Understanding mammal avoidance of human settlements.
Authors: Potts JR, Börger L, Tucker MA, Ossi F, Yanco SW, Ellis-Soto D, Müller T, Oliver RY, Alves MH, Arnold W, Attias N, Bastille-Rousseau G, Belant JL, Blount JD, Beyer DE, Cagnacci F, Chamaillé-Jammes S, Chan AN, Cole EK, Cornils JS, de Paula RC, DeNicola V, Desbiez ALJ, Dewey SR, Drake D, Egan M, Eikelboom JAJ, Farmer M, Garel M, Goheen JR, Hansen HP, Haugaard L, Hebblewhite M, Heim M, Ježek M, Jordán L, Kamaru DN, Krofel M, LaSharr TN, Leimgruber P, Loison A, Long RA, Loretto MC, Marchand P, Meisingset E, Melzheimer J, Monteith KL, Morgan JJ, Mortensen RM, Mueller R, Mysterud A, Olejarz A, Oliveira T, Panzacchi M, Portas R, Potočnik H, Prins HHT, Prugh LR, Ranc N, Roeder R, Rolandsen CM, Şekercioğlu Ç, Selimovic A, Smiley R, Solberg EJ, Strand O, Sunde P, Toïgo C, Van Moorter B, Verzuh TL, Wachter B, Wagler BL, Whittington J, Wilmers CC, Wittemyer G, Rutz C
Journal: The Journal of animal ecology
mental health
psychology
open access
Abstract
Serotonin (5-hydroxytryptamine; 5-HT), synthesized in the brain, is a key neurotransmitter responsible for regulating numerous physiological and behavioral processes. It has been shown to influence mood, appetite, breathing, stress homeostasis, cognition, impulsivity, aggressive behavior, maternal care, sexual behavior, thermoregulation, and pain sensation [–]. It has also been suggested to play a role in rest-related and energy-conserving activities like sleep, locomotion, and motivation [, , ]. Central 5-HT is produced in neurons of the brainstem raphe nuclei from the amino acid L-tryptophan (TRP), which is transported from the periphery. In the rate-limiting step, TRP is hydroxylated to 5-hydroxy-L-tryptophan (5-HTP) by the tryptophan hydroxylase type 2 (TPH2), an enzyme identified by Walther and Bader []. Subsequently, 5-HTP is decarboxylated to 5-HT by aromatic L-amino acid decarboxylase (AADC). Newly synthesized 5-HT is packaged into synaptic vesicles by the vesicular monoamine transporter type 2 (VMAT2) and released to the synaptic cleft. In the cytoplasm, 5-HT can be degraded by monoamine oxidase (MAO) into 5-hydroxyindoleacetic acid (5-HIAA), while extracellular 5-HT is transported back to the terminal by 5-HT transporter (5-HTT/SERT). The wide spectrum of 5-HT functions is mediated by 14 5-HT receptor subtypes, classified into seven subclasses − 5-HT, 5-HT, 5-HT, 5-HT, 5-HT, 5-HT, and 5-HT. These receptor families differ in their structure, signaling mechanisms, and functional roles, allowing 5-HT to exert diverse effects throughout the CNS []. This review focuses on presenting evidence on the influence of 5-HT dysfunction on alcohol use disorder (AUD) vulnerability, maintenance, relapse, heterogeneity, and treatment response. According to DSM-5 [], AUD is a chronic, relapsing condition characterized by compulsive alcohol use. Diagnosis of AUD requires the presence of at least two of eleven criteria within 12 months, including drinking in larger amounts or for longer than intended, craving, continued drinking despite negative consequences, and withdrawal symptoms. Depending on the number of symptoms present, AUD is classified as mild (2–3 symptoms), moderate (4–5 symptoms), or severe (≥6 symptoms).