FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2912158792> ?p ?o ?g. }

• W2912158792 endingPage "3107" @default.
• W2912158792 startingPage "3094" @default.
• W2912158792 abstract "High-trait anxiety is a risk factor for the development of affective disorders and has been associated with decreased cardiovascular and behavioral responsivity to acute stressors in humans that may increase the risk of developing cardiovascular disease. Although human neuroimaging studies of high-trait anxiety reveals dysregulation in primate cingulate areas 25 and 32 and the anterior hippocampus (aHipp) and rodent studies reveal the importance of aHipp glutamatergic hypofunction, the causal involvement of aHipp glutamate and its interaction with these areas in the primate brain is unknown. Accordingly, we correlated marmoset trait anxiety scores to their postmortem aHipp glutamate levels and showed that low glutamate in the right aHipp is associated with high-trait anxiety in marmosets. Moreover, pharmacologically increasing aHipp glutamate reduced anxiety levels in highly anxious marmosets in two uncertainty-based tests of anxiety: exposure to a human intruder with uncertain intent and unpredictable loud noise. In the human intruder test, increasing aHipp glutamate decreased anxiety by increasing approach to the intruder. In the unpredictable threat test, animals showed blunted behavioral and cardiovascular responsivity after control infusions, which was normalized by increasing aHipp glutamate. However, this aHipp-mediated anxiolytic effect was blocked by simultaneous pharmacological inactivation of area 25, but not area 32, areas which when inactivated independently reduced and had no effect on anxiety, respectively. These findings provide causal evidence in male and female primates that aHipp glutamatergic hypofunction and its regulation by area 25 contribute to the behavioral and cardiovascular symptoms of endogenous high-trait anxiety. SIGNIFICANCE STATEMENT High-trait anxiety predisposes sufferers to the development of anxiety and depression. Although neuroimaging of these disorders and rodent modeling implicate dysregulation in hippocampal glutamate and the subgenual/perigenual cingulate cortices (areas 25/32), the causal involvement of these structures in endogenous high-trait anxiety and their interaction are unknown. Here, we demonstrate that increased trait anxiety in marmoset monkeys correlates with reduced hippocampal glutamate and that increasing hippocampal glutamate release in high-trait-anxious monkeys normalizes the aberrant behavioral and cardiovascular responsivity to potential threats. This normalization was blocked by simultaneous inactivation of area 25, but not area 32. These findings provide casual evidence in primates that hippocampal glutamatergic hypofunction regulates endogenous high-trait anxiety and the hippocampal–area 25 circuit is a potential therapeutic target." @default.
• W2912158792 created "2019-02-21" @default.
• W2912158792 creator A5021093644 @default.
• W2912158792 creator A5023549981 @default.
• W2912158792 creator A5027874151 @default.
• W2912158792 creator A5028975346 @default.
• W2912158792 creator A5035188600 @default.
• W2912158792 creator A5041301118 @default.
• W2912158792 creator A5041563576 @default.
• W2912158792 creator A5053690189 @default.
• W2912158792 creator A5065225426 @default.
• W2912158792 creator A5067805366 @default.
• W2912158792 creator A5079589109 @default.
• W2912158792 creator A5083636574 @default.
• W2912158792 date "2019-02-04" @default.
• W2912158792 modified "2023-10-10" @default.
• W2912158792 title "Glutamate Within the Marmoset Anterior Hippocampus Interacts with Area 25 to Regulate the Behavioral and Cardiovascular Correlates of High-Trait Anxiety" @default.
• W2912158792 cites W1811662369 @default.
• W2912158792 cites W1941407864 @default.
• W2912158792 cites W1944954943 @default.
• W2912158792 cites W1967460486 @default.
• W2912158792 cites W1973950070 @default.
• W2912158792 cites W1975517878 @default.
• W2912158792 cites W1980300126 @default.
• W2912158792 cites W1986764568 @default.
• W2912158792 cites W1987940241 @default.
• W2912158792 cites W1990397347 @default.
• W2912158792 cites W1995756445 @default.
• W2912158792 cites W2001131875 @default.
• W2912158792 cites W2005992028 @default.
• W2912158792 cites W2006701125 @default.
• W2912158792 cites W2010767102 @default.
• W2912158792 cites W2013616234 @default.
• W2912158792 cites W2016918058 @default.
• W2912158792 cites W2023025832 @default.
• W2912158792 cites W2023443471 @default.
• W2912158792 cites W2023595618 @default.
• W2912158792 cites W2023961947 @default.
• W2912158792 cites W2026813655 @default.
• W2912158792 cites W2028636860 @default.
• W2912158792 cites W2032337752 @default.
• W2912158792 cites W2035462451 @default.
• W2912158792 cites W2039348342 @default.
• W2912158792 cites W2041457323 @default.
• W2912158792 cites W2044413038 @default.
• W2912158792 cites W2046616756 @default.
• W2912158792 cites W2048211160 @default.
• W2912158792 cites W2051246321 @default.
• W2912158792 cites W2051497760 @default.
• W2912158792 cites W2051823327 @default.
• W2912158792 cites W2058330488 @default.
• W2912158792 cites W2061657402 @default.
• W2912158792 cites W2068863027 @default.
• W2912158792 cites W2073031662 @default.
• W2912158792 cites W2081145596 @default.
• W2912158792 cites W2097699474 @default.
• W2912158792 cites W2100143444 @default.
• W2912158792 cites W2104047644 @default.
• W2912158792 cites W2108888119 @default.
• W2912158792 cites W2109699997 @default.
• W2912158792 cites W2117501598 @default.
• W2912158792 cites W2118281620 @default.
• W2912158792 cites W2118654942 @default.
• W2912158792 cites W2121970195 @default.
• W2912158792 cites W2122424266 @default.
• W2912158792 cites W2144116861 @default.
• W2912158792 cites W2148596080 @default.
• W2912158792 cites W2152032786 @default.
• W2912158792 cites W2153168156 @default.
• W2912158792 cites W2157305460 @default.
• W2912158792 cites W2158553737 @default.
• W2912158792 cites W2170969968 @default.
• W2912158792 cites W2180841008 @default.
• W2912158792 cites W2216855499 @default.
• W2912158792 cites W2254443919 @default.
• W2912158792 cites W2282110843 @default.
• W2912158792 cites W2306479064 @default.
• W2912158792 cites W2320863873 @default.
• W2912158792 cites W2404592340 @default.
• W2912158792 cites W2414381817 @default.
• W2912158792 cites W2500712516 @default.
• W2912158792 cites W2593999158 @default.
• W2912158792 cites W2604657615 @default.
• W2912158792 cites W2611279297 @default.
• W2912158792 cites W2787791202 @default.
• W2912158792 cites W2789974429 @default.
• W2912158792 cites W2900127046 @default.
• W2912158792 cites W3115097227 @default.
• W2912158792 cites W4247491791 @default.
• W2912158792 cites W565238098 @default.
• W2912158792 cites W849609062 @default.
• W2912158792 doi "https://doi.org/10.1523/jneurosci.2451-18.2018" @default.
• W2912158792 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6468106" @default.
• W2912158792 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30718320" @default.
• W2912158792 hasPublicationYear "2019" @default.
• W2912158792 type Work @default.
• W2912158792 sameAs 2912158792 @default.
• W2912158792 citedByCount "27" @default.

• next