STRUCTURAL DIFFERENCES BETWEEN GRANULE CELLS AND SEMILUNAR GRANULE CELLS: ROLE IN DIFFERENTIAL POST-TRAUMATIC PLASTICITY OF SYNAPTIC INPUTS
Abstract number :
1.006
Submission category :
1. Translational Research: 1A. Mechanisms
Year :
2013
Submission ID :
1749401
Source :
www.aesnet.org
Presentation date :
12/7/2013 12:00:00 AM
Published date :
Dec 5, 2013, 06:00 AM
Authors :
F. S. Elgammal, A. Gupta, A. Proddutur, B. Sweitek, O. Chika-Nwosuh, V. Santhakumar
Rationale: Concussive brain trauma increases the risk for acquired epilepsy and memory dysfunction. In earlier studies, we identified that semilunar granule cells (SGCs), glutamatergic neurons in the inner molecular layer with axonal projections to CA3 (Williams et al., 2007), show enhanced excitability after brain injury. SGCs receive significantly greater inhibitory inputs than granule cells and demonstrate a post-traumatic decrease in the frequency of inhibitory synaptic inputs rather than an increase observed in granule cells (Gupta et al., 2012). Here, we examined whether differences in dendritic morphology contribute to the divergent intrinsic pattern and post-traumatic plasticity of synaptic inputs between the two cell types.Methods: Young adult male rats were used to model brain injury. Whole-cell recordings from dentate neurons were obtained from acute hippocampal slices prepared 1 week after lateral fluid percussion injury (FPI) or sham-injury. Recorded neurons were filled with biocytin and processed for post-hoc cell identification. Neuronal reconstructions and morphometric analysis were performed on Neurolucida. Simulations done with NEURON.Results: In contrast to the differential post-injury changes in synaptic inhibition, both granule cells and SGCs showed an increase in the frequency spontaneous EPSCs one week after FPI. The frequency of sEPSCs in SGCs from sham-injured rats was significantly greater than in granule cells (sEPSC in Hz, GC median=1.65, IQR =0.88-3.68, n=3; SGC median=2.99, IQR=1.4-7.3, n=7). Molecular layer interneurons showed fewer spontaneous inhibitory inputs and a post-FPI increase in sIPSC frequency, indicating that location may not account for the differences in synaptic inputs between SGCs and granule cells. Morphometric analysis revealed a greater dendritic contraction angle in SGCs (in degrees, GC=59.1 6.8, n=4; SGC=119.7 8.1, n=6, p<0.05, t-test). However, the total dendritic length was not different between the two cell types (in m, GC=3206.9 377.4, n=5; SGC=2583.2 249.6, n=5). SGCs had more numerous first and second order branches and greater dendritic length in these low order, proximal branches than granule cells (dendritic length of first order branches in m, GC=32.2 15.4, n=5; SGC=396.2 148.9, n=5; p<0.05, t-test). However, granule cells had greater dendritic length than SGCs at locations distal to the somata. Detailed morphological simulations of granule cells and SGCs incorporating identical active and passive properties suggest that the difference in morphology cannot fully explain the distinctive intrinsic physiology of SGCs.Conclusions: These data reveal unique dendritic morphological characteristics of granule cells and SGCs that may contribute to the differences in their synaptic inputs and post-traumatic plasticity. However, our simulation studies indicate that, apart from the distinctive morphology, dissimilar channel distribution is likely to underlie differences in active properties between the cell types. Support NJCBIR 09.003.BIR1 to VS and NJCBIR 11-3223-BIR-E-O to AG
Translational Research