~ Neuroplasticity ~
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Neuroplasticity is a specialized process of adaptive learning that enables certain parts of the brain to reorganize itself due to changes in the environment, illness, and injury. Neuro (or neural) plasticity is based upon the concept of Hebbian learning, which in turn is a product of the now famous phrase neurons that fire together, wire together. Neuroplasticity can be defined as the process of synaptic plasticity enabling the bi-directionality of the brain to rewire, relearn and to adapt to changes over the course of time, all of which is independent of genetic heritability. Experience, |
AKA learning, in conjunction with the environment, can and does change both the structure and the function of the human brain.
In 1949, Canadian-born Donald Hebb, known as the father of neuropsychology, proposed an elegant yet profound postulation, that learning and experience change the brain. With thanks in large part to another extraordinary psychologist, Eric Kandel, it is incontrovertible that learning changes the very chemical composition of the brain at the level of the brain cell. This means that old dogs CAN and DO learn new tricks. Remember however, that neuroplasticity is bi-directional. This is to say while certain types of brain damage can e repaired, it also means that certain types of brain damage can be acquired. Addiction is an unfortunate but good example of this. It was not until he began working with Wilder Graves Penfield in 1937, that his work became laser-focused, in large part due to Penfield who as a neurosurgeon, was concerned with functionality and recovery of function in children who had significant brain injury.
In 1949 Hebb published the work that would catapult him into lasting fame with The Organization of Behavior: A Neuropsychological Theory. It was here that Hebb outlined his finding that areas of the prefrontal cortex would, post-operatively, demonstrate remarkable recovery of function. Through his work and the publication of his 1949 tome which stands today as one, if not thee, most significant achievements in neuroscience and neuropsychology, he was able to demonstrate that when two previously unrelated neurons fire together after injury or through repetition, they become wired together. And further, that through this neuroplastic process of being 'wired' together, if neuron 'A' fires all by itself, it will automatically trigger neuron 'B' to fire, without neuron 'B' actually doing anything to have caused it to fire, and visa versa.
Before Hebb, however, there was the remarkable 1906 Nobel Prize Laureate, neuroscientist, pathologist, artist, and father of neuroscience, Santiago Ramon y Cajal (1852-1934) from Spain, who coined the term neuronal plasticity. Ramon y Cajal both described and sketched the morphological changes of the brain and neurogenesis. This sketching of dendritic branching, is but one of many hundreds of Ramon y Cajal's neuroanatomical renditions. He drew the amazing depictions, with stunning detail and accuracy, of what he saw under the microscope.
Plasticity occurs at the molecular level and is closely tied if not synonymous to the mechanisms of learning and memory. These mechanisms are twinned with critical periods of neurological development. From the molecular to the cognitive, adult neurogenesis, synaptogenesis, dendritic branching, glutamate, protein phosphorylation , N-methyl-D-asparate (NMDA), long term potentiation (LTP), and the hippocampus and amygdaloid regions, are the basic underlying mechanisms that are deeply involved in neural plasticity of the central nervous system (CNS). In turn, these important processes and areas of the brain are responsible for producing specific disease and associated alteration of emotional and behavioral function.
Neurogenesis refers to the formation and the regeneration of neuronal cell growth and is literally translated to mean the beginning of the brain. Importantly, neurogenesis requires protein synthesis (phosphorylation) to evolve. Through neuronal communication, synaptic formation is a critical process of storing information and is obtained through experience. Additionally, synaptic transmision is a crucial underlying factor not just for learning, but essential for memory and cognition as well.Neurogenesis, and the subsequent amount of neuronal branching has been highly correlated with amount of education (Scheibel, 1993). Synaptogenesis is the formation and developmental plasticity of synapses between neurons. In its simplest terms, synaptogenesis refers to the interaction between pre- and post-synaptic neurons that result in the expression of the transmitter - and voltage-gated ion channels required for mature synaptic function.
Dendritic growth is an essential component of cortical growth, and is responsible for local processing which leads ultimately to axonal development and to the determination of specific properties of the cortex and resultant neural growth. We know that chronic and/or prolonged stress, along with considerable glucocorticoid exposure, effects dendritic atrophy and/or death. Dendrites actually seek out incoming activity and information and alter their responses (growth patterns that are represented by branching) dependent upon the stimuli received. It can be said that the branching and connectivity of dendritic activity, which is more pronounced in the limbic system and higher cortical areas, is the backbone of learning.
