Quantification of immunogold labelling reveals enrichment of glutamate in mossy and parallel fibre terminals in cat cerebellum

Somogyi, Péter; Halasy, Katalin; Somogyi, J.; Storm‐Mathisen, Jon; Ottersen, Ole Petter

doi:10.1016/0306-4522(86)90121-1

Cited by 332 publications

(160 citation statements)

References 22 publications

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“…These results may provide evidence for a neurotransmitter role of taurine in the cerebellum; however, taurine has been shown to modulate the synaptic release of transmitters such as ACh, norepinephrine, and GABA (Kuriyama, 1980). Researchers have proposed that some mossy fibers use the excitatory amino acid glutamate as a neurotransmitter (Freeman et al, 1983;Beitz et al, 1986;Somogyi et al, 1986;Wenthold et al, 1986). We believe that taurine is more likely to serve in a neuromodulatory role in these excitatory fibers than in a classical transmitter role.…”

Section: Discussionmentioning

confidence: 90%

Colocalization of taurine- and cysteine sulfinic acid decarboxylase- like immunoreactivity in the cerebellum of the rat with monoclonal antibodies against taurine

et al. 1988

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Two monoclonal antibodies against fixative-modified taurine, Tau1 and Tau2, were produced, characterized, and used in the present study to analyze the distribution of taurine in the cerebellum of the rat. In addition, immunohistochemical colocalization experiments were performed to determine whether cerebellar neurons contain both taurine and its synthesizing enzyme, cysteine sulfinic acid decarboxylase (CSADC). In ELISAs, both Tau1 and Tau2 displayed high affinities for taurine conjugated to various carrier proteins and possessed some cross- reactivity for other amino acids which are present in lower concentrations in the brain than taurine. Tau2 was found to recognize only taurine and hypotaurine when paraformaldehyde was used to fix the amino acids to carrier proteins. With the use of glutaraldehyde fixation, Tau1 cross-reacted with conjugates of beta-alanine and hypotaurine and Tau2 cross-reacted strongly with conjugates of cysteic acid and hypotaurine and weakly with cysteine sulfinic acid. Despite different cross-reactivities, Tau1 and Tau2 exhibited almost identical patterns of neuronal staining in bands of Purkinje cells in the cerebellum. Staining of Purkinje cell dendrites was more prominent than staining of the soma. Light immunoreactivity was present in Golgi, stellate, and basket cells. A scattered population of granule cells displayed taurine-like immunoreactivity at the electron microscopic level. Immunostaining was identified in some terminals in the Purkinje cell layer and in a limited number of mossy fibers. Tau2-like immunoreactivity was colocalized with CSADC-like immunoreactivity in the cerebellar neurons described above. These immunoreactive cells may represent a subpopulation of neurons that contain a higher concentration of taurine than neighboring cells due to their ability to synthesize taurine. The intense immunoreactive staining of Purkinje cell dendrites provides support for the hypothesis that calcium- dependent release of taurine in the cerebellum may originate primarily from dendritic rather than synaptic processes and suggests a neuromodulator role for taurine in the cerebellum.

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Section: Discussionmentioning

confidence: 90%

Colocalization of taurine- and cysteine sulfinic acid decarboxylase- like immunoreactivity in the cerebellum of the rat with monoclonal antibodies against taurine

et al. 1988

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“…Third, the presynaptic GABA neuron itself may be glutamatergic. Although not released by most GABAergic terminals (Somogyi et al, 1986), glutamate is a precursor for GABA synthesis. In some cases, both GABA and glutamate are stored by the same terminals (Sandler and Smith, 1991;Somogyi, 2002;Ottem et al, 2004) and may be coreleased.…”

Section: Discussionmentioning

confidence: 99%

Endogenous Activation of Metabotropic Glutamate Receptors Modulates GABAergic Transmission to Gonadotropin-Releasing Hormone Neurons and Alters Their Firing Rate: A Possible Local Feedback Circuit

