1. Synaptic Plasticity
Synaptic efficacy (strength) is changing with time.
Many of these changes are activity-dependent, i.e.
the magnitude and direction of change depend on
the activity of pre- and post-synaptic neuron.
Some of the mechanisms involved:
- Changes in the amount of neurotransmitter released.
- Biophysical changes in ion channels.
- Morphological alterations of spines or dendritic branches.
- Modulatory action of other transmitters.
- Changes in gene transcription.
- Synaptic loss or sprouting.
2. Hebb’s Postulate
“When an axon of cell A is near enough to
excite a cell B and repeatedly and 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.”
Donald Hebb, “Organization of Behavior”, 1949
3. Cross-section of the hippocampus:
Animal Models of Plasticity
Long-Term Potentiation (LTP)
4. Brain slice preparation of the hippocampus:
Animal Models of Plasticity
5. Typical LTP experiment: record from cell in hippocampus
area CA1 (receives Schaffer collaterals from area CA3). In
addition, stimulate two sets of input fibers.
6. Typical LTP experiment:
record EPSP’s in CA1 cells
Step 1: weakly stimulate input
1 to establish baseline
Step 2: give strong stimulus
(tetanus) in same fibers
Step 3: continue weak
stimulation to record increased
Step 4: throughout, check for
responses in control fibers
LTP is input specific.
LTP is long-lasting (hours, days, weeks).
LTP results when synaptic stimulation coincides with
postsynaptic depolarization (achieved by cooperativity of
many coactive synapses during tetanus).
The timing of the postsynaptic response relative to the
synaptic inputs is critical.
LTP has Hebbian characteristics (“what fires together wires
together”, or, in this case, connects together more
LTP may produce synaptic “sprouting”.
8. The NMDA Receptor
(a)At the resting potential
glutamate binds to the NMDA
channel, the channel opens,
but is “plugged” by a
magnesium ion (Mg2+
(b)Depolarization of the
relieves the magnesium block
and the channel open to
allow passage of sodium,
potassium and calcium.
9. The Associative Nature of LTP
Old(er) view: Associative requirement is
mediated by the voltage-dependent
characteristics of the NMDA receptor.
New discovery (1994): Active conductances in
dendrites mediate back-propagation of AP’s into
the dendritic tree.
10. Spike-Timing Dependent Plasticity
Basic Idea: Change in synaptic strength
depends on the precise temporal difference
between pre- and post-synaptic neuronal
11. The Neuron:
Integrator or Coincidence Detector?
Synchronous inputs really matter!
12. Data Analysis in Neurophysiology
Neuron in MT
13. Data Analysis in Neurophysiology
Desimone et al., 1984
Neuron in IT (object selective)
14. Data Analysis in Neurophysiology
Engel et al., 1991
Neurons in V1 (orientation selective)
PSTH (firing rate) Auto-Correlation
Cross-Correlation Shift Predictor
15. Neural Coding
Rate coding versus temporal coding
One major mechanism of how neurons encode information is
through their firing rate (number of AP’s per second). –
Example: orientation selectivity.
Another major mechanism is synchronization (AP’s occurring
together in time). – Example: perceptual grouping.
Synchrony could affect other neurons (e.g. through spatial
summation – see unit 1).
16. Computational Neuroscience
- Units and connections
- Inputs and outputs
- Activation function
- Learning rule
Components of (most) neural models:
17. The McCullogh-Pitts Neuron
18. The McCullogh-Pitts Neuron
19. “Why the Mind is in the Head”
“Why is the mind in the head? Because there,
and only there, are hosts of possible
connections to be formed as time and
circumstance demand. Each new connection,
serves to set the stage for others yet to
come and better fitted to adapt us to the
world, for through the cortex pass the
greatest inverse feedbacks whose function
is the purposive life of the human intellect.”
Warren S. McCullogh, Hixon Symposium 1951.