Developmental plasticity

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Developmental plasticity is a general term referring to changes in neural connections during development as a result of environmental interactions as well as neural changes induced by learning. [1] Much like neuroplasticity, or brain plasticity, developmental plasticity is specific to the change in neurons and synaptic connections as a consequence of developmental processes. A child creates most of these connections from birth to early childhood. There are three primary methods by which this may occur as the brain develops,[ citation needed ] but critical periods determine when lasting changes may form. Developmental plasticity may also be used in place of the term phenotypic plasticity when an organism in an embryonic or larval stage can alter its phenotype based on environmental factors. [2] However, a main difference between the two is that phenotypic plasticity experienced during adulthood can be reversible, whereas traits that are considered developmentally plastic set foundations during early development that remain throughout the life of the organism. [3]

Contents

Mechanisms

Time-lapse video of a developing dendrite.

During development, the central nervous system acquires information via endogenous or exogenous factors as well as learning experiences. In acquiring and storing such information, the plastic nature of the central nervous system allows for the adaptation of existing neural connections in order to accommodate new information and experiences, resulting in developmental plasticity. This form of plasticity that occurs during development is the result of three predominant mechanisms: synaptic and homeostatic plasticity, and learning.[ citation needed ]

Synaptic plasticity

The underlying principle of synaptic plasticity is that synapses undergo an activity-dependent and selective strengthening or weakening so that new information can be stored. [4] [5] Synaptic plasticity depends on numerous factors including the threshold of the presynaptic stimulus in addition to the relative concentrations of neurotransmitter molecules. Synaptic plasticity has long been implicated for its role in memory storage and is thought to play a key role in learning. [6] [5] However, during developmental periods, synaptic plasticity is of particular importance, as changes in the network of synaptic connections can ultimately lead to changes in developmental milestones. For instance, the initial overproduction of synapses during development is key to plasticity that occurs in the visual and auditory cortices. [7] In experiments conducted by Hubel and Wiesel, the visual cortex of kittens exhibits synaptic plasticity in the refinement of neural connections following visual inputs. Correspondingly, in the absence of such inputs during development, the visual field fails to develop properly and can lead to abnormal structures and behavior. [8] Furthermore, research suggests that this initial overproduction of synapses during developmental periods provides the foundation by which many synaptic connections can be formed, thus resulting in more synaptic plasticity. In the same way that synapses are abundant during development, there are also refining mechanisms that assist in the maturation of synapses in neural circuits. This regulatory process allows the strengthening of important or frequently used synaptic connections while reducing the amount of weak connections. [9]

Homeostatic plasticity

In order to maintain balance, homeostatic controls exist to regulate the overall activity of neural circuits, specifically by regulating the destabilizing effects of developmental and learning processes that result in changes of synaptic strength. Homeostatic plasticity also helps regulate prolonged excitatory responses, which lead to a reduction in all of a neuron's synaptic responses. [10] Numerous pathways have recently been associated with homeostatic plasticity, though there is still no clear molecular mechanism. Synaptic scaling is one method that serves as a type of autoregulation, as neurons can recognize their own firing rates and notice when there are alterations; calcium-dependent signals control the levels of glutamate receptors at synaptic sites in response. Homeostatic mechanisms may be local or network-wide. [11]

Learning

While synaptic plasticity is considered to be a by-product of learning, learning involves interaction with the environment to acquire the new information or behavior; synaptic plasticity merely represents the change in strength or configuration of neural circuits. [12] Learning is crucial, as there is considerable interaction with the environment, which is when the potential for acquiring new information is greatest. By depending largely upon selective experiences, neural connections are altered and strengthened in a manner that is unique to those experiences. [13] Experimentally, this can be seen when rats are raised in an environment that allows ample social interaction, resulting in increased brain weight and cortical thickness. In contrast, the inverse is seen following rearing in an environment devoid of interaction. [14] Also, learning plays a considerable role in the selective acquisition of information and is markedly demonstrated when children develop one language instead of another. Another example of such experience-dependent plasticity that is critical during development is the occurrence of imprinting. This occurs as a result of a young child or animal being exposed to a novel stimulus and rapidly implementing a certain behavior in response. [15]