Chu

Moenter

2005

Journal of Neuroscience

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Gonadotropin-releasing hormone (GnRH) neurons are the primary central regulators of fertility, receiving input from GABAergic afferents via GABA A receptors. We tested whether metabotropic glutamate receptors (mGluRs) regulate GABA transmission to GnRH neurons and GnRH neuronal firing pattern. Whole-cell recordings were performed under conditions isolating ionotropic GABA postsynaptic currents (PSCs) in brain slices. The broad-spectrum mGluR agonist 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) decreased the frequency of GABA A -mediated spontaneous PSCs in a reversible manner. Amplitude and kinetics were not altered, suggesting that afferent GABA neurons are the primary targets. TTX eliminated the effects of ACPD in most tested neurons. Group II [2-(2,3-dicarboxycyclopropyl) glycine] and III (L-AP-4) mGluR agonists mediated this response; a group I agonist (3,5-dihydroxyphenylglycine) was not effective. The broad-spectrum antagonist ␣-methyl-4-carboxyphenylglycine (MCPG) and/or (RS)-␣-cyclopropyl-4-phosphonophenylglycine (CPPG) (group III antagonist) enhanced spontaneous PSC frequency, particularly when initial frequency was low, suggesting that endogenous activation of mGluRs regulates GABA transmission to GnRH neurons. Extracellular recordings were used to evaluate GnRH neuron firing rate within the network. ACPD reduced firing rate, and MCPG plus CPPG had an opposite effect, indicating that mGluRs help control excitability of the GnRH network. GnRH neurons express vesicular glutamate transporters, suggesting they may corelease this transmitter. Simulation of firing activity in a GnRH neuron decreased PSC frequency in that cell, an effect blocked by antagonism of mGluRs but not GnRH receptors. These results demonstrate an inhibition of GABAergic inputs to GnRH neurons by mGluRs via a presynaptic mechanism. Through this mechanism, local glutamate milieu, possibly contributed by GnRH neurons themselves, plays an important role in modulating GnRH release and the central regulation of fertility.

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“…Our method relies on a flow-cytometry-based glutamate-immunodetection procedure using anti-glutamate antibodies to determine steadystate levels of vesicular glutamate. The specificity of glutamate antibodies has been extensively characterized (Somogyi et al, 1986;Storm-Mathisen et al, 1983;Storm-Mathisen et al, 1986). Moreover, these antibodies are a standard tool for identifying glutamatergic neurons in nerve tissue (Bramham et al, 1990;Somogyi et al, 1986).…”

Section: D) Coexpression Of Both Znt3 and Vglut1 Transporters Furthermentioning

confidence: 99%

Vglut1 and ZnT3 co-targeting mechanisms regulate vesicular zinc stores in PC12 cells

Salazar

Craige

Love

et al. 2005

Journal of Cell Science

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The lumenal ionic content of an organelle is determined by its complement of channels and transporters. These proteins reach their resident organelles by adaptordependent mechanisms. This concept is illustrated in AP-3 deficiencies, in which synaptic vesicle zinc is depleted because the synaptic-vesicle-specific zinc transporter 3 does not reach synaptic vesicles. However, whether zinc transporter 3 is the only membrane protein defining synaptic-vesicle zinc content remains unknown. To address this question, we examined whether zinc transporter 3 and the vesicular glutamate transporter Vglut1 (a transporter that coexists with zinc transporter 3 in brain nerve terminals) were co-targeted to synaptic-like microvesicle fractions in PC12 cells. Deconvolution microscopy and subcellular fractionation demonstrated that these two transporters were present on the same vesicles in PC12 cells. Vglut1 content in synaptic-like microvesicle fractions and brain synaptic vesicles was partially sensitive to pharmacological and genetic perturbation of AP-3 function. Whole-cell flow-cytometry analysis of PC12 cell lines expressing zinc transporter 3, Vglut1 or both showed that vesicular zinc uptake was increased by Vglut1 expression. Conversely, production of zinc transporter 3 increased the vesicular uptake of glutamate in a zincdependent fashion. Our results suggest that the coupling of zinc transporter 3 and Vglut1 transport mechanisms regulates neurotransmitter content in secretory vesicles.

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Quantification of immunogold labelling reveals enrichment of glutamate in mossy and parallel fibre terminals in cat cerebellum

Cited by 332 publications

References 22 publications

Colocalization of taurine- and cysteine sulfinic acid decarboxylase- like immunoreactivity in the cerebellum of the rat with monoclonal antibodies against taurine

Colocalization of taurine- and cysteine sulfinic acid decarboxylase- like immunoreactivity in the cerebellum of the rat with monoclonal antibodies against taurine

Endogenous Activation of Metabotropic Glutamate Receptors Modulates GABAergic Transmission to Gonadotropin-Releasing Hormone Neurons and Alters Their Firing Rate: A Possible Local Feedback Circuit

Vglut1 and ZnT3 co-targeting mechanisms regulate vesicular zinc stores in PC12 cells

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