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Printable Handouts
Navigable Slide Index
- Introduction
- The hypothalamo-neurohypophysial system
- Anatomical remodeling
- Unstimulated
- Stimulated
- Consequences of the anatomical remodeling
- Glutamatergic synapse (1)
- Glutamatergic synapse (2)
- Activation of the Glutamatergic synapse (1)
- Activation of the Glutamatergic synapse (2)
- Astrocytes control glutamate clearance
- Heterosynaptic transmission
- Anatomical remodeling causes increase in Glu
- Glutamate spillover and remodeling of the SON
- Diffusion: tortuosity and volume
- Heterosynaptic modulation: GABAergic terminal
- Heterosynaptic modulation due to Glu spillover
- Two-stimulations paradigm
- mGluRs and heterosynaptic depression of IPSCs
- Activation of GluR on neighboring synapses
- Retraction of the astrocytic process
- Heterosynaptic depression & SON of lactating rats
- Effects of limiting diffusion in extracellular space
- NMDA receptors
- NMDA receptor: model
- Serine racemase in the SON
- D-serine in the SON
- DAAO degrades D-serine
- AMPA and NMDA peak currents
- D-serine is the endogenous ligand of NMDAR
- NMDAR-mediated EPSCs in lactating rats
- D-serine rescues NMDAR activity in lactating rats
- D-serine levels in the cleft reduced in lactating rats
- Long-term synaptic plasticity (1)
- Ca2+ signaling requirement for LTD
- Long-term synaptic plasticity (2)
- Conclusions
- Acknowledgments
Topics Covered
- Anatomical remodelling of the hypothalamo-neurohypophysial system during specific physiological conditions
- Charactersiation of this remodelling by reduction in the astrocytic coverage of manocellular neurons and their synapses
- Electrophysiological approaches show changes in the glial environment of neurons and synapses can dramatically alter synaptic functions
- The hypothalamo-neurohypophysial system as an experimental model to study the contribution of astrocytes to synaptic transmission and plasticity
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Talk Citation
Oliet, S.H. (2013, November 5). Neuronal-glial anatomical plasticity in the hypothalamus [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 9, 2024, from https://doi.org/10.69645/XMLK9797.Export Citation (RIS)
Publication History
Financial Disclosures
- Dr. Stéphane H.R. Oliet 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
I'm Stephane Oliet from Neurocentre
Magendie in Bordeaux, France
and I'm going to tell you about
the neuronal-glial
anatomical plasticity
that takes place in
the hypothalamus.
0:12
The plasticity I'm
talking about takes
place in the
hypothalamo-neurohypophysial system.
The system is illustrated
in this diagram which
represents a sagittal view of
the basal part of the brain.
The hypothalamo-neurohypophysial
system is
made of neuroendocrine neurons,
shown here in yellow, and
that are localized in
both the supraoptic and
paraventricular nuclei.
The nuclei's perimeter here
is illustrated in green.
The magnocellular
neurons project
their axon directly into
the neurohypophysis
where they can release
in the bloodstream their
products of secretion,
namely oxytocin,
and vasopressin.
While oxytocin is important
for reproductive function,
alteration, and lactation,
vasopressin is essential for
cardiovascular and body
fluid homeostasis.
The release of these hormones in
the bloodstream is directly
dependent upon the
electrical activity
of the magnocellular
neuron activity,
which is itself controlled by
apparent excitatory and
arbitrary synaptic input.
1:19
There are some specific
physiological conditions that are
associated with a
strong stimulation
of the magnocellular system,
such as chronic dehydration,
lactation, parturition,
or stress.
The hypothalamo-neurohypophysial
system undergoes
striking anatomical remodeling.
This remodeling is
characterized in
particular by hypertrophy
of the neuron
proportional increase
in the number of
the synopsis both
excitatory and inhibitory;
and most interestingly, a pronounced
reduction in the astrocytic coverage of
magnocellular neurons that
results in an increased amount of
directly juxtaposed
neuronal surfaces.
All of these changes
are completely
irreversible upon the
cessation of the stimulation.