Journal club: Mechanisms of oscillation in dynamic clamp constructed two-cell half-center circuits

A. A. Sharp, F. K. Skinner, E. Marder
Journal of Neurophysiology Published 1 August 1996 Vol. 76 no. 2, 867-883

Dynamic clamping is merely current injection triggered by presynaptic voltage. The amount of current is determined mainly by postsynaptic voltage. There is nothing magical.

In this paper, the authors studied how systematic alterations in intrinsic and synaptic parameters affected the network behavior by using their newly-developed "dynamic clamping" on a pair of the gastric mill motor neurons, GMs. They isolated GMs by blocking synaptic transmission with picrotoxin and created reciprocally inhibitory two-cell circuits by the dynamic clamp.

The author demonstrated in this system that there was no bursting without the hyperpolarization-activated inward current (I_H). In the presence of additional I_H, a variety of circuit dynamics, including stable half-center oscillatory activity, was produced. The increase in synaptic conductance increased the burst period, whereas the increase in IH conductance reduced it. Discussion went on about synaptic threshold, saying that changes in the synaptic threshold might play a large role in turning on and off bursting activity. However,  these discussion are not so informative to others because nonspiking synapses are rarely seen other than crustaceans.

The authors often stated that they "depolarized" or "hyperpolarized" the thoreshold for synapse. This is wrong. The threshold does not "polarize." Membrane potential does. They should have stated that the threshold was changed to more depolarized or hyperpolarized levels.

Journal club: Gap junctions compensate for sublinear dendritic integration in an inhibitory network

Koen Vervaeke, Andrea Lőrincz, Zoltan Nusser, R. Angus Silver

Science 30 Mar 2012:

Vol. 335, Issue 6076, pp. 1624-1628

DOI: 10.1126/science.1215101

This paper describe how dendrites of cerebellar Golgi cells enhance synaptic signals by sharing them with neighboring Golgi cells via gap junctions rather than boosting them by generating action potentials.

Golgi cells are the inhibitory interneurons in the granular layer of the cerebellar cortex. They receive excitatory input from mossy fibres and parallel fibers.  In this study, the authors studied how the excitatory synaptic inputs onto Golgi cells are integrated by the dendrites and by electrical connections to other Golgi cells. Forming the gap junctions with neighboring cells counteracts with the dendritic attenuation due to membrane conductance.

The author first examined the efficiency of passive dendritic conduction of a local synaptic potential evoked by two-photon uncaging of glutamate. They found that the dendrite of Golgi cell is quite passive. Substantial attenuation of the electrotonic signals when occurred at many places at once.  This weakens the impact of distal excitatory inputs. 

 

However, the high density of dendritic gap junctions enables the synaptic potentials spread to the dendrites of neighboring GoCs. This gap junction-mediated lateral excitation counteracts the effects of sublinear dendritic behavior. Thus, electrical connections among GoCs counteract the dendritic attenuation without the need to boost electrically remote synaptic input with active dendritic conductances.  The combination of passive dendrites and dendritic gap junctions facilitates the excitatory synaptic signals by involving a larger number of interneurons to respond to localized patches of synaptic excitation.

The results also revealed how gap junctions on inhibitory interneuron dendrites could contribute to spatial averaging, which has been proposed in the retina, excitatory olfactory neurons in insects, and to the broad tuning of inhibitory interneurons in cortex.  These mechanisms are also likely to contribute to gain control in the granule cell layer through parallel-fiber mediated feedback.  The interneurons do not operate as fully independent neuronal units but share charge during chemical synaptic excitation and thus exhibit features of a syncitium.

 

Reveiw: Cortical reorganization after spinal cord injury: Always for good?

Neuroscience 283 (2014) 78–94

K. A. Moxon, A. Oliviero, J. Aguilar, and G. Foffani

http://dx.doi.org/10.1016/j.neuroscience.2014.06.056

This review paper gave me a vivid image of the plastic nature in brain function. The cortical map is not a static representation. It represents dynamic equilibrium of continuous interactions of the brain and the external world. Such fluidic nature of the brain is remarkable during the sensorimotor learning.  It becomes especially important when the brain goes through functional recovery after injury and rehabilitation. Upon spinal cord injury, a change in brain state occurs immediately to start cortical reorganization. 

   A complete thoracic spinal cord transection immediately changes the state of the brain, decreasing cortical spontaneous activity as evidenced by a slowing of the frequency of anesthesia-induced oscillations, while increases the cortical responses to stimuli delivered above the level of the lesion. The increased responses could be due to a change in the equilibrium between excitation and inhibition at cortical and subcortical levels.

   There is a species differences in the cortical reorganization. In human, the spinal lesion induces an enlargement of cortical sensorimotor areas representing preserved muscles above the level of lesion. Primates brain may be more flexible than rodents, in which spontaneous cortical reorganization is more limited.

   The authors discussed potential therapy that involves 5-HT and exercises. Activation of 5-HT receptors facilitates cortical reorganization by restructuring connections that could be relevant for behavioral recovery. Cortical reorganization can also be promoted by exercise therapy, which increases brain BDNF levels. This peptide and 5-HT together favors cortical reorganization and functional recovery after spinal cord injury.