Immunocytochemical localization of glutamate decar☐ylase in rat cerebellum with a new antiserum

Oertel, WH; Schmechel, D. E.; Mugnaini, Enrico; Tappaz, Marcel; Ij, Kopin

doi:10.1016/0306-4522(81)90115-9

Cited by 407 publications

(107 citation statements)

References 28 publications

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“…In all brain regions, the distribution of immunoreactive puncta appeared to correspond to the distribution of GABAergic terminals. Furthermore, the staining patterns produced in all brain regions by the patient's autoantibodies were strikingly similar to the previously described staining patterns produced by antibodies to GAD, which is the enzyme responsible for the biosynthesis of GABA (46,47). GAD antibodies are routinely used as markers of GABAergic neurons and, in particular, of GABAergic terminals, since anti-GAD antibodies appear to be localized in nerve terminals (8).…”

Section: At the Benchsupporting

confidence: 84%

Stiff-man syndrome: From the bedside to the bench

Helfgott

1999

Arthritis & Rheumatism

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Section: At the Benchsupporting

confidence: 84%

Stiff-man syndrome: From the bedside to the bench

Helfgott

1999

Arthritis & Rheumatism

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“…In the granular layer, distribution of GAD was almost the same as that of GABA (Oertel et al, 1981;Ottersen and Storm-Mathisen, 1984;Ribak and Roberts, 1990;Takayama, 1994). In the molecular and Purkinje cell layers, however, GABA is absent in the dendrites and cell bodies of Purkinje cells, although GAD is localized throughout the Purkinje cells.…”

Section: Introductionmentioning

confidence: 86%

Extrasynaptic localization of GABA in the developing mouse cerebellum

Takayama

Inoue

2004

Neuroscience Research

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In the adult brain, γ-amino butyric acid (GABA) is synaptically released and mediates inhibitory transmission. Recent studies have revealed that GABA is a trophic factor for brain development. To reveal the distribution of GABA and its secretion mechanisms during brain development, we investigated the immunohistochemical localization of two molecules, GABA and vesicular GABA transporter (VGAT), which is a GABAergic vesicle protein, in the developing mouse cerebellum by means of newly developed antibodies.Furthermore, we tested the relationship between developmental changes in distribution of above two molecules in the presynapses and ontogeny of GABAergic synapses. GABAergic synapses were detected by immunohistochemistry for the GABA A receptor α1 subunit, which is an essential subunit for inhibitory synaptic transmission in the mature cerebellar cortex.Until postnatal day 7 (P7), GABA was localized throughout the GABAergic neurons, and VGAT accumulated at axon varicosities and growth cones, where the α1 subunit did not accumulate. After P10, both GABA and VGAT became confined to the terminal sites where the α1 subunit was localized. These results suggested that GABA was extrasynaptically released from axon varicosities and growth cones by vesicular secretion 'exocytosis' and from all parts of GABAergic neurons during the cerebellar development by non-vesicular secretion 'diacrine'.

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“…Second, GAD-positive synaptic terminals in numerous other brain regions (Wood et al, 1976;Oertel et al, 1981;Ribak et al, 1981) predominantly display morphological characteristics that are very similar to those of the F terminals in the superior colliculus. Thus, there is circumstantial evidence supporting the possibility that GABAergic terminals in the superior colliculus might become reorganized in response to a loss of retinal innervation.…”

mentioning

confidence: 94%

Immunocytochemical localization of glutamic acid decarboxylase in normal and deafferented superior colliculus: evidence for reorganization of gamma-aminobutyric acid synapses

Cr¹,

Lee²,

Vaughn³

1983

J. Neurosci.

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There is circumstantial evidence that GABAergic synaptic terminals in the superior colliculus might become reorganized in response to a loss of the retinal innervation of this brain region. The present investigation tests this possibility by identifying y-aminobutyric acid (GABA) neurons and their synaptic relationships with an immunocytochemical localization of the GABA-synthesizing enzyme, glutamic acid decarboxylase (GAD), and by comparing these synaptic relationships in normal superior colliculus with those present 6 and 16 weeks after unilateral eye removal. In normal superior colliculus, light microscopy revealed a much denser concentration of GAD-positive reaction product in the superficial layers than in the intermediate and deep collicular layers. Most of this reaction product was contained within small, punctate structures, but GAD-positive somata and proximal dendrites also were observed. Electron microscopy showed that GAD was localized in numerous synaptic terminals, including those that were the presynaptic elements of dendrodendritic synapses. The vast majority of GAD-positive presynaptic elements formed symmetric synaptic junctions. In addition, GAD-positive profiles frequently were postsynaptic to unstained retinal terminals as well as presynaptic to unstained dendritic profiles and thus participated in serial synaptic relationships. Furthermore, both retinal and GAD-positive elements commonly were presynaptic to the same postsynaptic dendrite, and often these synaptic contacts were adjacent to each other. In deafferented specimens, profiles with the characteristics of retinal axon terminals were not observed, whereas there appeared to be no reduction of GAD-positive synaptic profiles. However, there was a marked and statistically significant increase in the proportion of GADpositive presynaptic terminals that formed asymmetric synaptic contacts in superior colliculus deprived of retinal input. This change indicates that partial deafferentation induces a reorganization of GAD-positive synapses. The long-term presence of the GABA-synthesizing enzyme within reorganized synaptic terminals also suggests that such presynaptic elements could produce and, presumably, release neurotransmitter.Previous investigations have sought evidence in a number of different brain regions for lesion-induced synaptic reorganization of neurons that use y-aminobutyric acid (GABA) as a neurotransmitter, but such alterations still remain to be demonstrated unequivocally.

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Immunocytochemical localization of glutamate decar☐ylase in rat cerebellum with a new antiserum

Cited by 407 publications

References 28 publications

Stiff-man syndrome: From the bedside to the bench

Stiff-man syndrome: From the bedside to the bench

Extrasynaptic localization of GABA in the developing mouse cerebellum

Immunocytochemical localization of glutamic acid decarboxylase in normal and deafferented superior colliculus: evidence for reorganization of gamma-aminobutyric acid synapses

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