Expression of the mRNAs encoding for the vesicular glutamate transporters 1 and 2 in the rat thalamus

Abstract

Vesicular glutamate transporters (VGLUTs) are responsible for glutamate trafficking and for the subsequent regulated release of this excitatory neurotransmitter at the synapse. Three isoforms of the VGLUT have been identified, now known as VGLUT1, VGLUT2, and VGLUT3. Both VGLUT1 and VGLUT2 have been considered definitive markers of glutamatergic neurons, whereas VGLUT3 is expressed in nonglutamatergic neurons such as cholinergic striatal interneurons. It is widely believed that VGLUT1 and VGLUT2 are expressed in a complementary manner at the cortical and thalamic levels, suggesting that these glutamatergic neurons fulfill different physiological functions. In the present work, we analyzed the pattern of VGLUT1 and VGLUT2 mRNA expression at the thalamic level by using single and dual in situ hybridization. In accordance with current beliefs, we found significant expression of VGLUT2 mRNA in all the thalamic nuclei, while moderate expression of VGLUT1 mRNA was consistently found in both the principal relay and the association thalamic nuclei. Interestingly, individual neurons within these nuclei coexpressed both VGLUT1 and VGLUT2 mRNAs, suggesting that these individual thalamic neurons may have different ways of trafficking glutamate. These results call for a reappraisal of the previously held concept regarding the mutually exclusive distribution of VGLUT transporters in the central nervous system.

Gene Expression Identifies Distinct Ascending Glutamatergic Pathways to Frequency-Organized Auditory Cortex in the Rat Brain

“…This expression pattern is consistent with a VGLUT2 protein-dense terminal field found within thalamic recipient layers of sensory cortex (Kaneko et al, 2002;Nahmani and Erisir, 2005;Graziano et al, 2008;Hackett and de la Mothe, 2009). However, recent studies find that type 1 glutamate transporter (VGLUT1) mRNA is coexpressed with VGLUT2 mRNA in a subset of MGBv neurons in rodents (Barroso-Chinea et al, 2007;. This raises the question of whether MGBv pathways to different frequencyorganized cortical fields have different gene expression patterns for glutamate transporter type.…”

“…The majority of the principal neurons in MGBv likely release glutamate neurotransmitter as they express the gene and corresponding mRNA encoding type 2 vesicular glutamate transporter (VGLUT2) which in turn is critical for loading glutamate into synaptic vesicles (Fremeau et al, 2004a;Barroso-Chinea et al, 2007;Hackett et al, 2011;. This expression pattern is consistent with a VGLUT2 protein-dense terminal field found within thalamic recipient layers of sensory cortex (Kaneko et al, 2002;Nahmani and Erisir, 2005;Graziano et al, 2008;Hackett and de la Mothe, 2009).…”

“…6). VGLUT2 gene expression is high throughout the caudal-to-rostral extent of MGBv (Barroso-Chinea et al, 2007;) and a high VGLUT2 protein expression in cortical layers III and IV (Fig. 2) suggests both thalamocortical pathways use glutamate as a neurotransmitter (Fig.…”

Coexpression of vesicular glutamate transporters 1 and 2, glutamic acid decarboxylase and calretinin in rat entorhinal cortex

“…In a follow-up study (Wouterlood et al 2007b) we report on entorhinal innervation from the NRT. The projection of this nucleus is known in detail (Wouterlood et al 1990;Vertes et al 2006), its neurophysiology studied in some detail (Dolleman-van der Weel et al 1997;Bertram and Zhang 1999), and it contains CR immunoreactive neurons (Arai 1994) as well as neurons rich in VGluT2 mRNA (Hur and Zaborszky 2005;Barroso-Chinea et al 2007). …”

Limiting glutamate transmission in a Vglut2 -expressing subpopulation of the subthalamic nucleus is sufficient to cause hyperlocomotion

“…If that is the case, it would allow direct control over each cell population, facilitating the investigation of their respective roles. In rodents, the STN is believed to be composed solely of glutamatergic neurons, characterized by expression of the subtype 2 Vesicular glutamate transporter (Vglut2), whereas the other two subtypes (Vglut1 and Vglut3) have not been detected (15,16). Selective targeted deletion of Vglut2 expression in this nucleus would therefore provide a specific loss-of-function model that would bypass a common problem presented by traditional lesions with pharmacological agents, which have patterns of diffusion that likely affect surrounding structures (17).…”