Complete summary of the literature for 3.6C "The Brain" Theme 2: Changing Brain for the Psychology "Brain and Cognition" specialisation. The summary covers the following book chapters:
- Purves et al. (2019): Chapters 25 and 26
- Carlson (2017): Chapter 13: Learning and Memory
Theme 2
Changing Brain
Purves et al. (2019): Chapter 25: Experience-Dependent Plasticity in the
Developing Brain
Neural Activity and Brain Development
Hebb’s postulate: the coordinated electrical activity of a presynaptic terminal and a
postsynaptic neuron strengthens the synaptic connection between them
Hebb’s postulate explains three phenomena:
1. behaviours not initially present in newborns emerge and are shaped by experience
throughout early life
2. the superior capacity for acquiring complex skills and cognitive abilities during early life
3. the brain continues to grow after birth, roughly in parallel with the emergence and
acquisition of increasingly complex behaviours and the addition of pre-and postsynaptic
processes
During the initial phases of progressive construction the brain gets larger because of postnatal
growth of dendrites, axons and synapses-but not because of the addition of neurons. During the
elimination phase, counterintuitively, the brain continues to grow. This reects the continued
elaboration of the synapses that remain, and the neurons that are their targets.
Intrinsic mechanisms establish the general circuitry required for most behaviours. These cellular
and molecular mechanisms, however, do not yield a nal connectivity pattern. Typical
experiences validate initial wiring and preserve, augment, or adjust the initial arrangement that
is established by intrinsic developmental mechanisms. In the case of "diminished" experiences
due to lack of sensory exposure or disrupted sensory transduction and relay, these adjustments
do not occur appropriately and brain connectivity and behavioural capacity can be altered
Critical Periods
These are periods when experience and the neural activity that reects that experience have
maximal effect on the acquisition or skilled execution of a particular behaviour. Critical periods
, for sensorimotor skills and complex behaviours end far less abruptly compared to other
behaviours, and provide far more time for environmentally acquired experience. The availability
of instructive experiences from the environment, as well as the neural capacity to respond to them,
is key for successful completion of the critical period.
Basic properties of critical periods:
● Each critical period encompasses the time during which a given behaviour is especially
susceptible to specic environmental inuences in order to develop normally
● Environmental inuence elicits neural activity in the relevant sensory or motor
pathway, and the nature of this activity (frequency, amplitude, duration, and
correlation) ultimately drives changes in
synaptic connections
● Once a critical period ends, the core features
of the behaviour are largely unaffected by
subsequent experience
● critical periods rely particularly on changes
in organisation and function of circuits in
the cerebral cortex
The Role of Oscillations in Establishing Critical Periods
Local oscillations of activity that are initially beneath the threshold for action potential
generation are essential for shaping circuit networks to be prepared for optimal experience-
driven activity.
Analyses of retinal waves, activity in the retina that begins before birth, provided the initial
evidence for oscillatory activity ⇒ The waves are initiated in amacrine cells, and subthreshold
activity leads to action potential ring by ganglion cells that is then relayed to the LGN. These
waves are asynchronous between the two eyes. The lack of correlated activity establishes a
modest competitive interaction-leading to Hebbian reinforcement-between the two eyes for
target space in the LGN and via the LGN to the V1. A nascent circuit that includes GABAergic,
acetylcholinergic, and glycinergic synaptic transmission from retinal amacrine cells combined
with glutamatergic release from bipolar cells to retinal ganglion cells is responsible for the
generation of retinal waves.
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