Unformatted text preview: Outline 13: Learning, Memory & Neural Plasticity- Part 1 (Cont.) Book Chapter Readings for this outline: Sections 11.6-11.8, 9.3-9.4 III. Hippocampal Place Cells
Cells that are most active when a rat is in a particular position relative to stable cues in the environment. A. Place cell properties: 1. Location specific-Intense activity only when a rat's head is in a certain position in the environment 2. Place fields develop within minutes in a new environment and are stable for weeks to months (maybe longer) 3. The same cell can have stable representations of different places within different environments 4. Place cells do not make up a topographic representation of space within hippocampus 5. Place cells can vary dependent upon what the rat is doing in the environment (e.g., directed versus random search for food pellets) B. Does the hippocampus form a cognitive map of space? Some believe that a major function of the hippocampus is to form cognitive maps of space. Others think that spatial processing by the hippocampus is just one component of a larger function, that of forming relationships between individual items in memory. In potential support of the latter, hippocampal neurons do respond to stimuli other than spatial positions, e.g., "head direction cells", "cue cells" and "stimulus sequence cells" 1 IV. Considerations for finding the "engram "
-Localization of Function -Distributed Processing -Hierarchical pathways -Parallel pathways It is now quite clear that: (1) The same type of learning can involve changes in many different brain regions. (2) Different types of learning can involve changes in different brain regions. Learning, Memory and Neural Plasticity, Part II:
************************************************ How does the brain change? ************************************************ I. Background
Donald Hebb (1949) The Organization of Behavior Hebb's Neurophysiological Postulate: "When an axon of cell A is near enough to excite 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." Today Hebbian synapses are those which are enhanced by coincident activity between the pre-synaptic and post-synaptic neuron i.e., coincident pre- and post-synaptic activity enhances the efficacy of the connections between neurons A and B This could work by (1) increasing the strength, or "efficacy", of existing synapses and (2) changing the numbers of synapses II. Long-term potentiation (LTP)- an example of how synapses may
become more efficacious LTP is a long lasting increase in neuronal activity induced by afferent activation (activation of the input to the neurons) 2 A. Some terms: pre-synaptic post-synaptic correlated pre- and post-synaptic activitypre-synaptic activation paired with post-synaptic depolarization tetanic stimulation, high frequency electrical stimulation (tetanic- "convulsant, spasmodic" rapidly repeating) B. An example of how LTP induction works: At "normal" low frequency stimulation or stimulation of only a few inputs, glutamate released from the pre-synaptic terminal binds with AMPA receptors on the post-synaptic membrane. This opens NA+ channels and results in a small depolarization (EPSP) in the post-synaptic cell. With repeated high frequency stimulation of several inputs, depolarization of the post-synaptic cell is greater (more Na+ channels are opened) This greater depolarization permits NMDA receptors on the post-synaptic cell to open Ca2+channels The Ca2+ influx via NMDA receptors results in the induction of LTP by initiating in a cascade of cellular changes that enhance post-synaptic responsiveness, such as the insertion of new AMPA receptors into the postsynaptic membrane. Now, when the cell is given normal low frequency stimulation again, the depolarization is greater than it was before (prior to the exposure to high frequency stimulation). 3 C. Properties of LTP: 1. Associativity: a. Pre- and post-synaptic associativity The post-synaptic neuron must be sufficiently depolarized for the pre-synaptic neuron's effects to be enhanced (i.e., NMDA receptor activation only occurs if there is already sufficient depolarization b. Associativity of afferent input Stimulation of a weak pathway (one with few inputs) alone does not produce LTP because it does not produce strong enough depolarization to activate NMDA receptors. However, paired stimulation of a weak pathway with a stronger pathway will result in LTP of the weak pathway (Why is this reminiscent of classical conditioning?) 2. Cooperativity: You can not produce LTP by stimulating only one axon's input onto a post-synaptic cell. It requires concurrent stimulation of at least several axons 3. Specificity: LTP is specific to the post-synaptic neurons that have been stimulated by the high frequency activation. 4 D. Is LTP Learning? NO, LTP models use artificial stimulation parameters. BUT, can learning work this way? Maybe-1. Behavioral LTP LTP (a long lasting increase in neuronal activity induced by afferent activation) can be induced by learning. Examples: in visual cortex-complex environment exposure (more on this later) motor cortex-motor skills training amygdala-fear conditioning hippocampus-spatial learning?? 2. Interfering with things that interfere with LTP interfere with leaning e.g., administering drugs that block NMDA receptors during exposure to a learning task blocks the learning (Aside - LTD- long lasting decrease in neuronal activity induced by afferent activation) 5 III. Changes in the number and structure of synaptic connections
