Summary: New study reveals that brain tissue use a muscle-like signaling system to switch data over longer distances. Researchers discovered that neurons, the branch-like additions of neurons, contain a planned system of touch sites that heighten magnesium signals—similar to how muscles contract. These touch sites control calcium release and activate important protein involved in memory and learning.
This method explains how neurons transmit information to the cell body through distinct channels. Understanding this method sheds light on neural flexibility, which underlies learning and memory creation. The results could lead to fresh insights into neurological conditions like Alzheimer’s.
Important Facts:
- Neurological Calcium Amplification: Head cells use structured ER call sites to intensify calcium signals, related to how muscles cells trigger contractions.
- Memory and Learning Connection: These calcium signals install CaMKII, a proteins important for strengthening synaptic connections and memory development.
- Prospective Disease Insights: Understanding this device may help explain cognitive function in conditions like Alzheimer’s illness.
Origin: HHMI
Our brain tissue and our biceps may share more than originally thought.
A system of subcellular buildings, similar to those concerned for propagating chemical signals that cause muscle contraction, are also responsible for transmitting signs in the mind that might aid learning and memory, according to new research from the Lippincott-Schwartz Lab.
” Einstein said that when he uses his mind, it is like he is using a body, and in that regard, there is some opposite here”, says Janelia Senior Group Leader Jennifer Lippincott-Schwartz.
” The same equipment is operating in both cases, but with diverse readouts.”
Janelia scientists discovered anything strange about the cellular reticulum, or ER, which are the membrane sheets and folds inside cells that are essential for several cellular functions.
When Lorena Benedetti noticed that the substances were tracing a repeated, ladder-like structure along the entire length of the neurons, the branch-like modifications on brain cells that receive coming signals, she noticed that the researchers were tracking them at high quality along the surface of the ER in mammal neurons.
Senior Group Leader Stephan Saalfeld gave Lippincott-Schwartz a heads-up about the high-resolution 3D electron microscopic pictures of neurons in the travel head, where the ER was also forming often spaced, quadrilateral structures around the same period.
The ER usually appears like a big, powerful online, but as soon as Lippincott-Schwartz saw the structures, she knew her facility needed to figure out what they were for.
” In technology, structure is work”, says Lippincott-Schwartz, who likewise heads Janelia’s 4D Cellular Physiology study area.
We just had the impression that this structure, which is strange and wonderful throughout the entire dendrite, must have some significant function.
The researchers, led by Benedetti, started by looking at the only different area of the body known to have related, ladder-like ER buildings: muscle tissue.
The ER and the blood layer, the cell’s external barrier, are arranged in body cells at regular contact points, which is controlled by a molecule called junctophilin.
The researchers discovered that dendrites also have a form of junctophilin, which regulates contact sites between their ER and plasma membrane, using high-resolution imaging.
Further, the team discovered that the same molecular machinery that controls calcium release at dendrite contact sites, where calcium controls neuronal signaling, is also present at muscle cell contact sites, where calcium causes muscle contraction.
The researchers guessed based on these hints that the molecular machinery at dendritic contact sites must also be involved in the transmission of calcium signals, which cells use to communicate.
They suspected that the contact sites along the dendrites might act like a repeater on a telegraph machine: receiving, amplifying, and propagating signals over long distances. This may help to explain how signals received at particular sites on dendrites are relayed to the cell body hundreds of micrometers away in neurons.  ,
Benedetti points out that it is unknown how that information travels over long distances and how the calcium signal is specifically amplified.
We believed that ER could play that role because these regularly distributed contact sites can receive and transmit calcium signals both locally and temporally. They can do this by receiving and transferring this calcium signal over a distance.
The researchers discovered that this process is triggered by a neuronal signal that passes through the contact sites of voltage-gated ion channel proteins. Although this initial calcium signal quickly disappears, it also causes the ER to release additional calcium at the contact site.
CaMKII, a protein known to be crucial for memory, is activated and attracted by this calcium-influx at the contact site. CaMKII alters the plasma membrane’s biochemical properties, changing the strength of the signal that is passed down the plasma membrane.
The neuron decides how it will communicate with other neurons, and this process extends from one contact site to another all along the dendrite to the cell body.
The new research uncovers a novel mechanism for signal transmission in brain cells and provides answers to an unanswered question in neuroscience regarding how intracellular signals travel over long distances in neurons, enabling information received at specific locations on dendrites to be processed in the brain.  ,
Additionally, it provides insight into the molecular mechanisms that underlie synaptic plasticity, which involves strengthening or weakening neuronal connections that facilitates memory and learning.
Understanding how the brain functions normally and in diseases where these processes go wrong, like Alzheimer’s, could be improved by understanding this process at the molecular level.
According to Lippincott-Schwartz,” we are showing that a structure that is operating at a level of subcellular organization is having a huge impact on the way the entire neuronal system is operating in terms of calcium signaling,”
” This is a great example of how, in doing science, if you see a beautiful structure, it can take you into a whole new world”.
About this information on memory and learning research
Author: Nanci Bompey
Source: HHMI
Contact: Nanci Bompey – HHMI
Image: The image is credited to Neuroscience News
Original Research: Open access.
” Periodic ER-plasma membrane junctions support long-range Ca2+ signal integration in dendrites” by Jennifer Lippincott-Schwartz et al. Cell
Abstract
Periodic ER-plasma membrane junctions support long-range Ca2+ signal integration in dendrites
The mechanisms by which activity-evoked intracellular signals propagate over macroscopic distances are not well understood, but neuronal dendrites are required to relay synaptic inputs over long distances.
Here, we discovered a system of periodically arranged endoplasmic reticulum-plasma membrane ( ER-PM) junctions tiling the plasma membrane of dendrites at ∼1 , μm intervals, interlinked by a meshwork of ER tubules patterned in a ladder-like array.
Populated with Junctophilin-linked plasma membrane voltage-gated Ca2+ , channels and ER Ca2+-release channels ( ryanodine receptors ), ER-PM junctions are hubs for ER-PM crosstalk, fine-tuning of Ca2+ , homeostasis, and local activation of the Ca2+/calmodulin-dependent protein kinase II.
Local spine stimulation activates the Ca2+ , modulatory machinery, facilitating signal transmission and ryanodine-receptor-dependent Ca2+ , release at ER-PM junctions over 20 , μm away.
Thus, interconnected ER-PM junctions support signal propagation and Ca2+ , release from the spine-adjacent ER.
Dendritic computations may be influenced by the ability of this subcellular architecture to alter both local and distant membrane-proximal biochemistry.
