Temporal Scales

The brain is also spread across many orders of magnitude in temporal scale. Figuring out the temporal ways in which the brain processes information, learns, and builds a generative model will be key to extending the deep learning structures that we have now. This is one of the biggest mysteries, and there are a lot of possibilities, so here are some highlights:

Action Potentials

• Millisecond timescale
• Main signaling mechanism, transfers information.
• Fast sodium and potassium voltage-sensitive channels are mechanism. Tons of other modifications.
• Adaptation
• Refractory period
• Bursting

Gap-Junction Signaling

• Rapid communication between neurons. Purely electrical, so extremely fast. 
• Probably important for synchronizing neurons (esp. FS cells). 
• Some evidence is emerging that these can be regulated. Normally, they are thought of as resistors connecting two cells electrically. 
• They can be uni-directional
• Neurotransmitters/modulators may be able to open/close gap junctions.

Synaptic Signaling

• Primary mechanism of computation. Holds majority of parameters of the system. Extremely modifiable.
• Pre-synaptic neurons virtually always only have a single neuro-transmitter. 
• Glutamate: primary excitatory transmitter
• GABA: primary inhibitory transmitter
• Dopamine: positive reinforcement modulator.
• Tons of other transmitters: Glycein, Serotonin, 
• Post-synaptic neurons, however, have receptors for almost every kind of neuro-transmitter. 
• AMPA (Glutamate): primary excitatory transmitter. These get modulated for long-term learning.
• NMDA (Glutamate): regulates plasticity. Triggers mechanisms for AMPA trafficking. Mechanism for STDP.
• Chloride Channels (GABA): these are inhibitory. 
• Can be as fast as 5ms to hundreds of ms.

Dendritic/Calcium Spikes

• Active mechanisms in dendrites that perform computation.
• NMDA, Volage-Gated Calcium Channels, Ca-Gated Calcium Channels, Voltage-Gated Sodium Channels all can contribute. 
• Kv4.2 potassium channnels can regulate "strength" of dendrites.
• Can last 10s to 100s of ms.

Short-term Plasticity

• Changes in strength of synapses over short time-scales. Can be extremely rapid
• Can be facilitating (each AP is stronger than previous), or depressing (each AP is weaker). Both of these can be in operation at different time-scales.
• i.e. Depressing if APs are greater than 50Hz, Facilitating if 20-50Hz
• 100s of ms to 10s of seconds
• Could be a mechanism for working memory: Mongillo et al, 2008

Long-term Plasticity

• Main mechanism for learning. AMPA receptors are recruited to or removed from synapse.
• Hebb: fire-together, wire-together.
• Spike-timing dependent plasticity
• Pre just before post -> stronger (temporally causal).
• Can be modulated by dopamine.

Neurogenesis

• Neurons in hippocampus (dentate gyrus) are constantly being born. These neurons have been implicated as a way to create our declarative memories: Aimone, 2006
• New-born neurons are very excitable and very plastic. These are storing your current memories, and easily associate with other new-born neurons.
• Old neurons become less excitable, and lose plasticity. Keep the information of old memories.