Synaptogenesis-- the formation of new synaptic connections (Historical misconception - the brains of adults are hard-wired. Changes in the brain must be limited to changes in the activity of pre-existing connections.) A. Experience induced changes in synapses in Adult animals 1. Learning of various types can change the number and configuration of synaptic connections in brain regions involved in the learned behaviors Examples: Complex environment housing - visual cortex, hippocampus, cerebellum, striatum... Maze training - visual cortex Reach training - motor cortex Acrobatic training - motor cortex, cerebellum 2. Changes in synapse number are often accompanied by changes in synaptic structure and configuration Question: Are there limits to synapse addition? There is little increase in synapse number in super-enriched rats in comparison to run-of-the-mill enriched rats. There may be a limit to adding synapses, after which more efficient use of synapses may be the route of change Given ongoing exposure to learning tasks, patterns of functional connectivity may be continuously altered whereas net numbers of synapses may be relatively stable. B. Experience dependent changes in developing animals 1. There are intrinsic forces during development that make the brain ready to be modified by experience 6 Synapse overproduction and selective elimination based on competitive processes During development, many more synapses are created than are maintained into adulthood. It is believed that more effective synapses are maintained and less effective synapses are lost. This process of selectively maintaining some synapses at the expense of others (selective elimination) is known as synaptic competition This is likely to be a widespread general brain process of establishing neural connections during development. 2. Examples a. Visual system Normally, inputs from the 2 eyes are represented in the cortex as adjacent ocular dominance columns-alternating strips of cortical columns showing responsiveness to visual stimuli presented to left or right eye. -Neurons in ocular dominance columns send converging input to binocular neurons. 7 1. Monocular deprivation - depriving visual stimulation to one eye Wiesel & Hubel (1963)-monocular deprivation during sensitive periods of development cause a loss of the neuronal responsiveness during later visual input. During early development, axonal projections to ocular dominance columns overlap. Their pruning back results in segregated columns responsive to left vs right eye input. This segregation is dependent upon exposure to visual stimuli to both eyes. 2. Alternating visual input Visual exposure to both eyes but never at the same time during sensitive stages in development prevents the development of neurons that are binocularly driven. Approximately half of this population gets "captured" by each eye, i.e., is responsive only to input to left or right eye, but not both. ---There are many other examples of experience-expectant processes: Barrel fields in rats, language, imprinting, audition, song learning in birds, olfaction, emotions (Harlow's monkeys), visuomotor integration (Gondola kittens) Question: Why would brain development work this way? Why not just hard wire everything? 8 IV. New neurons in adult brains
Neurogenesis - the production of new neurons Adult neurogenesis- " in adult animals A. Background-Historical misconception: We are born with all of the neurons we will ever have. Adult neurogenesis was discovered in the hippocampus of rats in the 1960'searly 1980's*. The findings were largely dismissed. 1980's-90's-Skepticism about adult neurogenesis in rats and mice gives way under mounting evidence, but this is thought one of those examples of how rodents are different from primates 1997- 1999 Elizabeth Gould finds neurogenesis in the dentate gyrus and cerebral cortex of new and old world monkeys 1998 Eriksson-identifies neurogenesis in the hippocampus of humans Currently, the importance and prevalence of neurogenesis in healthy adult humans is controversial and in need of more research. B. From where do the new neurons come? Germinal zones--zones where neuronal precursor cells are concentrated stem cells --> neural (or glial) progenitor cells --> differentiated cells (neurons or glia) There are two major germinal zones: 9 1. Subventricular Zone (around the lateral ventricles) This is the source of new neurons in the olfactory bulb. They migrate from around the lateral ventricles rostrally into the olfactory bulbs. The pathway they take is called the rostral migratory stream (RMS). Gould et al (1999) Science, "Neurogenesis in the neocortex of adult primates" This also appears to be a source of the new neurons that Gould has found in the cerebral cortex. The new neurons may differentiate into small interneurons. There may be other sources of new neurons in cerebral cortex-- 2. Subgranular Zone of the Dentate Gyrus Progenitor cells in this region are the source of new granule cell neurons in the dentate gyrus, a subregion of the hippocampus 10 Neural progenitor cells in these 2 germinal zones are found in close proximity to vascular progenitor cells. ("Angiogenesis"--the production of new blood vessels.) For this reason, areas of proliferative activity have been termed the "neurovascular niche" C. Is adult neurogenesis a plausible mechanism of learning? 1. Adult neurogenesis is sensitive to experience 2. Disrupting neurogenesis might impair learning (but the case is not very strong for this...yet?) Although there are differences in the particulars, the current general view of learning is that it results from the selective strengthening and weakening of subsets of neural connections of existing neurons. Is the addition of new neurons into a neural system: -a plausible alternative to modification of existing connections? -another way of doing it (in some brain areas; some of the time)? - something that is coordinated with modification of the connections of existing neurons? ------------------------------------------------------------------------------*Altman & Das (1965) Autoradiographic and histological evidence of postnatal hippocampal neurogenesis in rats. J Comp Neurol. 124:319-35. Kaplan & Hinds (1977) Neurogenesis in the adult rat: electron microscopic analysis of light radioautographs. Science. 197:1092-4. 11 ...
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This note was uploaded on 04/20/2008 for the course PSY 308 taught by Professor Jones during the Spring '08 term at University of Texas.
- Spring '08