Seminar: Plasticity of neuronal networks and single cell properties in the anterior cingulate cortex induced by neuropathic pain, by Prof. Thomas Nevian from University of Bern

The Graduate School would like to invite you to a seminar by Thomas Nevian, from University of Bern, Switzerland. This talk will be introduced by Prof. Jeff Wickens from Neurobiology Research Unit. 

--------------------------------------------------------------------------------------
Date:   Thursday, June 11, 2015
Time:  10:00 – 11:00
Venue: Seminar Room B503, Level B, Lab 1
--------------------------------------------------------------------------------------

Speaker:

Prof. Thomas Nevian
University of Bern, Department of Physiology, Bühlplatz

Title:

Plasticity of neuronal networks and single cell properties in the anterior cingulate cortex induced by neuropathic pain

Abstract:

Neuropathic pain caused by peripheral nerve injury is a debilitating neurological condition of high clinical relevance. On the cellular level, the elevated pain sensitivity is induced by plasticity of neuronal function along the pain pathway. Changes in cortical areas involved in pain processing contribute to the development of neuropathic pain. Yet, it remains elusive which plasticity mechanisms occur in cortical circuits. We investigated the properties of neural networks in the anterior cingulate cortex (ACC), a brain region mediating affective responses to noxious stimuli. 
We performed multiple whole-cell recordings from neurons in layer 5 (L5) of the ACC of adult mice after chronic constriction injury of the sciatic nerve of the left hind paw and observed a striking loss of connections between excitatory and inhibitory neurons in both directions. These experiments suggest that cortical disinhibition is a fundamental pathological modification associated with peripheral nerve damage. 
Furthermore, we investigated the single cell properties of the L5 pyramidal neurons on a subcellular level by performing dual whole-cell recordings from the soma and the apical dendrite. We found that nerve ligation resulted in a loss of function of the hyperpolarization activated and cyclic nucleotide dependent cation channel (HCN channel). We could demonstrate that this caused increased dendritic excitability by enhancing the temporal summation of EPSPs. We were able to reverse this pathological condition by activating 5-HT7 receptors that are specifically present in the dendrite. Activation of 5-HT7 receptors by 5-CT increased HCN channel function, decreased the temporal summation and the resulting increased cellular excitability. Specific delivery of 5-CT to the ACC could also reduce the allodynia like behaviour in vivo.
In conclusion, we find novel plastic changes in the ACC induced by peripheral nerve ligation. These changes at the cortical cellular and network level might therefore contribute to the neuropathic pain condition. 

We hope to see many of you there.

Sincerely,
Academic Services Section