«We were able to demonstrate for the first time that these specific cells — a small group of cells in the hippocampus — had undergone this augmentation
of synaptic strength,» Tonegawa says.
Repeated applications of serotonin, a facilitating transmitter important in behavioral dishabituation and sensitization, produced growth of the sensory neurons that paralleled the long - term enhancement
of synaptic strength.
This action can result in the activation of genes that had been switched off, and could be the cause of the recovery
of synaptic strength.
Not exact matches
Synaptic plasticity, the ability of neurons to alter the strength of their synaptic connections with activity and experience, is thought to play a critical role in memory
Synaptic plasticity, the ability
of neurons to alter the
strength of their
synaptic connections with activity and experience, is thought to play a critical role in memory
synaptic connections with activity and experience, is thought to play a critical role in memory storage.
These properties, which are believed to be important for the induction
of long - term changes in
synaptic strength, are imparted by asparagine residues in a putative channel - forming segment
of the protein, transmembrane 2 (TM2).
The same information can be represented as lines on paper, as electrical charges inside a PC's memory banks or as the
strength of the
synaptic connections among nerve cells.
Geoff Hinton, a leading neural networking theorist, argues the hardware is useless without the proper «learning algorithm» spelling out which factors change the
strength of the
synaptic connections and by how much.
They used a somewhat bizarre technique in which two mice were sutured together in such as way that they shared a circulatory system (known as parabiosis), and found old mice joined to their youthful counterparts showed changes in gene activity in a brain region called the hippocampus as well as increased neural connections and enhanced «
synaptic plasticity» — a mechanism believed to underlie learning and memory in which the
strength of neural connections change in response to experience.
So, rather than the number
of AMPA receptors themselves, the abundance
of scaffolding proteins appears to determine
synaptic strength, effectively allowing AMPA receptors to receive signals from glutamate.
Researchers have observed AMPA traveling from the inside
of a neuron to the downstream end
of a synapse, but they remain uncertain as to whether the migration into and out
of the synapse is the major component in determining
synaptic strength.
Moser demonstrated a number
of changes in the
strength of connections between nerve cells — a phenomenon called
synaptic plasticity — in the hippocampus as rats stored information in their long - term memory.
His lab is building detailed computer models
of synapses and the networks they sustain in order to determine how they collect firing statistics during wakefulness and sleep and when they change
synaptic strengths to reflect the difference.
At the cellular level, learning and memory require continuous readjustment
of the
strength of synaptic junctions — the functional connections between nerve cells.
«There is mounting evidence that the cellular machinery that controls cell death also controls the
strength and number
of synaptic connections,» Overstreet - Wadiche said.
They control the
strength and duration
of the
synaptic signal.
It has been known for decades that triggering new protein synthesis is vital to the formation
of long - term memories as well as for long - lasting
synaptic plasticity — the ability
of the neurons to change the collective
strength of their connections with other neurons.
Since morphology changes
of synapses underlie
synaptic plasticity and our learning and memory, this will provide us with many new insights into mechanisms
of how neurons store information in their morphology, how it changes
synaptic strength and ultimately how it creates new memory.
With the combined use
of genetics and pharmacology, the investigators altered the production
of proteins controlled by eIF2α in adult mice, essentially converting them into adolescents by making them more susceptible to cocaine - induced changes in
synaptic strength and behavior.
«There is mounting evidence that the cellular machinery that controls cell death also controls the
strength and number
of synaptic connections»
This conclusion is provocative because the dogma has been that a memory is instead stored by
synaptic strength,» says Susumu Tonegawa, the Picower Professor
of Biology and Neuroscience, the director
of the RIKEN - MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, and the study's senior author.
Long - term potentiation (LTP), a phenomenon in which brief repetitive activity causes a long lasting (many weeks) enhancement in the
strength of synaptic transmission, is generally accepted to be a key cellular substrate for learning and memory.
Activity - dependent and independent mechanisms regulate
synaptic size and
strength to ensure a balance between excitation and inhibition
of inputs and between input and output.
We use a number
of experimental approaches to gain a greater understanding
of translational control mechanisms necessary for maintaining long - lasting changes in
synaptic strength and memory.
Based on evidence from electrophysiological studies showing that both
synaptic plasticity and
strength of inputs to hippocampal region CA1 vary systematically with ongoing theta oscillations (Hyman et al., 2003; Brankack et al., 1993), it has been suggested that the theta rhythm functions to separate periods
of encoding
of current sensory stimuli and retrieval
of episodic memory cued by current stimuli so as to avoid interference that would occur if encoding and retrieval were simultaneous.
At the same time, she found that circuits can generate similar neuronal and network outputs from many different configurations
of intrinsic neuronal excitability and
synaptic strength.