The document discusses developmental neuroplasticity in the visual cortex. It describes how thalamic input first establishes basic mapping in the cortex during early development. During the critical period, visual experience can alter circuit structure and function. Neurons in the primary visual cortex develop orientation and direction selectivity. Early abnormal visual experience can lead to lasting impairment, while normal experience is important for maturation. Neurotrophins released with coordinated neural activity strengthen synapses during development and recovery.

1. Developmental
neuroplasticity
Domina Petric, MD

2. Cortical columns functions:
•AMPLIFICATION
•COMPUTATION
•COMMUNICATION
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3. Visual cortex development
Thalamic input is recieved first in the cortical layer 4
(stellate cells).
Precritical fase of the development: establishment of
basic mapping function that allows the thalamus to map
into layer 4 of the cortex.
Critical fase is when the visual experience can alter the
structure and the function of the circuits.
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4. Primary visual cortex and topographic map
Topographic map: fovea is encoded in
the most posterior parts of the primary
visual cortex, perhipheral parts of the
retina are encoded in the more anterior
parts of the visual cortex.
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5. Ocular dominance
Two eyes project to separate layers of cells within the
lateral geniculate nucleus.
The contralateral eye projects to layers 1, 4 and 6.
The ipsilateral eye projects to layers 2, 3 and 5.
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6. Layer 5
Layer 4
Layer 3
Layer 6
Layer 2
Layer 1
Parvocellular layers project
to layer C4β of the visual cortex
and those cells and axons
are concerned with shape
and color of objects.
Magnocellular layers project
to layer C4 of the visual cortex
and those cells and
axons are concerned with
motion of objects.
Koniocellular layers synapse in the zones rich
with oxidative metabolism in the layer 3 of the
visual cortex.Their function is unknown.
Contralateral
eye projections
Ipsilateral eye projections

7. Critical period
• In the early postnatal life neuronal circuits are
sensitive to changes in activity dependent
modulation of ongoing neural activity by sensory
experience.
• Cortical blindness will persist if the onset of eye
deprivation was in the early postnatal life.
• If there is correctible eye disorder, it should be treated
early in life to prevent life long visual impairment.
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8. Orientation selectivity and preference
Visual cortex neurons are
specialised to specifically
oriented visual receptive
field.
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9. Direction selectivity and preference
Visual cortex neurons are
also specialised to
specifically directed visual
receptive field.
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10. Receptive fields in retina and thalamus
Receptive fields in visual cortex
And so on...

11. Pinwhell centers
Pinwheel centers in the visual
cortex contain the cortical columns
that represent all possible
orientations for a given set of
overlapping receptive fields.
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12. Pinwhell centers
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PINWHEEL

13. Key factors of neuronal self-organisation
• Neuronal circuits are dynamical systems: activity
dependent plasticity.
• Neuronal circuits grow long ranging axonal
connections that are able to bind together the
activity of different cortical columns with similar
preferences.
• Visual cortex self organises into pinwheel
formations with π density.
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14. Bad vs. NO experience
Bad experience (abnormal
vision) is worse (more
detrimental to the
development of visual cortical
circuits) than NO experience
(lack of experience).
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15. Conclusions for orientation preference of
receptive fields in visual cortex
• Normally, self-organization operates synergistically with
sensorimotor experience to promote full functional
maturation.
• When there is abnormal experience, synergy is broken and
the neuronal circuits are functionally impaired.
• Neuronal circuits that underlie orientation columns, self
organise to adapt to the quality of the incoming sensory
signals.
• Neuronal circuits are harmed by abnormal experience.
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16. Conclusions for direction preference of
receptive fields in visual cortex
The neuronal circuits that underlie direction columns
can not self-organize.
They must be instructed (trained) by visual experience
with moving stimuli.
The window of opportunity for the motion training is
very brief: early experience is critical.
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17. Final concluding marks
• Normal sensorimotor experience has a profound effect on the
formation and maturation of neural circuits in the cerebral
cortex.
• Some properties (timing-based properties like direction
selectivity) may not develop without normal experience in the
early critical period.
• Abnormal sensorimotor experience in early critical period may
lead to lasting functional impairment.
• Normal experience in early life is critical!
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18. Neurotrophins and
developmental neuroplasticity
II.
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19. Hebb´s postulate
Coordinated activity of a presynaptic
terminal and a postsynaptic cell will
strengthen that synaptic connection.
Uncoordinated activity of a presynaptic
terminal and a postsynaptic cell will
weaken that synaptic connection.
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20. Neurotrophins
• The production and release of neurotrophins is activity
dependent.
• Interconnected and coordinated neurons will strengthen
their interconnections (synapses) and will be nourished via
the release and retrograde activity of neurotrophins in
presynaptic neurons.
• Circuits driven by abnormal experience (connected neurons,
but not functionally coordinated) will weaken their
interconnections (synapses): insufficient neurotrophic
support.
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21. Neurotrophins
In maturity the regulated secretion of trophic factors
may help shape neuronal connections in response to
injury or adaptation to new patterns of neural activity.
In recovering brain BDNF (brain derived neurotrophic
factor) activity has been linked to adaptive circuit
plasticity.
Variations in BDNF gene render cortical circuits more or
less adaptive to challenges in motor learning and
cognition.
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22. Literature
https://www.coursera.org/learn/medical-
neuroscience: Leonard E. White, PhD,
Duke University
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