Asset Details
Do you wish to reserve the book?
Inactivation of the Mouse L-Proline Transporter PROT Alters Glutamatergic Synapse Biochemistry and Perturbs Behaviors Required to Respond to Environmental Changes
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Inactivation of the Mouse L-Proline Transporter PROT Alters Glutamatergic Synapse Biochemistry and Perturbs Behaviors Required to Respond to Environmental Changes
Do you wish to request the book?
Inactivation of the Mouse L-Proline Transporter PROT Alters Glutamatergic Synapse Biochemistry and Perturbs Behaviors Required to Respond to Environmental Changes
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Inactivation of the Mouse L-Proline Transporter PROT Alters Glutamatergic Synapse Biochemistry and Perturbs Behaviors Required to Respond to Environmental Changes
2018
Overview
The endogenous neutral amino acid L-proline exhibits a variety of physiological and behavioral actions in the nervous system, highlighting the importance of accurately regulating its extracellular abundance. The L-proline transporter PROT (
) is believed to control the spatial and temporal distribution of L-proline at glutamatergic synapses by rapid uptake of this amino acid into presynaptic terminals. Despite the importance of members of the
transporter family regulating neurotransmitter signaling and homeostasis in brain, evidence that PROT dysfunction supports risk for mental illness is lacking. Here we report the disruption of the PROT gene by homologous recombination. Mice defective in PROT displayed altered expression of glutamate transmission-related synaptic proteins in cortex and thalamus. PROT deficiency perturbed mouse behavior, such as reduced locomotor activity, decreased approach motivation and impaired memory extinction. Thus, our study demonstrates that PROT regulates behaviors that are needed to respond to environmental changes
and suggests that PROT dysfunctions might contribute to mental disorders showing altered response choice following task contingency changes.
