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Related Concept Videos

Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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If over time, all...
Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when presynaptic neurons...
The Retina01:32

The Retina

The retina is a layer of nervous tissue at the back of the eye that transduces light into neural signals. This process, called phototransduction, is carried out by rod and cone photoreceptor cells in the back of the retina.
Anatomy of the Eyeball01:20

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The eye is a spherical, hollow structure composed of three tissue layers. The outer layer — the fibrous tunic, comprises the sclera — a white structure — and the cornea, which is transparent. The sclera encompasses some of the ocular surface, most of which is not visible. However, the 'white of the eye' is distinctively visible in humans compared to other species. The cornea, a clear covering at the front of the eye, enables light penetration. The eye's middle layer, the vascular tunic,...

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Electrophysiological Investigations of Retinogeniculate and Corticogeniculate Synapse Function
09:09

Electrophysiological Investigations of Retinogeniculate and Corticogeniculate Synapse Function

Published on: August 7, 2019

LTD and LTP at the developing retinogeniculate synapse.

Jokūbas Ziburkus1, Emily K Dilger, Fu-Sun Lo

  • 1Department of Biology and Biochemistry, University of Houston, Houston, Texas, USA.

Journal of Neurophysiology
|September 25, 2009
PubMed
Summary
This summary is machine-generated.

Retinal activity drives long-term changes in synaptic strength within the developing dorsal lateral geniculate nucleus (LGN). Calcium influx through L-type channels mediates this synaptic plasticity during critical developmental periods.

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Synaptic Plasticity

Background:

  • The developing visual system undergoes significant structural and functional remodeling.
  • Retinal activity patterns are crucial for shaping neuronal connections in the dorsal lateral geniculate nucleus (LGN).
  • Understanding the mechanisms of synaptic plasticity in the LGN is key to comprehending visual circuit development.

Purpose of the Study:

  • To investigate if retinal activity can induce long-term changes in synaptic strength in the developing LGN.
  • To determine the role of specific ion channels in mediating this developmental synaptic plasticity.
  • To correlate synaptic plasticity with critical periods of retinogeniculate connection refinement.

Main Methods:

  • Utilized a rodent in vitro explant preparation of the LGN with intact retinal afferents.
  • Applied a high-frequency tetanus stimulation protocol to the optic tract, mimicking spontaneous retinal waves.
  • Measured changes in extracellular field potentials evoked by retinal stimulation.
  • Administered pharmacological antagonists for specific receptors and ion channels.

Main Results:

  • High-frequency stimulation induced long-term depression (LTD) in early development (postnatal day 1-14) and long-term potentiation (LTP) in later development (postnatal day 16-30).
  • LTD was not affected by GABA-A or NMDA receptor antagonists.
  • Both LTD and LTP were blocked by L-type Ca(2+)-channel antagonists, indicating their critical role.
  • Calcium influx via L-type channels is essential for inducing synaptic plasticity.

Conclusions:

  • Retinal activity patterns directly influence synaptic plasticity in the developing LGN.
  • L-type Ca(2+) channels are critical mediators of synaptic plasticity during retinogeniculate development.
  • This plasticity mechanism may guide the pruning and stabilization of visual connections.