Exocytosis from large dense cored vesicles outside the active synaptic zones of terminals within the trigeminal subnucleus caudalis: A possible mechanism for neuropeptide release

Zhu, Pei-Chun; Thureson‐Klein, Åsa; Klein, Richard L.

doi:10.1016/0306-4522(86)90004-7

Cited by 192 publications

(97 citation statements)

References 59 publications

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“…For these reasons rab3A could be a local targeting/controlling factor to ensure correct targeting of small synaptic vesicles to the active zone of the nerve terminal. Because large, dense-cored vesicles are targeted differentially (not to the active zone; Zhu et al, 1986;Thureson-Klein and Klein, 1990;Verhage, 1991b) and rab3A may be absent from large, dense-cored vesicles (which represents pinched off Golgi sacs), these vesicles may exploit different factors, probably other members of the tab-family.…”

Section: The Availability Of Transmitters For Releasementioning

confidence: 99%

“…Finally, the group of neuropeptides induces even slower effects. They are believed to be released distant from the active zone and at non-synaptic sites (see Zhu et al, 1986) with slow kinetics (Verhage et al, 1991a(Verhage et al, , 1992b and in minute amounts. In the case of isolated nerve terminals their release is in the order of fmoles per mg synaptosomal protein.…”

Section: Differential Transmitter Release: Co-transmission and Changementioning

confidence: 99%

“…In addition, the actual release process exhibits unique characteristics for different transmitters, especially between the group of transmitters accumulated in small synaptic vesicles and those in large, dense-cored vesicles. Small synaptic vesicles containing classical transmitters and large, dense-cored vesicles containing neuropeptides and catecholamines are differentially distributed in the nerve terminal (see Zhu et al, 1986;Verhage et al, 1991b). Small clear cored vesicles occur in clusters,…”

Section: Differential Release Of Differeni Transmittersmentioning

confidence: 99%

See 2 more Smart Citations

Presynaptic plasticity: The regulation of Ca2+-dependent transmitter release

Verhage

Ghijsen

Silva

1994

Progress in Neurobiology

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Section: The Availability Of Transmitters For Releasementioning

confidence: 99%

Section: Differential Transmitter Release: Co-transmission and Changementioning

confidence: 99%

Section: Differential Release Of Differeni Transmittersmentioning

confidence: 99%

See 1 more Smart Citation

Presynaptic plasticity: The regulation of Ca2+-dependent transmitter release

Verhage

Ghijsen

Silva

1994

Progress in Neurobiology

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“…Coexistence of substance P, in primary glutamatergic fibers, was reported in the superficial laminae of rat spinal cord (De Biasi and Rustioni, 1988) and has been suggested for the adrenocorticotropic hormone in the pigeon vestibular ganglion (Gtinttirkiin and Deviche, 1992). In addition, the presence of DCVs in the LMCEs, away from the presynaptic grid, suggests that somatostatin could be released independently from glutamate at nonspecialized areas as suggested for another system (Zhu et al, 1986) and given this disposition, it could act on adjacent synapses as shown for glycine (Faber and Korn, 1988).…”

Section: Discussionmentioning

confidence: 98%

Colocalization of somatostatin with GABA or glutamate in distinct afferent terminals presynaptic to the Mauthner cell

1994

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The presence of somatostatin in afferent fibers impinging on the goldfish Mauthner (M-) cell was determined using immunohistochemical methods, combined with confocal and electron microscopy, and the relationship of this peptide with inhibitory and excitatory terminals was studied. Somatostatin-reactive boutons were present only on the distal part of the M-cell's lateral dendrite. Somatostatin immunoreactivity was observed in typical large myelinated club endings (LMCEs) corresponding to mixed (electrical and chemical) eighth nerve primary afferent fibers. The axoplasm of these fibers contained dense- core vesicles (DCVs) dispersed among round vesicles. We have made a novel finding that the excitatory transmitter glutamate is present in LMCEs. Colocalization of this amino acid with somatostatin was detected in 75% of these endings using postembedding staining with gold particles of various sizes. The other structures labeled by somatostatin antibody were found to be small vesicle boutons (SVBs), which establish symmetrical synapses and contain a population of pleiomorphic vesicles with DCVs scattered among them. Double labeling with antibodies against glutamic acid decarboxylase and GABA allowed the definition of three types of biochemically characterized terminals: [somatostatin-GABA], [GABA], and [somatostatin]. However, the occurrence of DCVs in SVBs stained for GABA alone suggests that neuropeptides other than somatostatin may also coexist with GABA in this class of boutons. The coexistence of somatostatin with both inhibitory and excitatory neurotransmitters acting on the same region of a postsynaptic cell is discussed in relation to the role postulated for this peptide in synaptic plasticity.

