Medical Neuroscience explores the functional organization and neurophysiology of the human central nervous system, while providing a neurobiological framework for understanding human behavior. In this course, you will discover the organization of the neural systems in the brain and spinal cord that mediate sensation, motivate bodily action, and integrate sensorimotor signals with memory, emotion and related faculties of cognition. The overall goal of this course is to provide the foundation for understanding the impairments of sensation, action and cognition that accompany injury, disease or dysfunction in the central nervous system. The course will build upon knowledge acquired through prior studies of cell and molecular biology, general physiology and human anatomy, as we focus primarily on the central nervous system. This online course is designed to include all of the core concepts in neurophysiology and clinical neuroanatomy that would be presented in most first-year neuroscience courses in schools of medicine. However, there are some topics (e.g., biological psychiatry) and several learning experiences (e.g., hands-on brain dissection) that we provide in the corresponding course offered in the Duke University School of Medicine on campus that we are not attempting to reproduce in Medical Neuroscience online. Nevertheless, our aim is to faithfully present in scope and rigor a medical school caliber course experience. This course comprises six units of content organized into 12 weeks, with an additional week for a comprehensive final exam: - Unit 1 Neuroanatomy (weeks 1-2). This unit covers the surface anatomy of the human brain, its internal structure, and the overall organization of sensory and motor systems in the brainstem and spinal cord. - Unit 2 Neural signaling (weeks 3-4). This unit addresses the fundamental mechanisms of neuronal excitability, signal generation and propagation, synaptic transmission, post synaptic mechanisms of signal integration, and neural plasticity. - Unit 3 Sensory systems (weeks 5-7). Here, you will learn the overall organization and function of the sensory systems that contribute to our sense of self relative to the world around us: somatic sensory systems, proprioception, vision, audition, and balance senses. - Unit 4 Motor systems (weeks 8-9). In this unit, we will examine the organization and function of the brain and spinal mechanisms that govern bodily movement. - Unit 5 Brain Development (week 10). Next, we turn our attention to the neurobiological mechanisms for building the nervous system in embryonic development and in early postnatal life; we will also consider how the brain changes across the lifespan. - Unit 6 Cognition (weeks 11-12). The course concludes with a survey of the association systems of the cerebral hemispheres, with an emphasis on cortical networks that integrate perception, memory and emotion in organizing behavior and planning for the future; we will also consider brain systems for maintaining homeostasis and regulating brain state.
Brain Development Across the Lifespan, part 1
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來自 Duke University 的課程
Medical Neuroscience
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從本節課中
The Changing Brain: The Brain Across the Lifespan
This module represents another turning point in Medical Neuroscience. Now that we have surveyed human neuroanatomy and our sensory and motor systems, we are ready to take a step back and consider how this magnificent central nervous system came to be the way that it is. We will also learn how the brain re-wires itself across the lifespan as genetic specification, experience-dependent plasticity and self-organization continue to interact, re-shaping the structure and function of neural circuits throughout the central nervous system.
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Leonard E. White, Ph.D.Associate Professor
Department of Neurology, Department of Neurobiology, Duke University School of Medicine; Department of Psychology & Neuroscience, Trinity College of Arts & Sciences; Director of Education, Duke Institute for Brain Sciences; Duke University
Welcome to the final tutorial in Unit five, which is all about the changing
brain. And today's tutorial is entitled, The
Changing Brain Across the Lifespan, Development, Repair, and Regeneration.
Today's tutorial relates to two of our core concepts in the field of
neuroscience. First, that life experiences change the
nervous system. We'll spend some time in this tutorial
talking about a variety of life experiences that have an impact on
nervous system structure and function, including injuries to the nervous system.
And, hopefully, what you'll see is that fundamentals, discoveries promote healthy
living in the treatment of disease. And the more we know about the basic
mechanisms of nervous system change in plasticity, and the response of nervous
tissue to injury and disease. the more we are likely to develop
strategic interventions that will do just this.
promote healthy living, and the treatment of human disease.
Well I have several learning objectives for in this tutorial.
first I'd like for you to be able to discuss neurobiological basis for changes
in gray matter and white matter volume, that occur in the developing brain,
throughout the years of childhood. I'd like for you to be able to discuss
the mechanisms of regeneration of peripheral nerves following injury.
And I'd like for you to be able to discuss the mechanisms of plasticity in
adult sensorimotor maps following peripheral injury.
I'd like for you to be able to discuss the mechanisms of plasticity in adult
neural circuits following central injury. That is, injury to the brain or the
spinal cord itself. And lastly, I would like for you to be
able to have a cogent discussion of the evidence regarding neurogenesis in the
adult central nervous system. And that will include evidence for
neurogenesis, as well as evidence against neurogenesis.
Well we will begin this tutorial as we have the last several.
just recognizing that there are three principle forces at work to shape brain
development. certainly these are powerful forces in
embryogenesis and in early life. But they continue to interact with one
another throughout the lifespan as genes are expressing their protein product.
So, there's the contribution of nature or genetic specification cells continue to
interact with one another in a dynamical way through activity based mechanisms,
whether that activity is holy endogenous or modulated by experience.
So, so there's the potential for self organization to continue to play out.
