Presynaptic cytomatrix protein Bassoon is localized at both excitatory and inhibitory synapses of rat brain

Abstract

Bassoon is a 420‐kDa protein specifically localized at the active zone of presynaptic nerve terminals. It is thought to be involved in the structural organization of the neurotransmitter release site. We studied the distribution of Bassoon transcripts and protein in rat brain and assessed which types of presynaptic terminals contain the protein. As shown by in situ hybridization, Bassoon transcripts are widely distributed in the brain and occur primarily in excitatory neurons. In addition, examples of γ‐aminobutyric acid (GABA)‐ergic neurons expressing Bassoon are detected. At the light microscopic level, Bassoon immunoreactivity is found in synaptic neuropil regions throughout the brain, with the strongest expression in the hippocampus, the cerebellar cortex, and the olfactory bulb. Immunoelectron microscopy showed that Bassoon immunoreactivity is found in both asymmetric type 1 and symmetric type 2 synapses. Immunopositive asymmetric synapses include mossy fiber boutons and various spine and shaft synapses in the hippocampus and mossy fiber terminals and parallel fiber terminals in the cerebellum. Bassoon‐containing symmetric synapses are observed, e.g., between basket and granule cells in the hippocampus, between Golgi cells and granule cells, and between basket cells and Purkinje cells in the cerebellum. Within synaptic terminals, Bassoon appears highly concentrated at sites opposite to postsynaptic densities. In cultured hippocampal neurons, Bassoon was found to colocalize with GABAA and glutamate (GluR1) receptors. These data indicate that Bassoon is a component of the presynaptic apparatus of both excitatory glutamatergic and inhibitory GABAergic synapses. J. Comp. Neurol. 408:437–448, 1999. © 1999 Wiley‐Liss, Inc.

Lack of Molecular-Anatomical Evidence for GABAergic Influence on Axon Initial Segment of Cerebellar Purkinje Cells by the Pinceau Formation

“…6 A, D, single arrowheads), as reported previously (Richter et al, 1999;Patrizi et al, 2008). However, no such clusters were found along AnkG ϩ portions of the AIS (Fig.…”

“…To clarify whether, and how, the molecular machinery for GABAergic transmission is organized in the pinceau formation, we investigated immunohistochemical localization of GAD, VIAAT, bassoon, NL2, and GABA A R␣1, because all are highly accumulated at GABAergic synapses on somatodendritic elements in PCs (Oertel et al, 1981;Fritschy and Mohler, 1995;Chaudhry et al, 1998;Richter et al, 1999;Varoqueaux et al, 2004). Our examination confirmed that these molecules were clustered at perisomatic sites of PCs, thus ensuring the specificity and sensitivity of the present immunohistochemistry.…”

SynGAP regulates synaptic strength and mitogen-activated protein kinases in cultured neurons

“…To test whether SynGAP overexpression regulates synapses in general, we transfected cultured neurons with GFP-SynGAP and subsequently labeled neurons for Bassoon or NR1. Bassoon has been shown to be a component of nearly all synapses in the forebrain, rendering it an ideal marker for changes in synapse number (15). We observed no changes in total synaptic density or excitatory synapse number as measured by Bassoon and NMDA receptor immunolabeling (Fig.…”

Preferential Localization of Muscarinic M1Receptor on Dendritic Shaft and Spine of Cortical Pyramidal Cells and Its Anatomical Evidence for Volume Transmission

“…These anatomical features sharply contrasted to those of the glutamatergic system; GluA2 subunit and mGluR5 were accumulated to the synaptic or perisynaptic membrane, respectively, facing glutamatergic terminals. Furthermore, prominent accumulation of Bassoon, one of the cytomatrix active zone (CAZ) proteins considered to act as a platform for active zone vesicles (Richter et al, 1999), was observed near the presynaptic membrane in glutamatergic terminals, whereas no such accumulation was discernible in cholinergic varicosities. This finding implies that the molecular machinery for ACh release is not integrated into a specific site of given varicosities, unlike the active zone at glutamatergic synapses.…”