Expression of trkB and trkC receptors and their ligands brain‐derived neurotrophic factor and neurotrophin‐3 in the murine amygdala

Abstract

The neurotrophin brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) and their cognate receptors, trkB and trkC, have a variety of physiological brain functions, ranging from cell survival to mechanisms involved in learning and memory and long-term potentiation (LTP). LTP can be induced in the cortex and hippocampus, as well as within the amygdala. However, the role of neurotrophins in amygdalar LTP is largely unknown. Expression patterns of BDNF and NT-3 and their cognate receptors in the adult mouse amygdala have not been analyzed in detail. We have therefore examined the expression of trkB, trkC, BDNF, and NT-3 mRNA and protein in different amygdalar nuclei as well as in the hippocampal areas CA1-CA3 and the dentate gyrus. The distribution pattern of trkB, trkC, BDNF, and NT-3 mRNA in the murine hippocampus is comparable to that seen in rats. Within most amygdalar nuclei, a moderate BDNF mRNA expression was found; however, BDNF mRNA was virtually absent from the central nucleus. No expression of NT-3 mRNA was found within the amygdala, but trkC mRNA-expressing cells were widely distributed within this brain region. trkB mRNA was strongly expressed in the amygdala. Because trkB is expressed in a full-length and a truncated form (the latter form is also expressed by nonneuronal cells), we also investigated the distribution of full-length trkB mRNA-expressing cells and could demonstrate that this version of trkB receptors is also widely expressed in the amygdala. These results can serve as a basis for studies elucidating the physiological roles of these receptors in the amygdala.

Ethanol–BDNF interactions: Still more questions than answers

“…As discussed above, these data are in contrast to anatomical studies showing no BDNF mRNA in CeA, but heavy staining of fibers and terminals in this area Krause et al, 2008). Ethanol induces expression of BDNF mRNA in structures not identified in classical expression studies in normal animals, such as the CeA and dorsolateral striatum (McGough et al, 2004).…”

“…TrkB is expressed on the majority of mesencephalic DA neurons while a subpopulation also produce BDNF (Numan and Seroogy, 1999). BDNF, NT-4 and TrkB are often expressed in the same cell populations within the CNS but there are subtle differences between mRNA expression and localization by immunohistochemistry (Altar et al, 1997;Conner et al, 1997;Krause et al, 2008). For example, BDNF mRNA is expressed in the Basolateral Amygdala (BLA) and Lateral Amygdala (LA), CA3 and dentate gyrus with less expression in CA1.…”

“…Neurotrophins are often synthesized in one area and retrogradely or anterogradely transported. Areas such as the striatum, NAc, Central Amygdala (CeA) and Bed Nucleus of the Stria Terminalis (BNST) are devoid of BDNF mRNA detected by in situ hybridization but rich in BDNF-containing fibers detected by enzymatically amplified immunohistochemistry (Altar et al, 1997;Baquet et al, 2004;Conner et al, 1997;Guillin et al, 2001;Agassandian et al, 2006;Krause et al, 2008). Recent studies on alcoholism using commercially available antibodies coupled to immunogold, in situ PCR and RT-PCR have challenged these initial observations, however (for examples see Pandey et al, 2006 andMcGough et al, 2004).…”

Bdnf Deletion or TrkB Impairment in Amygdala Inhibits Both Appetitive and Aversive Learning

“…Although our infusions spanned multiple amygdalar nuclei, bdnf mRNA is absent from the CeA and expression is most prominent in the BLA (Krause et al, 2008). Some, but not all, of our infusions extended beyond the amygdala to surrounding cortical areas that are positive for bdnf mRNA (e.g., endopiriform nulei and, less frequently, the piriform cortex), but infection was not strong in these areas and did not seem to affect behavioral outcomes.…”

“…In addition to its demonstrated role in hippocampal-dependent learning, interest in the influence of BDNF and its primary receptor, tyrosine kinase receptor B (TrkB), in amygdala-dependent learning has also grown rapidly in recent years. Cell bodies in the basolateral amygdala (BLA) strongly express bdnf mRNA, and the TrkB receptor is expressed throughout the amygdala, including the BLA and the central nucleus (CeA) (Krause et al, 2008). The BLA is known to facilitate the acquisition and consolidation of appetitive and aversive learning events, and recent studies have shown that bdnf mRNA is significantly upregulated in this region of the amygdala following Pavlovian fear conditioning (Rattiner et al, 2004;Ou and Gean, 2006).…”