The nerve cells or neurons They are the fundamental component of our nervous system. They have the ability to drive nerve impulses, as well as to transmit information to other neurons. These very special cells also have a unique functioning. Next we will explain what happens in the nerve tissue after an injury.
Neural plasticity refers to the ability of neurons to change their form and function in response to alterations in their environment. It is a continuous process that allows remodeling and neuronosynaptic reorganization, with the aim of optimizing the functioning of neural networks during phylogeny, ontogeny, learning and after a brain injury.
- 1 Neural Degeneration
- 2 Neural Regeneration
- 3 Neural regeneration in mammalian SNP
- 4 Neural Reorganization
Neurodegeneration is a process of irreversible neuronal damage and even death, present in aging and neurodegenerative diseases. Neurodegenerative disorders are characterized by a gradual loss of neurons, which often cause death.
In lesions of the Nervous System, after the section of a neuronal axon or from a group of axons (axotomy) there are two types of neuronal degeneration, which are the following:
- Antegrade degeneration: consists of degeneration of the distal segment.
- Retrograde degeneration: consists of degeneration of the proximal segment.
On the other hand, these two axon segments must also be distinguished after an axotomy:
- The distal segment: It is the part of the axon that lies between the cut and the axon terminals.
- The proximal segment: It is the part of the axon that lies between the cut and the cell body.
Antegrade degeneration occurs rapidly (the axon without the soma cannot survive), but retrograde degeneration is slower. In fact, after the injury changes begin to occur in the cell body, which can be degenerative or regenerative:
- Degenerative changes, such as the decrease in cell body size, indicate that the neuron will die.
- Regenerative changes, such as increasing the size of the soma, may indicate that the neuron is making a massive protein synthesis to replace the degenerated axon. Keep in mind that these regenerative changes do not guarantee the survival of the neuron, since it is not enough to regenerate the axon, but also to establish the appropriate synaptic contacts.
Keep in mind that the effects of an injury, in this case of an axotomy, are not limited to the injured neuron, but can extend to the neurons that the injured neuron is related to.
The transneuronal degeneration It involves the degeneration of neurons related to the axotomulated neuron.
We can distinguish two types of transneuronal degeneration: antegrade and retrograde.
- Antegrade transneuronal degeneration it is the degeneration of a neuron due to the injury of a neuron on which it established synapses.
- Retrograde transneuronal degeneration it is the degeneration of a neuron due to the injury of a neuron from which information is subtracted.
Neural regeneration is the growth of injured neurons.
The neuronal regeneration It is clear in most invertebrates and lower vertebrates, but it is hardly seen in mammals and other higher vertebrates. We must differentiate, however, the regeneration in the SNC (Central Nervous System), which is practically null, of the regeneration in the SNP (Peripheral Nervous System), which in certain occasions can be successful.
Neural regeneration in the mammalian SNP
Three forms of axon regeneration to the peripheral nerves of mammals.
Shortly after an injury, after two or three days, the axon begins to grow. This growth does not guarantee the survival of the neuron, nor the success of the regeneration.
But why doesn't this regeneration occur in the CNS?
Curiously, CNS neurons can regenerate when they are transplanted into the SNP, but SNP neurons cannot regenerate if they are transplanted centrally. It seems that what is decisive for regeneration is the environment in which neurons are found.
The Schawnn cells they promote the regeneration of the SNP of mammals, and produce neurotrophic factors and cell adhesion molecules.
These neurotrophic factors produced by Schawnn cells, which, as you will remember, form the myelin layer in the SNP, stimulate the growth of neurons, and the cell adhesion molecules of the cell membranes of Schawnn cells mark the path by that axons must grow.
The oligodendroglia of the central nervous system does not stimulate or guide axonal regeneration.
Growth of collateral outbreaks after neuronal degeneration.
When an axon degenerates, nearby healthy axons grow branches that establish synapses with the empty sites left by the degenerated axon. This process is called growth of collateral outbreaks.
While the main changes that take place in mammalian SNs occur in the early stages of development, the mature mammalian SN maintains the ability to reorganize.
The majority of SN reorganization studies have focused on the capacity of sensory systems and engine of reorganizing in response to an injury or experience.
In an experiment conducted on nonhuman primates it was revealed that, if the sensory information of an arm is prevented from reaching the crust zone corresponding (injuring the sensory pathways that carry this type of information), the area of the cortex that originally processes the information of the arm ends up processing sensory information from the face. And therefore, the reorganization that occurs after the injury expands the cortical areas that process the sensory information of the face.
Keep in mind that functional reorganization is not always accompanied by functional recovery.
Neural reorganization could contribute to the recovery of a brain injury, but little is currently known about recoveries of brain injuries. The problem is that many times the brain injury produces a series of changes that can be confused with the recovery of function. Sometimes, the improvement of function after an injury can be the result of learning new cognitive strategies or new behaviors and not tissue regeneration.