Pathological gamma oscillations, impaired XXXX release, synapse loss and reduced dynamic range of unitary glutamatergic synaptic transmission in the striatum of hypokinetic Q175 Huntington @entity19 .

@entity1 @entity57557 @entity2003 @entity19 @entity10406 @entity935 @entity2033 @entity2845 @entity18358 @entity4365 @entity46236 @entity4149 @entity14827
UNASSIGNED: @entity2033 ( @entity2033 ) is a severe genetically @entity14827 . @entity1 present with three principal phenotypes of motor symptoms: choreatic, @entity2003 and mixed. The Q175 @entity19 model of disease offers an opportunity to investigate the cellular basis of the @entity2003 form of @entity2033 . At the age of 1year homozygote Q175 @entity19 exhibited the following signs of @entity2845 : Reduced frequency of spontaneous movements on a precision balance at daytime (-55%), increased total time spent without movement in an open field (+42%), failures in the execution of unconditioned avoidance reactions (+32%), reduced ability for conditioned avoidance (-96%) and increased reaction times (+65%) in a shuttle box. Local field potential recordings revealed @entity4365 in the striatum as a characteristic feature of @entity2033 @entity19 at rest. There was no significant loss of @entity46236 immunolabeled striatal projection neurons (SPNs) although the level of @entity46236 immunoreactivity was lower in @entity2033 . As a potential cause of @entity2845 , @entity2033 @entity19 revealed a strong reduction in striatal @entity10406 -induced @entity935 release, accompanied by a decrease in the number of @entity4149 hydroxylase-(TH)- and @entity57557 -positive synaptic varicosities. The presynaptic TH fluorescence level was also reduced. Patch-clamp experiments were performed in slices from 1-year-old @entity19 to record unitary EPSCs (uEPSCs) of presumed cortical origin in the absence of G-protein-mediated modulation. In @entity2033 @entity19 , the maximal amplitudes of uEPSCs amounted to 69% of the WT level which matches the loss of @entity18358 +/SYP+ synaptic terminals in immunostained sections. These results identify impairment of cortico-striatal synaptic transmission and @entity935 release as a potential basis of @entity2845 in @entity2033 .
