Seminar "Loss of GABAB-mediated interhemispheric synaptic inhibition in stroke periphery" by Dr. Bojana Kokinovic
Date
Wednesday, April 18, 2018 - 11:00 to 12:00
Location
D015, Lab1
Description
Sensory and Behavioural Neuroscience Unit (Fukuanga Unit) would like to invite you a seminar by Dr. Bojana Kokinovic from Umea University.
Date: Wendesday, April 18th
Time: 11:00 - 12:00
Venue: D015, Lab1
Speaker: Dr. Bojana Kokinovic
Title: Loss of GABAB-mediated interhemispheric synaptic inhibition in stroke periphery
Abstract: Recovery after stroke is mediated by plastic changes largely occurring in the lesion
periphery. However, little is known on the microcircuit changes underlying recovery, at
which extent perilesional plasticity occurs at synaptic input vs spike output level, and on
the connectivity behind such synaptic plasticity. We combined intrinsic imaging with
extra- and intra-cellular recordings and pharmacological inactivation in a focal stroke in
mouse somatosensory cortex (S1). In vivo whole-cell recordings in hindlimb S1 (hS1)
showed synaptic responses also to forelimb stimulation in controls, and such responses
were abolished by stroke of neighboring forelimb area (fS1), suggesting that in normal
conditions they originate via horizontal connections from neighboring fS1. Synaptic and
spike responses to forelimb stimulation in hS1 recovered to quasi-normal levels 2 weeks
after stroke, without changes in intrinsic excitability and hindlimb-evoked spike
responses. Recovered synaptic responses had longer latencies, suggesting a long-range
origin of the recovery, prompting us to investigate the role of callosal inputs in the
recovery process. Contralesional S1 silencing unmasked significantly larger responses
to both limbs in controls, a phenomenon that was not observed when GABAB receptors
were antagonized in the recorded area. Conversely, such GABAB-mediated
interhemispheric inhibition was not detectable after stroke: callosal input silencing
failed to change hindlimb responses, whereas it robustly reduced recovered forelimb
responses. Thus, recovery of subthreshold responsiveness in the stroke periphery is
accompanied by a loss of interhemispheric inhibition and due to a pathway-specific
facilitatory action on the affected sensory response from contralateral cortex.
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