Dendritic branching is responsible for learning, the result, in part, of experience (sensation and perception) and the processing of incoming information. The more learning, the more branching for higher cortical areas. Dendrites function as what Quartz and Sejnowski (1997) refer to as detectors of correlated activity and growth preferentially in such regions. NMDA receptors play a particular role, along with glutamate and protein phosphorylation, in dendritic branching and development and neuronal plasticity.
Cortical plasticity is dependent upon proteins and protein synthesis throughout the brain, and neuronal processes are governed by protein phosphorylation. Phosphorylation is a process that alters protein (among other things) within a cell by changing configuration and cell permeability and the release of neurotransmitter substances. It also modulates neuronal activity and neurotransmitter receptors important for second (and third) messenger systems. This then ultimately accounts for the bigger picture of complex behaviors that are mediated by factors such as stress and short-term memory .
The hippocampus and amygdala are key structures of the limbic system and are said to be the most plastic regions of the brain, with the hippocampus reigning supreme in matters of plasticity. Located at the junction between the cortex and the lower diencephalon, the hippocampus is essential for declarative and spatial learning and memory and prevents conversion of short-term memory into long-term memory, while the amygdala is known to modulate emotional states.
According to the earlier work by Jay Belsky, et al (2009), they maintain that not all children (or adults) are equally susceptible to the effects of neuroplasticity. They maintain that there are at minimum, three determinants, early childhood temperament, the individual's physiological reactivity, and what they call measured genes referring to genetic inheritance such as the plasticity marker 7R-DRD4 allele.
It was the life and work of Donald Hebb that drew me, mercilessly, into the realm singularly inhabited by cognitive neuroscience.
Want to know more? You can follow my blogs, take a webinar, seminar, or e-course.
(c) Copyrighted, All Rights Reserved, May not be copied or shared without written permission of author
From: Ullman, S (2006). Neurobiological substrates of plasticity, In S. Ullman (Ed), A Neuropsychological Examination of Neural Plastic Alteration in the Dorsolateral and Orbital Prefrontal Functions Secondary to Early Childhood Sexual Traumatic Exposure in Diagnosed Adult Male Sexual Addicts (pp. 44-49).
In 1949, Canadian-born Donald Hebb, known as the father of neuropsychology, proposed an elegant yet profound postulation, that learning and experience change the brain. With thanks in large part to another extraordinary psychologist, Eric Kandel, it is incontrovertible that learning changes the very chemical composition of the brain at the level of the brain cell. This means that old dogs CAN and DO learn new tricks. Remember however, that neuroplasticity is bi-directional. This is to say while certain types of brain damage can e repaired, it also means that certain types of brain damage can be acquired. Addiction is an unfortunate but good example of this. It was not until he began working with Wilder Graves Penfield in 1937, that his work became laser-focused, in large part due to Penfield who as a neurosurgeon, was concerned with functionality and recovery of function in children who had significant brain injury.
In 1949 Hebb published the work that would catapult him into lasting fame with The Organization of Behavior: A Neuropsychological Theory. It was here that Hebb outlined his finding that areas of the prefrontal cortex would, post-operatively, demonstrate remarkable recovery of function. Through his work and the publication of his 1949 tome which stands today as one, if not thee, most significant achievements in neuroscience and neuropsychology, he was able to demonstrate that when two previously unrelated neurons fire together after injury or through repetition, they become wired together. And further, that through this neuroplastic process of being 'wired' together, if neuron 'A' fires all by itself, it will automatically trigger neuron 'B' to fire, without neuron 'B' actually doing anything to have caused it to fire, and visa versa.
Before Hebb, however, there was the remarkable 1906 Nobel Prize Laureate, neuroscientist, pathologist, artist, and father of neuroscience, Santiago Ramon y Cajal (1852-1934) from Spain, who coined the term neuronal plasticity. Ramon y Cajal both described and sketched the morphological changes of the brain and neurogenesis. This sketching of dendritic branching, is but one of many hundreds of Ramon y Cajal's neuroanatomical renditions. He drew the amazing depictions, with stunning detail and accuracy, of what he saw under the microscope.
