain and spinal cord nuclei in adult rodents continue to express predominantly SNAP-25a into adulthood (Bark et al, 1995;Boschert et al, 1996;Jacobsson et al, 1999), although its selective function remains unclear. Nevertheless, the behavioral affect of seizures and premature death seen in these mutant mice suggests that generalized maintenance of SNAP-25a expression might disrupt normal brain function.…”

Section: Discussionmentioning

confidence: 99%

“…This results in a developmental switch between 1 and 3 weeks of age from expression of predominately SNAP-25a to SNAP-25b transcripts that ultimately constitute Ͼ80% of SNAP-25 mRNA in adult mouse brain (Bark et al, 1995;Boschert et al, 1996;Jacobsson et al, 1999). In contrast, SNAP-25a remains the predominant isoform in adult neuroendocrine cells (Bark et al, 1995;Gonelle-Gispert et al, 1999;Grant et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Developmentally Regulated Switch in Alternatively Spliced SNAP-25 Isoforms Alters Facilitation of Synaptic Transmission

Bark¹,

Bellinger²,

Kaushal³

et al. 2004

J. Neurosci.

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Although the basic molecular components that promote regulated neurotransmitter release are well established, the contribution of these proteins as regulators of the plasticity of neurotransmission and refinement of synaptic connectivity during development is elaborated less fully. For example, during the period of synaptic growth and maturation in brain, the expression of synaptosomal protein 25 kDa (SNAP-25), a neuronal t-SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) essential for action potentialdependent neuroexocytosis, is altered through alternative splicing of pre-mRNA transcripts. We addressed the role of the two splicevariant isoforms of SNAP-25 with a targeted mouse mutation that impairs the shift from SNAP-25a to SNAP-25b. Most of these mutant mice die between 3 and 5 weeks of age, which coincides with the time when SNAP-25b expression normally reaches mature levels in brain and synapse formation is essentially completed. The altered expression of these SNAP-25 isoforms influences short-term synaptic function by affecting facilitation but not the initial probability of release. This suggests that mechanisms controlling alternative splicing between SNAP-25 isoforms contribute to a molecular switch important for survival that helps to guide the transition from immature to mature synaptic connections, as well as synapse regrowth and remodeling after neural injury.

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“…Despite compelling evidence for the involvement of these synaptic proteins in transmitter release, there are several indications that they may not be expressed uniformly in all populations of neurons (Bark et al, 1995; Jacobsson et al, 1999; Safieddine and Wenthold, 1999; von Kriegstein et al, 1999; Hellstrom et al, 1999; Morris et al, 2000; Greenlee et al, 2001). There also is variation in expression of SNARE proteins at different presynaptic domains of the same nerve terminal that is positively correlated with variation in the probability of transmitter release (Macleod et al, 1998, 1999).…”

mentioning

confidence: 99%

Heterogeneous expression of SNAP‐25 and synaptic vesicle proteins by central and peripheral inputs to sympathetic neurons

Gibbins

Jobling

Teo

et al. 2003

J of Comparative Neurology

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Neurons in prevertebral sympathetic ganglia receive convergent synaptic inputs from peripheral enteric neurons in addition to inputs from spinal preganglionic neurons. Although all inputs are functionally cholinergic, inputs from these two sources have distinctive neurochemical and functional profiles. We used multiple-labeling immunofluorescence, quantitative confocal microscopy, ultrastructural immunocytochemistry, and intracellular electrophysiologic recordings to examine whether populations of inputs to the guinea pig coeliac ganglion express different levels of synaptic proteins that could influence synaptic strength. Boutons of enteric intestinofugal inputs, identified by immunoreactivity to vasoactive intestinal peptide, showed considerable heterogeneity in their immunoreactivity to synaptosome-associated protein of 25 kDa (SNAP-25), synapsin, synaptophysin, choline acetyltransferase, and vesicular acetylcholine transporter. Mean levels of immunoreactivity to these proteins were significantly lower in terminals of intestinofugal inputs compared with terminals of spinal preganglionic inputs. Nevertheless, many boutons with undetectable levels of SNAP-25 immunoreactivity formed morphologically normal synapses with target neurons. Treatment with botulinum neurotoxin type A (20-50 nM for 2 hours in vitro) generated significant cleavage of SNAP-25 and produced similar dose- and time-dependent inhibitions of synaptic transmission from all classes of inputs, regardless of their mean level of SNAP-25 expression. The simplest interpretation of these results is that only synaptic boutons with detectable levels of SNAP-25 immunoreactivity contribute significantly to fast cholinergic transmission. Consequently, the low synaptic strength of intestinofugal inputs to final motor neurons in sympathetic pathways may be due in part to the low proportion of their boutons that express SNAP-25 and other synaptic proteins.

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Differential expression of SNAP-25a and SNAP-25b RNA transcripts in cranial nerve nuclei

Cited by 12 publications

References 40 publications

The role of the t-SNARE SNAP-25 in action potential-dependent calcium signaling and expression in GABAergic and glutamatergic neurons

The role of the t-SNARE SNAP-25 in action potential-dependent calcium signaling and expression in GABAergic and glutamatergic neurons

Developmentally Regulated Switch in Alternatively Spliced SNAP-25 Isoforms Alters Facilitation of Synaptic Transmission

Heterogeneous expression of SNAP‐25 and synaptic vesicle proteins by central and peripheral inputs to sympathetic neurons

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