Quantitation of nerve terminal populations: Synaptic vesicle‐associated proteins as markers for synaptic density in the rat neostriatum

Walaas, S. Ivar; Jahn, Reinhard; Greengard, Paul

doi:10.1002/syn.890020507

Cited by 86 publications

(34 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…To determine the spatial relationship between nerve endings and TNF-producing macrophages in spleen, we looked for the distribution pattern of the presynaptic vesicleassociated protein synaptophysin, a synaptic vesicle protein (24,25). Synaptophysin punctae were distributed in networks in the parenchyma of the white pulp and around the central artery.…”

Section: Nerve Terminals In the Spleen Are Found Adjacent To Tnf-prodmentioning

confidence: 99%

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

Rosas-Ballina¹,

Ochani²,

Parrish³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

621

569

View full text Add to dashboard Cite

The autonomic nervous system maintains homeostasis through its sympathetic and parasympathetic divisions. During infection, cells of the immune system release cytokines and other mediators that cause fever, hypotension, and tissue injury. Although the effect of cytokines on the nervous system has been known for decades, only recently has it become evident that the autonomic nervous system, in turn, regulates cytokine production through neural pathways. We have previously shown that efferent vagus nerve signals regulate cytokine production through the nicotinic acetylcholine receptor subunit ␣7, a mechanism termed ''the cholinergic antiinflammatory pathway.'' Here, we show that vagus nerve stimulation during endotoxemia specifically attenuates TNF production by spleen macrophages in the red pulp and the marginal zone. Administration of nicotine, a pharmacological agonist of ␣7, attenuated TNF immunoreactivity in these specific macrophage subpopulations. Synaptophysin-positive nerve endings were observed in close apposition to red pulp macrophages, but they do not express choline acetyltransferase or vesicular acetylcholine transporter. Surgical ablation of the splenic nerve and catecholamine depletion by reserpine indicate that these nerves are catecholaminergic and are required for functional inhibition of TNF production by vagus nerve stimulation. Thus, the cholinergic antiinflammatory pathway regulates TNF production in discrete macrophage populations via two serially connected neurons: one preganglionic, originating in the dorsal motor nucleus of the vagus nerve, and the second postganglionic, originating in the celiacsuperior mesenteric plexus, and projecting in the splenic nerve.brain ͉ cytokine ͉ innate ͉ spleen ͉ vagus T he autonomic nervous system is divided into two major branches based on anatomy and function. These divisions, sympathetic and parasympathetic, control organ function through a set of two serially connected neurons, the first of which is located in the CNS and the second in the peripheral ganglia. Typically, parasympathetic neurons originate in the brainstem medulla and sacral portion of the spinal cord, and the ganglia are located close to or within the innervated organ. Sympathetic neurons originate in the thoracic and lumbar portion of the spinal cord, and the ganglia are situated close to the spinal cord.

show abstract

Section: Nerve Terminals In the Spleen Are Found Adjacent To Tnf-prodmentioning

confidence: 99%

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

Rosas-Ballina¹,

Ochani²,

Parrish³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

621

569

View full text Add to dashboard Cite

show abstract

“…In the present study we found no changes in expression of the mRNA for synaptophysin in animals with a flattened corticosterone rhythm. SynaptophysinFa synaptic protein with roles in vesicle biogenesis and fusion (Elferink and Scheller, 1995)Fis a wellestablished synaptic marker (Walaas et al, 1988;Eastwood and Harrison, 1995). Furthermore, it has been shown that synaptophysin protein correlates well with synaptic number when this is measured by morphometric methods (McEwen et al, 1999;Brake et al, 2001), and also that synaptophsyin mRNA correlates with synaptophysin protein levels (see Eastwood and Harrison, 1995).…”

Section: Corticosterone-induced Changes In Hippocampal Expression Of mentioning

confidence: 99%

Flattening the Glucocorticoid Rhythm causes Changes in Hippocampal Expression of Messenger RNAs Coding Structural and Functional Proteins: Implications for Aging and Depression