Plasticity occurs at the molecular level and is closely tied if not synonymous to the mechanisms of learning and memory. These mechanisms are twinned with critical periods of neurological development. From the molecular to the cognitive, adult neurogenesis, synaptogenesis, dendritic branching, glutamate, protein phosphorylation , N-methyl-D-asparate (NMDA), long term potentiation (LTP), and the hippocampus and amygdaloid regions, are the basic underlying mechanisms that are deeply involved in neural plasticity of the central nervous system (CNS). In turn, these important processes and areas of the brain are responsible for producing specific disease and associated alteration of emotional and behavioral function.
Neurogenesis refers to the formation and the regeneration of neuronal cell growth and is literally translated to mean the beginning of the brain. Importantly, neurogenesis requires protein synthesis (phosphorylation) to evolve. Through neuronal communication, synaptic formation is a critical process of storing information and is obtained through experience. Additionally, synaptic transmision is a crucial underlying factor not just for learning, but essential for memory and cognition as well.Neurogenesis, and the subsequent amount of neuronal branching has been highly correlated with amount of education (Scheibel, 1993). Synaptogenesis is the formation and developmental plasticity of synapses between neurons. In its simplest terms, synaptogenesis refers to the interaction between pre- and post-synaptic neurons that result in the expression of the transmitter - and voltage-gated ion channels required for mature synaptic function.
Dendritic growth is an essential component of cortical growth, and is responsible for local processing which leads ultimately to axonal development and to the determination of specific properties of the cortex and resultant neural growth. We know that chronic and/or prolonged stress, along with considerable glucocorticoid exposure, effects dendritic atrophy and/or death. Dendrites actually seek out incoming activity and information and alter their responses (growth patterns that are represented by branching) dependent upon the stimuli received. It can be said that the branching and connectivity of dendritic activity, which is more pronounced in the limbic system and higher cortical areas, is the backbone of learning.
Dendritic branching is responsible for learning, the result, in part, of experience (sensation and perception) and the processing of incoming information. The more learning, the more branching for higher cortical areas. Dendrites function as what Quartz and Sejnowski (1997) refer to as detectors of correlated activity and growth preferentially in such regions. NMDA receptors play a particular role, along with glutamate and protein phosphorylation, in dendritic branching and development and neuronal plasticity.
Cortical plasticity is dependent upon proteins and protein synthesis throughout the brain, and neuronal processes are governed by protein phosphorylation. Phosphorylation is a process that alters protein (among other things) within a cell by changing configuration and cell permeability and the release of neurotransmitter substances. It also modulates neuronal activity and neurotransmitter receptors important for second (and third) messenger systems. This then ultimately accounts for the bigger picture of complex behaviors that are mediated by factors such as stress and short-term memory .
The hippocampus and amygdala are key structures of the limbic system and are said to be the most plastic regions of the brain, with the hippocampus reigning supreme in matters of plasticity. Located at the junction between the cortex and the lower diencephalon, the hippocampus is essential for declarative and spatial learning and memory and prevents conversion of short-term memory into long-term memory, while the amygdala is known to modulate emotional states.
According to the earlier work by Jay Belsky, et al (2009), they maintain that not all children (or adults) are equally susceptible to the effects of neuroplasticity. They maintain that there are at minimum, three determinants, early childhood temperament, the individual's physiological reactivity, and what they call measured genes referring to genetic inheritance such as the plasticity marker 7R-DRD4 allele.
It was the life and work of Donald Hebb that drew me, mercilessly, into the realm singularly inhabited by cognitive neuroscience.
Want to know more? You can follow my blogs, take a webinar, seminar, or e-course.
(c) Copyrighted, All Rights Reserved, May not be copied or shared without written permission of author
From: Ullman, S (2006). Neurobiological substrates of plasticity, In S. Ullman (Ed), A Neuropsychological Examination of Neural Plastic Alteration in the Dorsolateral and Orbital Prefrontal Functions Secondary to Early Childhood Sexual Traumatic Exposure in Diagnosed Adult Male Sexual Addicts (pp. 44-49).