Distribution and morphological characterization of phosphate-activated glutaminase-immunoreactive neurons in cat visual cortex

Gucht, Estel Van der; Jacobs, Sandy; Kaneko, Takeshi; Vandesande, Frans; Arckens, Lutgarde

doi:10.1016/s0006-8993(03)03332-8

Cited by 27 publications

(16 citation statements)

References 84 publications

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“…To further specify the type of neurons with SLC38 expression, double-labeling was performed together with phosphate-activated glutaminase (PAG). PAG is an enzyme which generates glutamate and ammonia from glutamine and is a marker for glutamatergic neurons [30], [31]. Extensive overlap between SLC38A6 and PAG was observed showing that SLC38A6 is highly expressed in glutamatergic neurons (Figure 2E with higher magnification and 2F with lower magnification).…”

Section: Resultsmentioning

confidence: 96%

Histological Analysis of SLC38A6 (SNAT6) Expression in Mouse Brain Shows Selective Expression in Excitatory Neurons with High Expression in the Synapses

et al. 2014

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SLC38A6 is one of the newly found members of the solute carrier 38 family consisting of total 11 members, of which only 6 have been characterized so far. Being the only glutamine transporter family expressed in the brain, this family of proteins are most probably involved in the regulation of the glutamate-glutamine cycle, responsible for preventing excitotoxicity. We used immunohistochemistry to show that SLC38A6 is primarily expressed in excitatory neurons and is not expressed in the astrocytes. Using proximity ligation assay, we have quantified the interactions of this SLC38 family protein with other proteins with known localization in the cells, showing that this transporter is expressed at the synapses. Moreover, this study has enabled us to come up with a model suggesting sub-cellular localization of SLC38A6 at the synaptic membrane of the excitatory neurons.

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Section: Resultsmentioning

confidence: 96%

Histological Analysis of SLC38A6 (SNAT6) Expression in Mouse Brain Shows Selective Expression in Excitatory Neurons with High Expression in the Synapses

et al. 2014

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“…We injected equal biological titers (IVP) of pVGLUT1lac-Pr&Intron or pVGLUT1lac-BasalPr, or 6.6-fold more physical particles (VG) of pVGLUT1lac-BasalPr than pVGLUT1lac-Pr&Intron (Table 1), into POR cortex, sacrificed the rats 4 days later, and performed costaining for β-galactosidase immunoreactivity (β-gal-IR) and PAG-IR, a marker for glutamatergic neocortical neurons (Kaneko and Mizuno, 1988; Kaneko et al, 1992; Sakata et al, 2002; Van der Gucht et al, 2003). Representative photomicrographs confirmed that pVGLUT1lac-Pr&Intron supports expression predominately in glutamatergic neurons (Fig.…”

Section: Resultsmentioning

confidence: 99%

The vesicular glutamate transporter-1 upstream promoter and first intron each support glutamatergic-specific expression in rat postrhinal cortex

Zhang

Zhao

et al. 2011

Brain Research

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Multiple applications of direct gene transfer into neurons require restricting expression to glutamatergic neurons, or specific subclasses of glutamatergic neurons. Thus, it is desirable to develop and analyze promoters that support glutamatergic-specific expression. The three vesicular glutamate transporters (VGLUTs) are found in different populations of neurons, and VGLUT1 is the predominant VGLUT in the neocortex, hippocampus, and cerebellar cortex. We previously reported on a plasmid (amplicon) Herpes Simplex Virus vector that contains a VGLUT1 promoter. This vector supports long-term expression in VGLUT1-containing glutamatergic neurons in rat postrhinal (POR) cortex, but does not support expression in VGLUT2-containing glutamatergic neurons in the ventral medial hypothalamus. This VGLUT1 promoter contains both the VGLUT1 upstream promoter and the VGLUT1 first intron. In this study, we begin to isolate and analyze the glutamatergic-specific regulatory elements in this VGLUT1 promoter. We show that the VGLUT1 upstream promoter and first intron each support glutamatergic-specific expression. We isolated a small, basal VGLUT1 promoter that does not support glutamatergic-specific expression. Next, we fused either the VGLUT1 upstream promoter or the first intron to this basal promoter. The VGLUT1 upstream promoter or the first intron, fused to the basal promoter, each supported glutamatergic-specific expression in POR cortex.

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“…Interestingly, we recently found a dramatic increase in the expression of phosphate-activated glutaminase (PAG), i.e., a key enzyme in the production of glutamate, in neurons located in this very same brain region in aggressive, adolescent AAS-treated animals [21]. PAG expression has been used in a number of previous studies to visualize and quantify glutamate-transmitting neurons [1,[38][39][40]48,75]. Glutamate has been firmly established as the predominant excitatory transmitter in the hypothalamus [5,51,74], and it's activity has been extensively linked to aggression in a range of animal models, including rats, mice, cats, and fighting bulls [6,30,36,56,57,71,76], where it appears be positively associated with the aggressive behavioral phenotype.…”

Section: Discussionmentioning

confidence: 99%

Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters

Ricci

Grimes

Melloni

2007

Behavioural Brain Research

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Repeated exposure to anabolic/androgenic steroids (AAS) during adolescence stimulates high levels of offensive aggression in Syrian hamsters. The current study investigated whether adolescent AAS exposure activated neurons in areas of hamster forebrain implicated in aggressive behavior by examining the expression of FOS, i.e., the protein product of the immediate early gene c-fos shown to be a reliably sensitive marker of neuronal activation. Adolescent AAS-treated hamsters and sesame oil-treated littermates were scored for offensive aggression and then sacrificed 1 day later and examined for the number of FOS immunoreactive (FOS-ir) cells in regions of the hamster forebrain important for aggression control. When compared with non-aggressive, oil-treated controls, aggressive AAS-treated hamsters showed persistent increases in the number of FOS-ir cells in select aggression regions, namely the anterior hypothalamus and lateral septum. However, no differences in FOS-ir cells were found in other areas implicated in aggression such as the ventrolateral hypothalamus, bed nucleus of the stria terminals, central and/or medial amygdala or in nonaggression areas such as the samatosensory cortex and the suprachiasmatic nucleus. These results suggest that adolescent AAS exposure may constitutively activate neurons in select forebrain areas critical for the regulation of aggression in hamsters. A model for how persistent activation of neurons in one of these brain regions (i.e., the anterior hypothalamus) may facilitate the development of the aggressive phenotype in adolescent-AAS exposed animals is presented.

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Distribution and morphological characterization of phosphate-activated glutaminase-immunoreactive neurons in cat visual cortex

Cited by 27 publications

References 84 publications

Histological Analysis of SLC38A6 (SNAT6) Expression in Mouse Brain Shows Selective Expression in Excitatory Neurons with High Expression in the Synapses

Histological Analysis of SLC38A6 (SNAT6) Expression in Mouse Brain Shows Selective Expression in Excitatory Neurons with High Expression in the Synapses

The vesicular glutamate transporter-1 upstream promoter and first intron each support glutamatergic-specific expression in rat postrhinal cortex

Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters

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