Neural development

The formation of the nervous system is one of the most crucial events in the developing embryo. The differentiation of stem cell precursors into specialized neurons gives rise to the formation of synapses and neural circuits, which is key to the principle of plasticity. [16] During this pivotal point in development, consequent developmental processes like the differentiation and specialization of neurons are highly sensitive to exogenous and endogenous factors. [17] For example, in utero exposure to nicotine has been linked to adverse effects, such as severe physical and cognitive deficits, due to the impediment of the normal acetylcholine receptor activation. In a recent study, the connection between such nicotine exposure and prenatal development was assessed. It was determined that nicotine exposure in early development can have a lasting and encompassing effect on neuronal structures, underlying the behavioral and cognitive defects observed in exposed humans and animals. Additionally, when proper synaptic function is disrupted through nicotine exposure, the overall circuit may become less sensitive and responsive to stimuli, resulting in compensatory developmental plasticity. [18] It is for this reason that exposure to various environmental factors during developmental periods can cause profound effects on subsequent neural functioning.

Neural refinement and connectivity

Initial stages of neural development begin early on in the fetus with spontaneous firing of the developing neuron. [19] These early connections are weak and often overlap at the terminal ends of the arbors. [20] The young neurons have complete potential of changing morphology during a time span classified as the critical period to achieve strengthened and refined synaptic connections. It is during this time that damaged neuronal connections can become functionally recovered. Large alterations in length and location of these neurons can occur until synaptic circuitry is further defined. [21] Although organization of neural connections begins at the earliest stages of development, activity-driven refinement only begins at birth when the individual neurons can be recognized as separate entities and start to enhance in specificity. [22] The gradual pruning of the initially blurry axonal branching occurs via competitive and facilitative mechanisms, relying on electrical activity at the synapses; axons that fire independently of each other tend to compete for territory, whereas axons that synchronously fire mutually amplify connections. [23] Until this architecture has been established, retinal focus remains diffuse. Perpetuation of these newly formed connections or the lack thereof depends on maintenance of electrical activities at the synapses. Upon refinement, the elaborate connections narrow and strengthen to fire only in response to specific stimuli to optimize visual acuity. [24] These mechanisms can malfunction with the introduction of toxins, which bind to sodium channels and suppress action potentials and consequently electrical activity between synapses. [25]

Quantification of synaptic networks has primarily been through retinal wave detection using Ca2+ fluorescent indicators. Prior to birth, retinal waves are seen to originate as clusters that propagate through the refractory region. These assays have been shown to provide spatiotemporal data on the random bursts of action potentials produced in a refractory period. [26] Another assay recently developed to assess the depth of neuronal connections utilizes the trans-neuronal spread of rabies. [27] This method of tracing employs the migration of a neurotropic virus through tightly interconnected neurons and specific site labeling of distinct connections. [28] Patch-clamping experiments and calcium imaging are often conducted based on preliminary results from this assay in order to detect spontaneous neuronal activity. [29] A method for in vitro synaptic quantification has been developed that uses immunofluorescence to measure synaptic density in different cell cultures. [30]

Critical period

The concept of critical periods is a widely accepted and prominent theme in development, with strong implications for developmental plasticity. Critical periods establish a time frame in which the shaping of neural networks can be carried out. During these critical periods in development, plasticity occurs as a result of changes in the structure or function of developing neural circuits. Such critical periods can also be experience-dependent, in the instance of learning via new experiences, or can be independent of the environmental experience and rely on biological mechanisms including endogenous or exogenous factors. [31] Some of the most pervading examples of this can be seen through the development of the visual cortex in addition to the acquisition of language as a result of developmental plasticity during the critical period. [8] [32] A lesser known example, however, remains the critical development of respiratory control during developmental periods. At birth, the development of respiratory control neural circuits is incomplete, requiring complex interactions from both the environment and intrinsic factors. Experimentally exposing two-week-old kittens and rats to hyperoxic conditions completely eliminates the carotid chemoreceptor response to hypoxia, resulting in respiratory impairment. This has remarkable clinical significance, as newborn infants are often supplemented with considerable amounts of oxygen, which could detrimentally affect the way in which neural circuits for respiratory control develop during the critical period. When stimuli appear or experiences occur outside of the critical period, any potential outcome is typically not long-lasting. [33]

