Journal club: The cortex as a central pattern generator

NATURE REVIEWS NEUROSCIENCE 6(6) 2005

by Rafael Yuste, Jason N. MacLean, Jeffrey Smith and Anders Lansner

A vast number of neurons in the brain cortex together generates synchronized oscillatory activity. In this review paper, the authors discuss how the neocortex neural network shares basic designs with the central pattern generator circuits in the spinal cord and brain stem.

For rhythmogenesis in a neural network, it seems like the general rule that self-boosting excitation within a functional unit is more important than reciprocal inhibition.  In the neocortical circuit, a population of neurons forms an excitatory kernel by being interconnected through recurrent excitation. Such excitatory neuronal population is capable of producing synchronized oscillatory activity through their active membrane properties and short-term synaptic plasticity. This circuit architecture is similar to the CPGs in the spinal cord and brain stem of vertebrates. The inhibitory connections are necessary for the regulation of the rhythm and spatiotemporal pattern of the network output.

The extent of spatial distribution is one of the major differences between the cortical network and the CPG in the brain stem/spinal cord.  In the cortex, the recurrent excitatory network is widely spread out over the neocortex, whereas in those for locomotion and breathing have bilaterally-grouped functional units. The other difference is high plasticity in the cortical network in contrast to the hard-wired CPGs in the spinal cord and brain stem. The connectivity in the cortex develops through activity-dependent Hebbian plasticity. We can call the cortex network as a learning CPG that is based on Hebbian assemblies and is specialized for learning and storing or retrieving memories.  Because of these properties, the neocortex network is highly fluidic.

Long-Term Modifications in Motor Cortical Dynamics Induced by Intensive Practice

Bjørg E. Kilavik, Sébastien Roux, Adrián Ponce-Alvarez, Joachim Confais, Sonja Grün, and Alexa Riehle

The timing of the task is represented in the temporal structure of significant spike synchronization at the population level. By practice, the temporal structure of synchrony was shaped. Synchrony became stronger and more localized in time during late experimental sessions, in parallel with a behavioral improvement, whereas the firing rate in the same neurons mainly decreased.




The brain processes in parallel sensory, temporal, and contextual information, which has to be combined appropriately to organize a movement.

It is widely accepted that sensorimotor funcitons are based on activity modulations in neuronal networks distributed over various brain structures. (Wise, 1984; Tanji and Kurata 1989; Riehle, 2005).
The timing of modulation of synchrony and firing rate at the population level in motor cortex suggests that synchrony may be preferentially involved in early preparatory and cognitive processes, whereas rate modulation may rather control movement initiation and execution (Riehle et al., 2000; Grammont and Riehle, 2003).

Homeostatic and nonhomeostatic modulation of learning in human motor cortex

By Patric Jung and Ulf Ziemann

Introduction
- Motor learning is of crucial importance throughout life for acquisition of new skills and reaccquisition of formerly known but, attributable to brain lesion, lost skills (Sanes, 2003; Krakauer, 2006).

- There is now substantial evidence that many types of motor learning occur in the primary motor cortex (M1) and involve synaptic plasticity in the form of long-term potentiation (LTP) (Rioult-Pedotti et al., 2000; Monfils and Teskey, 2004).

Neocortical mechanisms in motor learning

by Jerome N Sanes

- Incontrovertible evidence: Many neocortical regions, including the motor-related areas, exhibit plasticity and are likely to contribute to motor- skill learning.

Leaning mechanisms

- Candidate mechanisms include fundamental modification in neural-spiking properties, the formation of new intrinsic or extrinsic synaptic contacts, the long-term potentiation or long-term depression of network synapses, and changes in intracortical processing.

- LTP and LTD have been proposed as mechanisms for learning and memory functions throughout the brain, although definitive proof of the relationship between synaptic plasticity and learning often is lacking.

Mechanisms for recovery of motor function following cortical damage

by Randolph J. Nudo

- Intact tissue undergoes structural and functional changes that could play a substantial role in neurological recovery after focal injury to the cerebral cortex.
- Waves of growth promotion and inhibition modulate the self-repair processes of the brain.
- Entire cortical networks participate in the recovery process.

Early demonstrasions of post-injury plasticity
- Behavioral experience is a potent modulator of post-injury cortical plasticity.

New insights into the cellular and molecular mechanisms underlying local reorganization
- Neurite outgrowth in the peri-infarct region (increased GAP-43 immunoreactivity).
- Synaptogenesis (elevated synaptophysin staining).
- Axonal sprouting (traact-tracting methods).
- Surviving neurons becme hyperexcitable with upregulation of NMDA receptors and downregulation of GABA_A receptors.
- Growth-promoting gene expression.
- Exploiting this new understanding of cellular and molecular events following injury might provide new treatment approaches for recovery after CNS injury.


Plastic events remotes from the cortical injury
- The excitability of areas remote from the site of infarct is altered for significant periods of time after injury by upregulation of NMDA receptors and downregulation of GABA_A receptors.
- Alteration of intercortical wiring patterns among different cortical fields.
- Dendritic arborization and synaptogenesis (2 weeks ~ 1 month) in contralateral side.
- role of neural stem cells is still unclear.

Re-emmergence of the mass action principle

Is there a sensitive period for post-injury plasticity and recovery potential?
- Behavioral training is most effective if done within 1 week.

Conclusions
- A disruption of cortical motor network triggers a major reassembly of inter- and intra-areal cortical networks.
- Post-injury behavioral experience appears to be crucial to the reassemby of adaptive modules.
- Basic intracortical wiring plan is substancially altered.

Synaptic Bombardment Modulates Muscarinic Effects in Forelimb Motor Cortex

Niraj S. Desai and Elisabeth C. Walcott

Continuous synaptic bombardment with a complex barrage of excitatory and inhibitory inputs alter many aspects of neuronal responsiveness (by depolarizing neurons, increasing membrane conductance, and introducing fluctuations). This study shows how it shapes neuromodulation of postsynaptic responses by examining muscarinic modulation of forelimb motor cortex, a brain area in which cholinergic stimulation is known to be necessary for modifications during motor skill learning. Using a dynamic clamp system to inject simulated conductances
into pyramidal neurons, they mimicked in vivo-like activity by introducing a random background of excitatory and
inhibitory inputs. The presence of such background conductances strongly attenuated most muscarinic neuromodulatory effects, with the notable exception that sustained firing responses to trains of inputs were well preserved. This may be important for promoting plasticity in vivo.

The Journal of Neuroscience, February 22, 2006 • 26(8):2215–2226


Similar thing may be happening in the slug's CPG in the sea water. Most of my experiments testing neuromodulation have been done in HiDi saline, which suppresses anonymous synaptic bombardment.