Gartside

Leitch

McQuade

et al. 2002

Neuropsychopharmacol

View full text Add to dashboard Cite

Subtle changes in glucocorticoid levels, including a flattening of the diurnal rhythm with raised nadir, are prevalent, being characteristic of both aging and major depression. Both these conditions are also associated with deficits in hippocampally mediated cognitive functions. We hypothesized that this profile of glucocorticoid levels causes structural and functional changes in the hippocampus, which in turn may engender cognitive deficits. We implanted slow-release corticosterone pellets into adrenally intact adult male rats to produce a flattened glucocorticoid rhythm with levels clamped midway between the normal nadir and zenith. Using density profile analysis we measured hippocampal expression of messenger RNAs encoding structural and functional proteins. In rats with a flattened glucocorticoid rhythm, the expression of the mRNA coding for microtubule associated protein-2b (MAP2b) was reduced in CA3 relative to sham-operated controls, but unchanged in dentate gyrus and CA1. In contrast, the expression of the mRNA coding the alpha subunit of calciumcalmodulin dependent kinase (CAMKIIa) was reduced in dentate gyrus in animals with a flattened glucocorticoid rhythm, but unchanged in CA3. The expression of the mRNA coding the synaptic vesicle protein synaptophysin was unchanged in both CA3 and dentate gyrus. The data indicate that a flattening of the normal diurnal glucocorticoid rhythm decreases the hippocampal expression of mRNAs coding key structural and functional proteins, and does so in a regionally selective manner. The data may have relevance for cognitive deficits characteristic of aging and depression.

show abstract

“…The homo-oligomeric protein is a major calcium-binding component of synaptic vesicles [ 18] and it seems to play a crucial role in vesicular uptake and release of secondary compounds at the synap ses [19]. Therefore, immunostaining with monoclonal an tibodies against synaptophysin has been used to investi gate synapse formation during ontogenesis [20] and to quantify nerve terminal populations [21,22].…”

mentioning

confidence: 99%

MAP2, Synaptophysin Immunostaining in Rat Brain and Behavioral Modifications after Cerebral Postischemic Reperfusion

Martinez¹,

Giacomo

Carnazza³

et al. 1997

Dev Neurosci

View full text Add to dashboard Cite

Plasticity in the central nervous system after cerebral ischemia is a controversial issue; focal cerebral ischemia produces an area of infarction that is surrounded by neurons that may respond to nearby damage by creating new synapses. In the present study the expression of the postsynaptic microtubule-associated protein 2 (MAP2) and the presynaptic marker protein, synaptophysin, was investigated by immunocytochemical techniques in the CA1 sector of hippocampus and in cerebellum of rats made ischemic by bilateral clamping of common carotid arteries and reperfused for 7 and 30 days. In addition, ischemia-induced behavioral alterations were also evaluated after 7 and 30 days of reperfusion. The present study demonstrates a decreased postsynaptic MAP2 immunoreactivity, representative of neuronal loss, particularly in CA1 sector of hippocampus and in cerebellum of ischemic rats reperfused for 7 days. After 30 days of reperfusion, MAP2 immunostaining was similar to control. In the same brain sections an increased presynaptic synaptophysin immunoreactivity has been observed only after 30 days of reperfusion. These data suggest compensatory regenerative changes associated with synaptic remodelling and are supported by behavioral recovery observed under the same experimental conditions.

show abstract

Quantitation of nerve terminal populations: Synaptic vesicle‐associated proteins as markers for synaptic density in the rat neostriatum

Cited by 86 publications

References 50 publications

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia

Flattening the Glucocorticoid Rhythm causes Changes in Hippocampal Expression of Messenger RNAs Coding Structural and Functional Proteins: Implications for Aging and Depression

MAP2, Synaptophysin Immunostaining in Rat Brain and Behavioral Modifications after Cerebral Postischemic Reperfusion

Contact Info

Product

Resources

About