And of course we interact with the environment through our sensory and motor
systems, and this allows for these endogenous patterns of activity to be
shaped by the stimuli that we encounter. The way that we actually use our body, so
this would be sensory motor experience. And what is particularly interesting to
consider, and I wish we could do more, but our knowledge is limited and so is
our time as you all well know. these three factors, I think become
especially intriguing and important to consider when we think about how the
brain responds to injury. For example, we might imagine that when
the brain is injured then the dynamical system of that network is perturbed in
some way. And this very likely is going to alter
they way these ongoing patterns of activity are shaped by interactions with
the environment. Likely these dynamical systems will
fluctuate, and have an impact on the expression of genes, perhaps the
expression of genes that have been dormant since the early days of
embryogenesis. And likewise the gene products then will
interact with our neural systems that will affect the way they transduce
electrical impulses and encode information about the conditions of the
body and the outside world. So, these three factors continue to shape
how the brain responds to injury. So, that's just a thought I'd like for
you to keep in your mind, as we consider some of those contexts later in this
tutorial. But let's begin by picking up the story
of the changing brain across the lifespan.
Where we left off last time, which is in neonatal life at a time when the brain is
especially sensitive to the impact, and the influence of nurture or environmental
interactions, be they for the better or for the worse.
So, I'd like to continue the story of development and extend now the context
out, throughout childhood. And one very important consideration that
we should mention as we consider how the brain changes in childhood, is the
creation of new synaptic connections, and we call this synaptogenesis.
And there had been a variety of reports about synaptogenesis in the human brain
throughout the 70's and the 80's, and I think largely these data were somewhat
flawed. simply because the methods, just are
extremely difficult to employ successfully, in human tissue.
So, no, no fault to the investigators. But just that, we have not yet developed
the methods that allow for the generation of reliable data on this, on this front.
While there was a heroic series of studies that led by Pasko Rakic at Yale
University, and his collaborators and his students over the years that
systematically looked at the density of synaptic connections in an animal model.
A very excellent model for understanding synaptogenesis in our brain.
They've looked at the rhesus monkey, and they examined a variety of cortical
regions over a series of studies that spanned the decade of the 90's and into
the early 2000's. And the results of these studies are
summarized in this slide here, which is taken from our textbook.
And what is being plotted here is the density of synapses across early life in
the rhesus monkey. And, what is very clear from these data
is that in all the cortical areas that we're examining.
This includes primary sensory cortex, motor cortex dorsolateral prefrontal
cortex, and cortex that's close to the limbic forebrain of the medial temporal
lobe. What's very clear is that, at the time of
birth there are relatively few synaptic connections that are established and, and
fully functional. thereafter, however, there's an explosive
increase in the numbers of synaptic connections.
So, we see that in all of our cortical areas that have been studied.
in the months after birth, and this might correspond to the first couple of years
of infancy in humans, there's a tremendous increase in the numbers of
synapses that are being proliferated in the cerebral cortex.
Now that's not to say that there may not be some loss of some synaptic
connections. Indeed there will be loss of some
synaptic connections. But rather it's to emphasize that in
early infancy, there is a net gain in synaptic connections, by at least two or
three fold over the numbers of synapses that we're born with in the cortical
mantle. So, it's reasonable to conclude then
that, part of critical period plasticity, where the brain is especially sensitive
to the influence of the environment, has to do with this phenomenal rate of
synaptogenesis. That we see during the onset and near the
peak of the critical periods, in each of these areas.
Well for a variety of reasons, we know that the critical period does indeed
begin to wane after the first few years of life.
Here's just an example of an apparent critical period for the acquisition of
the English language. Compared to native speakers the
development of fluency begins to fall rather steeply after the first few years
of life. As it's shown here in this plot.
So after about age seven there's now a progressive decline in the relatively
fluency for those individuals for whom English is not their native language.
And they're trying to acquire English language skills.
Now, before I say more about this, decline of the critical period.
and what happens as synaptogenesis, wanes.
I should point out that in this early constructive phase, when synapses are
being added at a phenomenal rate. Is an opportunity for brain development,
to go, in a different direction. A direction that may be related to
various kinds of learning disabilities, or other kinds of disorders of cognition.
let me give you just a few examples of this.
what seems to be known about individuals that are somewhere on the autism spectrum
disorder is that, there appears to be an acceleration of this capacity for
synaptogenesis. Such that, if one simply looks at overall
brain size in children that are beginning to be evaluated and diagnosed with autism
spectrum disorder. It's very possible that there is actually
an acceleration of the rate of synaptogenesis and their cerebral cortex,
which results in an overgrowth of the brain.
Especially involving the cortex of the frontal and the temporal lobes.
As well as the amygdala, that we'll say more about in the next unit of the
course, as well as the cerebellum. And these are brain structures that are
involved in social cognition communication, and the executive control
of motor actions. Now as development proceeds in these
children they, the overgrowth tends to normalize.
towards where a typically developing child might be.
But that's not to say that connections are restored to normal structure and
function. It very well may be that aberrate
connections that may have been developed during this period of overgrowth may
persists, throughout the childhood and adolescent years, and indeed even into
adulthood. Now, I'll give you just one other
example, and that's the example of attention deficit hyperactivity disorder.
And this disorder commonly known as ADHD, rather than there being an acceleration
of synaptogenesis there seems to be a decrease in the rate of synaptogenesis.
Such that the cerebral cortex again mainly in the frontal lobe and in parts
of the temporal lobe, seems to be thinner than typically developing children that
don't have this disorder. So, it very well may be that this
decrease in cortical thickness is attributable to a relative, delay or
perhaps, a relative reduction in the total numbers of synaptic connections
that are established. we still don't really understand the full
consequences from a functional perspective, but its reasonable to at
least, hypothesize. That this reduced rate of synaptogenesis
is leading to the construction of dysfunctional circuits that can modulate
behavioral control, and perhaps this is part of the phenotype associated with
this particular disorder.
