Skip to content

Latest commit

 

History

History
57 lines (31 loc) · 3.08 KB

Literature-Search.md

File metadata and controls

57 lines (31 loc) · 3.08 KB
Raw

We observed colocalization of GabaR and VGlut1 (it seems like Jesse has also observed that).

There are 3 possibilities here:

  1. Neuroscience (existing knowledge) is wrong

  2. Our analysis is wrong

  3. The data is wrong

It is unlikely that our analysis is wrong since Jesse and us independently replicated that result.

In order to gauge our sanity here, I have conducted a literature search.

In summary, it is not unheard of that neurons can release both glutamate and GABA, and in certain systems across different organisms there has been lots of published evidence of colocalizations.

Many papers indicate that VGlut colocalizes with GABAR, but also with VGAT/GAD.

Rough manual look at NeuroDataViz indicates that colocalization is not an impossibility. The glutamatergic stacka and the GABAergic stack looks like they correspond very well.

The core question is not why VGlut colocalizes with GABAR, but rather why VGlut does not colocalize with VGAT/GAD etc given that it colocalizes with GABAR

Fattorini et al 2015 (shows in cortex)

-In adult neocortex, VGLUT1 (also known as SLC17A7), the main glutamate vesicular transporter, and VGAT (also known as SLC32A1), the γ‐aminobutyric acid (GABA) vesicular transporter, are co‐expressed in a subset of axon terminals forming both symmetric and asymmetric synapses, where they are sorted into the same vesicles.

From Valente et al 2015

  • displayed pictures of colocalization between VGlut1 and GabaRs

  • displayed evidence that there could be GABAergic release from glutamatergic neurons

  • also showed that VGlut should colocalize with GAD and VGAT (since these are what associates with GABAR)

  • their summary:

In the last years, an increasing amount of experimental evidence has demonstrated an abundant coexpression of VGLUT1 and VGAT in retina bipolar cells as well as in cortical and hippocampal glutamatergic synapses . Moreover, electrophysiological studies suggested that GABA is coreleased from glutamatergic hippocampal mossy fiber terminals (MFTs) during postnatal development or in the adult after induction of hyperexcitability. Although initially argued , the growing and convincing experimental evidence strengthened considerably the notion of GABA corelease at MFs. Previous data have shown that GABA, coreleased at these glutamatergic synapses, mainly activates postsynaptic and presynaptic ionotropic type A GABA receptors (GABAARs).

Zander et al 2010

-Using immunoisolation of synaptic vesicles, we now show that VGLUT2 and VGAT, and also VGLUT1 and VGLUT2, coexist in a sizeable pool of vesicles. VGAT immunoisolates transport glutamate in addition to GABA. Furthermore, VGLUT activity enhances uptake of GABA and monoamines. Postembedding immunogold double labeling revealed that VGLUT1, VGLUT2, and VGAT coexist in mossy fiber terminals of the hippocampal CA3 area.

From Kao et al 2004, Yang and Yazulla, 1994

  • displayed evidence that certain neurons in retina in different organisms use both glutamate and GABA

From Walker et al 2001, Safiulina et al 2006

  • hippocampal mossy fibers uses both glutamate and GABA