|dc.description.abstract||The reticular thalamic nucleus (RTN) is located between cerebral cortex, motor thalamus and the basal ganglia and thought to be implicated in the inhibitory-mediated regulation of motor control. Parkinson’s disease is a neurodegenerative motor disorder caused by the significant degenerative loss of dopamine neurons from the substantia nigra pars compacta. This loss results in abnormal electrophysiological activity throughout the basal ganglia-thalamo-cortical network. Interestingly, the role of the RTN in modulating basal ganglia-thalamo-cortical network activity is poorly understood in control conditions and has not been explored at all in parkinsonism.
To address this, the present study characterized neuronal activity of rostral RTN (rRTN) neurons in urethane-anesthetized rats. Furthermore, this study investigated the effect that 6-hydroxydopamine (6-OHDA) induced chronic dopamine neurodegeneration of the substantia nigra pars compacta had on rRTN neural activity. Extracellular spike train data were recorded for at least five minutes using glass electrodes.
Consistent with existing literature, electrophysiological and immunohistochemical data indicate that the rRTN contains primarily putative GABAergic neurons (AP spike width ≤0.47 ms). These neurons had a mean firing rate of 4.9 ± 1.1 spikes/s. Approximately 60% of GABAergic neurons demonstrated low threshold calcium spike (LTS) bursts (~200 Hz), which are characteristic of thalamic activity. LTS bursting in GABAergic neurons of the rRTN was dominated by doublets. Dopaminergic lesion significantly decreased the firing rate (p<0.05) and increased the incidence (~80%) of LTS bursting in GABAergic rRTN neurons (X2 = 38.37, p<0.0001) and non-doublet LTS bursts became dominant.
Interestingly, the electrophysiological and immunohistochemical data suggested the presence of non-GABAergic neurons in the rRTN (AP spike width ≥0.52 ms). Based on the available data these neurons were putatively defined as glutamatergic. These neurons had a mean firing rate of 6.2 ± 1.9 spikes/s. Approximately half of these neurons demonstrated LTS bursts, which were dominated by non-doublet LTS bursts.
Parkinsonism appeared to affect the glutamatergic neuronal population in a similar manner to how it affected the GABAergic population. Parkinsonism significantly decreased (p<0.05) the firing rate and increased the incidence of LTS bursting activity (~80%) in glutamatergic neurons, compared to control (X2 = 38.37, p<0.0001). Interestingly, the incidence of non-doublet LTS bursts was unaffected by parkinsonism, however the incidence of doublet LTS bursts was increased.
These data indicate that: 1) parkinsonism significantly affects the firing rate and LTS bursting characteristics of rRTN neurons and 2) there are possibly two distinct neuronal phenotypes present in the rRTN. Considering the reciprocal connections between RTN, basal ganglia nuclei and motor thalamus, it is possible that the RTN might be involved in producing some of the changes in the basal ganglia-thalamo-cortical network activity that underlie parkinsonian symptoms. Fully characterizing the neuronal characteristics of the rRTN, especially the novel population, will be important for understanding the role of the rRTN in information processing, particularly in future studies examining its role in movement control.||