Spontaneous network activity

Another lesser known element of developmental plasticity includes spontaneous bursts of action potentials in developing neural circuits, also referred to as spontaneous network activity. During the early development of neural connections, excitatory synapses undergo spontaneous activation, resulting in elevated intracellular calcium levels that signal the onset of numerous signaling cascades and developmental processes. For example, prior to birth, neural circuits in the retina undergo spontaneous network activity, which has been found to elicit the formation of retinogeniculate connections. [34] Developmental spontaneous network activity is also exhibited in the proper formation of neuromuscular circuits. [35] It is believed that spontaneous network activity establishes a scaffold for subsequent learning and information acquisition following the initial establishment of synaptic connections during development.

Phenotypic plasticity

Reaction norms

Graphical representation of a reaction norm, which determines distribution of potential phenotypes. Trait-scale-norm.png
Graphical representation of a reaction norm, which determines distribution of potential phenotypes.

The norm of reaction, or reaction norm, is a pattern of phenotypic plasticity that describes how a single genotype can produce an array of different phenotypes in response to different environmental conditions. [2] Furthermore, a reaction norm can be a graphical representation of organismal variation in phenotype in response to numerous environmental circumstances. The graphical representation of reaction norms is commonly parabolic in shape, which represents the variation in plasticity across a population. [36] Additionally, reaction norms allow organisms to evaluate the need for various phenotypes in response to the magnitude of the environmental signal. [2]

Polyphenisms

Example of phenotypic plasticity in the desert locust Schistocerca gregaria. The green pigment locust (top) has miniature wings that result from a low-density population. The deep pigmentation locust (bottom) has leg and wing development suitable for migration, which arose due to a high-density environment. DesertLocust.jpeg
Example of phenotypic plasticity in the desert locust Schistocerca gregaria. The green pigment locust (top) has miniature wings that result from a low-density population. The deep pigmentation locust (bottom) has leg and wing development suitable for migration, which arose due to a high-density environment.

Polyphenism refers to the ability of a single genotype to produce a variety of phenotypes in response to different environmental conditions. In contrast to reaction norms, which produce a continuous range of phenotypes, polyphenisms allow a distinct phenotype to arise from altering environmental conditions. [37] An example of polyphenism can be seen in the Florida carpenter ant, Camponotus floridanus. For a developing ant embryo, a multitude of environmental signals can ultimately determine the adult ant morphology. For Florida carpenter ants, the end phenotype and behavior are determined by the morphology; developing ants can either become minor workers, major workers, or queen ants. Although the polyphenism of the ants has been documented, research is still needed to determine the molecular mechanisms for the induction of each unique phenotype. [38]

Environmental cues

Environmental cues in either the maternal or the embryonic environment can result in changes in the embryo. Embryonic development is a sensitive process and can be impacted by cues from predators, [39] light, [40] and/or temperature. [41] For example, in Daphnia , neonates exposed to predator cues displayed higher expression of genes related to digestion, reproductive function, and defense. It was hypothesized that this increase in gene expression would allow the Daphnia to defend themselves and that an increase in growth would result in a larger investment in future offspring. Subsequent generations exhibited a similar pattern, despite not being exposed to any predator cues, suggesting an inheritance of epigenetic expression factors. [39] An organism's sensitivity to light during development could be useful in predicting what phenotype may be the most beneficial in the future based on the foliage of the mature organism. [40] Several species, including alligators and tortoises, have temperature-dependent sex determination, where the sex of the organism is dependent on the environmental temperature during a crucial thermosensitive period. An active area of research involves the mechanisms of temperature sex determination, which have been hypothesized to be associated with the methylation of specific genes. [41]

See also

Related Research Articles

The development of the nervous system, or neural development (neurodevelopment), refers to the processes that generate, shape, and reshape the nervous system of animals, from the earliest stages of embryonic development to adulthood. The field of neural development draws on both neuroscience and developmental biology to describe and provide insight into the cellular and molecular mechanisms by which complex nervous systems develop, from nematodes and fruit flies to mammals.