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“…The dense core vesicles in unlabeled axon terminals contacting dendrites containing both CRFr and μOR are often clustered at the perimeter of the axon terminals suggesting that the receptive sites for the CRF and opioid peptide may be more complex because release may occur from dense core vesicles at extrasynaptic sites [35]. Nevertheless, unlabeled axon terminals formed symmetric or asymmetric synapse with dendritic processes containing both CRFr and μOR.…”

mentioning

confidence: 99%

Ultrastructural evidence for co-localization of corticotropin-releasing factor receptor and μ-opioid receptor in the rat nucleus locus coeruleus

Reyes

Glaser

Bockstaele

2007

Neuroscience Letters

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Previous studies have shown that corticotropin-releasing factor (CRF), an integral mediator of the stress response, and opioids regulate the activity of the locus-coeruleus-norepinephrine (LC-NE) system during stress in a reciprocal manner. Furthermore, repeated opiate exposure sensitizes noradrenergic neurons to CRF. Previous studies have shown that μORs are prominently distributed within somatodendritic processes of catecholaminergic neurons in the LC and axon terminals containing opioid peptides and CRF converge within the LC. To further examine cellular sites for interactions between CRF receptor type 1 (CRFr) and μOR, immunofluorescence and electron microscopic analysis of the rat LC was conducted. Triple immunofluorescence showed prominent co-localization of the CRFr and μOR in noradrenergic somata in the LC. Ultrastructural analysis confirmed dual localization of CRFr and μOR in common dendritic processes in the LC. Semiquantitative analysis showed that of the dendrites exhibiting CRFr immunolabeling, 57% expressed μOR immunoreactivity. These data provide ultrastructural evidence that CRFr and μOR are colocalized in LC neurons, a cellular substrate that may underlie opiate-induced sensitization of brain noradrenergic neurons to CRF. Keywordscorticotropin-releasing factor receptor 1; μ-opioid receptor; immunocytochemistry; electron microscopy Corticotropin-releasing factor (CRF), the hypothalamic neurohormone that initiates release of adrenocorticotropin in response to stress [20] also serves as a neurotransmitter that activates neurons of the noradrenergic nucleus locus coeruleus (LC). CRF administration increases the spontaneous discharge rate of LC neurons [21]. Microinfusion of CRF receptor antagonists into the LC abrogates increases in LC discharge activity elicited by both intracerebroventricularly (icv) administered CRF [6] and certain stimuli [24]. Likewise, hypotensive stress-induced activation of LC neurons is blocked by microinfusion of CRF directly into the LC [24]. Taken together, these data suggest that CRF release in the LC increases activity of noradrenergic neurons. In addition, CRF potently activates forebrain electroencephalographic (EEG) activity [7]. Consistent with physiological findings, Corresponding Author: Beverly A. S. Reyes, Ph.D., Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, PA 19107, Voice: (215) FAX: (215) 955-7921, e-mail: bsr103@jefferson.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The LC is densely innervated by process...

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Exocytosis from large dense cored vesicles outside the active synaptic zones of terminals within the trigeminal subnucleus caudalis: A possible mechanism for neuropeptide release

Cited by 192 publications

References 59 publications

Presynaptic plasticity: The regulation of Ca2+-dependent transmitter release

Presynaptic plasticity: The regulation of Ca2+-dependent transmitter release

Colocalization of somatostatin with GABA or glutamate in distinct afferent terminals presynaptic to the Mauthner cell

Ultrastructural evidence for co-localization of corticotropin-releasing factor receptor and μ-opioid receptor in the rat nucleus locus coeruleus

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