Distinct synaptic and neurochemical changes to the granule cell-CA3 projection in Bassoon mutant mice
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Distinct synaptic and neurochemical changes to the granule cell-CA3 projection in Bassoon mutant mice. / Dieni, Sandra; Nestel, Sigrun; Sibbe, Mirjam; Frotscher, Michael; Hellwig, Sabine.
in: FRONT SYNAPTIC NEURO, Jahrgang 7, 23.10.2015, S. 18.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Distinct synaptic and neurochemical changes to the granule cell-CA3 projection in Bassoon mutant mice
AU - Dieni, Sandra
AU - Nestel, Sigrun
AU - Sibbe, Mirjam
AU - Frotscher, Michael
AU - Hellwig, Sabine
PY - 2015/10/23
Y1 - 2015/10/23
N2 - Proper synaptic function depends on a finely-tuned balance between events such as protein synthesis and structural organization. In particular, the functional loss of just one synaptic-related protein can have a profound impact on overall neuronal network function. To this end, we used a mutant mouse model harboring a mutated form of the presynaptic scaffolding protein Bassoon (Bsn), which is phenotypically characterized by: (i) spontaneous generalized epileptic seizure activity, representing a chronically-imbalanced neuronal network; and (ii) a dramatic increase in hippocampal brain-derived neurotrophic factor (BDNF) protein concentration, a key player in synaptic plasticity. Detailed morphological and neurochemical analyses revealed that the increased BDNF levels are associated with: (i) modified neuropeptide distribution; (ii) perturbed expression of selected markers of synaptic activation or plasticity; (iii) subtle changes to microglial structure; and (iv) morphological alterations to the mossy fiber (MF) synapse. These findings emphasize the important contribution of Bassoon protein to normal hippocampal function, and further characterize the Bsn-mutant as a useful model for studying the effects of chronic changes to network activity.
AB - Proper synaptic function depends on a finely-tuned balance between events such as protein synthesis and structural organization. In particular, the functional loss of just one synaptic-related protein can have a profound impact on overall neuronal network function. To this end, we used a mutant mouse model harboring a mutated form of the presynaptic scaffolding protein Bassoon (Bsn), which is phenotypically characterized by: (i) spontaneous generalized epileptic seizure activity, representing a chronically-imbalanced neuronal network; and (ii) a dramatic increase in hippocampal brain-derived neurotrophic factor (BDNF) protein concentration, a key player in synaptic plasticity. Detailed morphological and neurochemical analyses revealed that the increased BDNF levels are associated with: (i) modified neuropeptide distribution; (ii) perturbed expression of selected markers of synaptic activation or plasticity; (iii) subtle changes to microglial structure; and (iv) morphological alterations to the mossy fiber (MF) synapse. These findings emphasize the important contribution of Bassoon protein to normal hippocampal function, and further characterize the Bsn-mutant as a useful model for studying the effects of chronic changes to network activity.
U2 - 10.3389/fnsyn.2015.00018
DO - 10.3389/fnsyn.2015.00018
M3 - SCORING: Journal article
C2 - 26557085
VL - 7
SP - 18
JO - FRONT SYNAPTIC NEURO
JF - FRONT SYNAPTIC NEURO
SN - 1663-3563
ER -