Cortical Stoke Alters Physiology of Reticular Thalamic Nucleus
/An article published today in the Journal of Neuroscience describes the effect of focal cortical lesions on the reticular thalamic nucleus. The research, conducted by Stanford's Jeanne Paz (with help from Catherine Christian and Isabel Parada from the Huguenard and Prince labs) shows that focal cortical injuries significantly alter the intrinsic properties and synaptic excitability of inhibitory neurons in the reticular thalamus. Focal cortical injury (as will occur following a cortical stroke) causes significant damage or death to the thalamocortical relay neurons that project to the affected cortical area. Neurons of the inhibitory reticular thalamic nucleus general survive, although many of their corticothalamic and thalamocortical inputs are destroyed. The physiological properties of the survivng reticular neurons would determine recovery of the thalamocortical circuit after injury, however, these properties were not known.
The research by Jeanne and company looked at the physiology of inhibitory reticular thalamic neurons in a focal cortical stroke model. Their main findings are that:
- Changes to reticular thalamic neuron physiology occur by the end of the first week after injury.
- Reticular neurons have:
- decreased membrane input resistance
- reduced low-threshold calcium burst responses
- weaker evoked excitatory synaptic responses.
Jeanne and company conclude that such alterations in excitability of the inhibitory neuronal population could lead to loss of inhibition of surviving relay nuclei, which would in turn increase the output of those surviving thalamocortical relay neurons, enhancing thalamocortical excitation and potentially facilitate recovery of thalamic and cortical sensory circuits. Of course, these enhancements in excitability could (and often do) go too far, inducing a hyper-excitable thalamocortical circuit. These results are therefore notable, in that they provide clues as to the pathophysiology of post-stroke epilepsy.
