Abstract
Teneurin C-terminal associated peptides (TCAPs) are an evolutionarily ancient family of 40- to 41-residue bioactive peptides located on the extracellular end of each of the four teneurin transmembrane proteins. TCAP-1 may exist as a tethered peptide at the teneurin-1 carboxy end or as an independent peptide that is either released via post-transcriptional cleavage from its teneurin-1 pro-protein or independently expressed as its own mRNA. In neurons, soluble TCAP-1 acts as a paracrine factor to regulate cellular activity and neuroplastic interactions. In vitro studies indicate that, by itself, synthetic TCAP-1 promotes neuron growth and protects cells from chemical insult. In vivo, TCAP-1 increases hippocampal neuron spine density, reduces stress-induced behavior and ablates cocaine-seeking behaviors. Together, these studies suggest that the physiological effects of TCAP-1 are a result of an inhibition of corticotropin-releasing factor (CRF) activity leading to increased energy production. This hypothesis is supported by in vivo functional positron emissions tomography studies, which demonstrate that TCAP-1 significantly increases glucose uptake in rat brain. Complimentary in vitro studies show that enhanced glucose uptake is the result of TCAP-1-induced insertion of the glucose transporter into the neuronal plasma membrane, leading to increased glucose uptake and ATP production. Interestingly, TCAP-1-mediated glucose uptake occurs through a novel insulin-independent pathway. This review will focus on examining the role of TCAP on neuronal energy metabolism in the central nervous system.
Highlights
The teneurins are a family of type-II transmembrane glycoproteins that are widely expressed in the central nervous system (Baumgartner et al, 1994; Levine et al, 1994)
To determine if terminal associated peptides (TCAPs) exists as a separate gene that produces a soluble peptide independent of teneurin, the existence of TCAPspecific mRNA was investigated by Northern blot (Chand et al, 2013a)
The full-length teneurins, do possess the hydrophobic transmembrane region that allow them to be inserted into the plasma membrane via fusion with secretory vesicles (Baumgartner et al, 1994; Levine et al, 1994). This distinction in cellular localization is apparent in the differential expression of immunoreactive teneurin-1, which is primarily found at the plasma membrane, and immunoreactive TCAP-1, which is confined to the cytosol (Chand et al, 2013a). These findings indicate that a soluble TCAP peptide could be liberated by direct cleavage from the teneurins, or in the case of TCAP-1 and possibly TCAP-3, transcribed as a smaller, independent mRNA that encodes the TCAP region
Summary
TCAP-1 increases hippocampal neuron spine density, reduces stressinduced behavior and ablates cocaine-seeking behaviors. Together, these studies suggest that the physiological effects of TCAP-1 are a result of an inhibition of corticotropin-releasing factor (CRF) activity leading to increased energy production. These studies suggest that the physiological effects of TCAP-1 are a result of an inhibition of corticotropin-releasing factor (CRF) activity leading to increased energy production This hypothesis is supported by in vivo functional positron emissions tomography studies, which demonstrate that TCAP-1 significantly increases glucose uptake in rat brain. Complimentary in vitro studies show that enhanced glucose uptake is the result of TCAP-1-induced insertion of the glucose transporter into the neuronal plasma membrane, leading to increased glucose uptake and ATP production.
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