We noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- First description of neuroglia
- Proposed active role of neuroglia in the brain
- GFAP: an astrocytic marker
- Six mechanisms of astrocytic glutamate release
- Removal of extracellular glutamate by astrocytes
- Astrocytic plasma membrane Glu transporters
- Reverse operation of glutamate transporters
- Cystine-glutamate exchanger
- Cystine-glutamate exchanger localizes to glia
- The cystine-glutamate exchanger operation
- Glutamatergic secretory machinery in astrocytes
- Ca2+- dependent release of glutamate
- Glu release exhibits exocytotic characteristics
- The presence of secretory proteins in astrocytes
- Intracellular localization of secretory proteins
- Approach to study exocytotic glutamate release
- Intracellular calcium dynamics in astrocytes
- Glutamate release into extracellular space
- Glutamatergic exocytotic machinery in astrocytes
- Morphological correlates of exocytosis
- Visualization of vesicular fusions
- Report of vesicular fusions in astrocytes
- Ca2+ signaling system as a trigger for exocytosis
- Ca2+ sources for exocytotic glutamate release
- SOC entry through TRPC1
- The role of mitochondrial Ca2+ handling
- Ca2+ sources for glutamate release
- Volume-regulated anion channels
- Hypo-osmotically induced glutamate release (1)
- Hypo-osmotically induced glutamate release (2)
- Purinergic receptor activation and cell swelling
- ATP-induced swelling and glutamate release
- The purinergic P2X7 ion channel
- P2X7 receptors - expression in astrocytes
- Astrocytes possess functional P2X7 receptors
- P2X7 channels mediate the release of glutamate
- Gap junction channels and connexons
- Hemichannels
- Astrocytes possess functional hemichannels
- Release of glutamate via Cx43 hemichannels
- Possible future mechanisms
- Summary
- Thank you
Topics Covered
- Reversal of glutamate uptake
- Anion channel opening induced by cell swelling
- Ca2+-dependent exocytosis
- Glutamate exchange via the cystine-glutamate antiporter
- Release through ionotropic purinergic receptors
- Functional unpaired connexons, 'hemichannels'
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Parpura, V. (2020, May 1). Mechanisms of glutamate release from astrocytes [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 5, 2024, from https://doi.org/10.69645/RYAP2062.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Vladimir Parpura has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Neurology
Transcript
Please wait while the transcript is being prepared...
0:00
My name is Vladimir Parpura.
I will talk about various mechanisms
of glutamate release from astrocytes,
a subtype of glial cell
in the nervous system.
0:13
Neuroglia was first time
described in 1856 by the German
neuropathologist Rudolf Virchow
as a putty that binds nervous
elements together, somewhat like
cement that binds the bricks.
0:31
The Spanish neuroanatomist Santiago
Ramon Y Cajal proposed that neuroglia,
shown in dark brown in his drawing,
have a more active role in the brain,
since their position at
the interface between blood vessels,
shown in A, and neurons, shown in C and D.
We know today that the gold
sublimate stain that he used
targeted intermediate filaments
that consist mainly of
glial fibrillary acidic
protein abbreviated as GFAP,
which is used today as
an astrocytic marker.
1:07
This slide shows an image of purified
cultures of astrocytes stained
using indirect immunocytochemistry with
an antibody against GFAP, shown in red.
The cell nuclei shown in
blue are stained using DAPI.
Such cells in culture were
instrumental in describing various
mechanisms utilized by astrocytes for
the release of the major
excitatory transmitter glutamate
as summarized in the next slide.
1:40
There are six known mechanisms of
glutamate release from astrocytes,
shown clockwise in the order
of their discoveries,
along with original references.
1, swelling induced opening of
volume regulated anion channels.
2, reverse operation of excitatory
amino acid transporters.
3, calcium dependent exocytosis.
4, the cysteine glutamate exchanger.
5, connexin hemichannels.
And 6, the purinergic P2X7 receptors.
I'll discuss each of these mechanisms,
although not in order
of their discoveries.
I will start the discussion of glutamate
release through plasma membrane
transporters, such as the reversal
of uptake by excitatory amino acid
transporters, and exchange by
the cysteine glutamate antiporter.
Then I will follow up by
a more detailed discussion
of glutamate release through
calcium dependent exocytosis.
And finally I will discuss glutamate
release through channels on the cell
surface, such as anion channel
opening induced by cell swelling,
released ionotropic purinergic receptors,
and by unpaired connexin.