<span class="mw-page-title-main">Dendritic spine</span> Small protrusion on a dendrite that receives input from a single axon

A dendritic spine is a small membranous protrusion from a neuron's dendrite that typically receives input from a single axon at the synapse. Dendritic spines serve as a storage site for synaptic strength and help transmit electrical signals to the neuron's cell body. Most spines have a bulbous head, and a thin neck that connects the head of the spine to the shaft of the dendrite. The dendrites of a single neuron can contain hundreds to thousands of spines. In addition to spines providing an anatomical substrate for memory storage and synaptic transmission, they may also serve to increase the number of possible contacts between neurons. It has also been suggested that changes in the activity of neurons have a positive effect on spine morphology.

Hebbian theory is a neuropsychological theory claiming that an increase in synaptic efficacy arises from a presynaptic cell's repeated and persistent stimulation of a postsynaptic cell. It is an attempt to explain synaptic plasticity, the adaptation of brain neurons during the learning process. It was introduced by Donald Hebb in his 1949 book The Organization of Behavior. The theory is also called Hebb's rule, Hebb's postulate, and cell assembly theory. Hebb states it as follows:

Let us assume that the persistence or repetition of a reverberatory activity tends to induce lasting cellular changes that add to its stability. ... When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased.

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory.

In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.

Synaptogenesis is the formation of synapses between neurons in the nervous system. Although it occurs throughout a healthy person's lifespan, an explosion of synapse formation occurs during early brain development, known as exuberant synaptogenesis. Synaptogenesis is particularly important during an individual's critical period, during which there is a certain degree of synaptic pruning due to competition for neural growth factors by neurons and synapses. Processes that are not used, or inhibited during their critical period will fail to develop normally later on in life.

<span class="mw-page-title-main">Neural circuit</span> Network or circuit of neurons

A neural circuit is a population of neurons interconnected by synapses to carry out a specific function when activated. Multiple neural circuits interconnect with one another to form large scale brain networks.

Neuroplasticity, also known as neural plasticity or brain plasticity, is the ability of neural networks in the brain to change through growth and reorganization. It is when the brain is rewired to function in some way that differs from how it previously functioned. These changes range from individual neuron pathways making new connections, to systematic adjustments like cortical remapping or neural oscillation. Other forms of neuroplasticity include homologous area adaptation, cross modal reassignment, map expansion, and compensatory masquerade. Examples of neuroplasticity include circuit and network changes that result from learning a new ability, information acquisition, environmental influences, practice, and psychological stress.

Schaffer collaterals are axon collaterals given off by CA3 pyramidal cells in the hippocampus. These collaterals project to area CA1 of the hippocampus and are an integral part of memory formation and the emotional network of the Papez circuit, and of the hippocampal trisynaptic loop. It is one of the most studied synapses in the world and named after the Hungarian anatomist-neurologist Károly Schaffer.

Metaplasticity is a term originally coined by W.C. Abraham and M.F. Bear to refer to the plasticity of synaptic plasticity. Until that time synaptic plasticity had referred to the plastic nature of individual synapses. However this new form referred to the plasticity of the plasticity itself, thus the term meta-plasticity. The idea is that the synapse's previous history of activity determines its current plasticity. This may play a role in some of the underlying mechanisms thought to be important in memory and learning such as long-term potentiation (LTP), long-term depression (LTD) and so forth. These mechanisms depend on current synaptic "state", as set by ongoing extrinsic influences such as the level of synaptic inhibition, the activity of modulatory afferents such as catecholamines, and the pool of hormones affecting the synapses under study. Recently, it has become clear that the prior history of synaptic activity is an additional variable that influences the synaptic state, and thereby the degree, of LTP or LTD produced by a given experimental protocol. In a sense, then, synaptic plasticity is governed by an activity-dependent plasticity of the synaptic state; such plasticity of synaptic plasticity has been termed metaplasticity. There is little known about metaplasticity, and there is much research currently underway on the subject, despite its difficulty of study, because of its theoretical importance in brain and cognitive science. Most research of this type is done via cultured hippocampus cells or hippocampal slices.

