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SUMMARY:BMI Seminar // Abnormal release of neurotransmitter and Ca2+ influ
 x in presynaptic terminals in cortical neurons of a knock-in mouse model o
 f  Huntington’s disease
DTSTART:20170830T121500
DTEND:20170830T131500
DTSTAMP:20260501T102457Z
UID:179634c006b26e7f5f664b24b5cea99baca453fba21fec0c68bf07b1
CATEGORIES:Conferences - Seminars
DESCRIPTION: Hyokeun Park\, Division of Life Science\, Hong Kong Universi
 ty and Technology\, Hong Kong\, China\nHong Kong\nHuntington’s disease (
 HD) is a genetic neurodegenerative disorder caused by an abnormal expansio
 n of CAG trinucleotide repeats in the huntingtin gene. Mutant huntingtin (
 mhtt) proteins induce the progressive neuronal loss from the striatum and 
 cortex\, despite of their ubiquitous expression. One possible mechanism of
  this selective degeneration is that dysfunction in synaptic transmission 
 in the corticostriatal synapses could lead to the selective degeneration o
 f these striatal neurons.  However\, the release of neurotransmitters as 
 an input of corticostriatal synapses in HD has not fully understood yet. T
 hus we examined (or estimated) the release of neurotransmitters  and the 
 influx of Ca2+ during the stimulation at single presynaptic terminals in p
 rimary cortical neurons using real-time imaging with FM 1-43 labeled synap
 tic vesicles and Cal-520 (an ultrasensitive Ca2+ indicator). The released 
 neurotransmitters at presynaptic terminals in heterozygous neurons of a HD
  knock-in mouse model (Q175) were significantly higher than wild-type neur
 ons. The influx of Ca2+ in presynaptic terminals (distal from cell bodies)
  in heterozygous neurons was significantly higher compared with wild-type\
 , implying that higher Ca2+ increase release of neurotransmitters in HD. T
 he abnormal increase was rescued by the application of Ca2+ chelators and 
 N-type voltage-gated Ca2+ channel blockers. Our results suggest that the i
 ncreased release of neurotransmitter caused by higher influx of Ca2+ in pr
 esynaptic terminals of cortical neurons contribute to damage striatal and 
 cortical neurons\, which may underlie the selective neurodegeneration in H
 D. \n 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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