<span class="mw-page-title-main">Synapse</span> Structure connecting neurons in the nervous system

In the nervous system, a synapse is a structure that permits a neuron to pass an electrical or chemical signal to another neuron or to the target effector cell.

In neuroscience, homeostatic plasticity refers to the capacity of neurons to regulate their own excitability relative to network activity. The term homeostatic plasticity derives from two opposing concepts: 'homeostatic' and plasticity, thus homeostatic plasticity means "staying the same through change".

<span class="mw-page-title-main">Synaptic pruning</span> Process of synapse elimination that occurs between early childhood and the onset of puberty

Synaptic pruning, a phase in the development of the nervous system, is the process of synapse elimination that occurs between early childhood and the onset of puberty in many mammals, including humans. Pruning starts near the time of birth and continues into the late-20s. During pruning, both the axon and dendrite decay and die off. It was traditionally considered to be complete by the time of sexual maturation, but this was discounted by MRI studies.

A cultured neuronal network is a cell culture of neurons that is used as a model to study the central nervous system, especially the brain. Often, cultured neuronal networks are connected to an input/output device such as a multi-electrode array (MEA), thus allowing two-way communication between the researcher and the network. This model has proved to be an invaluable tool to scientists studying the underlying principles behind neuronal learning, memory, plasticity, connectivity, and information processing.

Activity-dependent plasticity is a form of functional and structural neuroplasticity that arises from the use of cognitive functions and personal experience; hence, it is the biological basis for learning and the formation of new memories. Activity-dependent plasticity is a form of neuroplasticity that arises from intrinsic or endogenous activity, as opposed to forms of neuroplasticity that arise from extrinsic or exogenous factors, such as electrical brain stimulation- or drug-induced neuroplasticity. The brain's ability to remodel itself forms the basis of the brain's capacity to retain memories, improve motor function, and enhance comprehension and speech amongst other things. It is this trait to retain and form memories that is associated with neural plasticity and therefore many of the functions individuals perform on a daily basis. This plasticity occurs as a result of changes in gene expression which are triggered by signaling cascades that are activated by various signaling molecules during increased neuronal activity.

<span class="mw-page-title-main">Nonsynaptic plasticity</span> Form of neuroplasticity

Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.

In neuroscience, synaptic scaling is a form of homeostatic plasticity, in which the brain responds to chronically elevated activity in a neural circuit with negative feedback, allowing individual neurons to reduce their overall action potential firing rate. Where Hebbian plasticity mechanisms modify neural synaptic connections selectively, synaptic scaling normalizes all neural synaptic connections by decreasing the strength of each synapse by the same factor, so that the relative synaptic weighting of each synapse is preserved.

Addiction is a state characterized by compulsive engagement in rewarding stimuli, despite adverse consequences. The process of developing an addiction occurs through instrumental learning, which is otherwise known as operant conditioning.

<span class="mw-page-title-main">Heterosynaptic plasticity</span>

Synaptic plasticity refers to a chemical synapse's ability to undergo changes in strength. Synaptic plasticity is typically input-specific, meaning that the activity in a particular neuron alters the efficacy of a synaptic connection between that neuron and its target. However, in the case of heterosynaptic plasticity, the activity of a particular neuron leads to input unspecific changes in the strength of synaptic connections from other unactivated neurons. A number of distinct forms of heterosynaptic plasticity have been found in a variety of brain regions and organisms. These different forms of heterosynaptic plasticity contribute to a variety of neural processes including associative learning, the development of neural circuits, and homeostasis of synaptic input.

<span class="mw-page-title-main">Synaptic stabilization</span> Modifying synaptic strength via cell adhesion molecules

Synaptic stabilization is crucial in the developing and adult nervous systems and is considered a result of the late phase of long-term potentiation (LTP). The mechanism involves strengthening and maintaining active synapses through increased expression of cytoskeletal and extracellular matrix elements and postsynaptic scaffold proteins, while pruning less active ones. For example, cell adhesion molecules (CAMs) play a large role in synaptic maintenance and stabilization. Gerald Edelman discovered CAMs and studied their function during development, which showed CAMs are required for cell migration and the formation of the entire nervous system. In the adult nervous system, CAMs play an integral role in synaptic plasticity relating to learning and memory.

References

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