Neurotensin receptors in the human amygdaloid complex. Topographical and quantitative autoradiographic study

Lantos, T; Palkovits, Miklós; Rostène, William; Bérod, Anne

doi:10.1016/0891-0618(96)00162-7

Cited by 10 publications

(3 citation statements)

References 62 publications

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“…The functional significance of this interaction is further supported by a behavioral study showing that neurotensin in the PAG is partially involved in analgesia produced by opioids injected into the amygdala (Tershner and Helmstetter, 2000). In humans and rodents, the amygdala has a dense distribution of both the neurotensin peptide and receptors (Tay et al, 1989; Benzing Lantos et al, 1996). This peptide is localized at the soma, axons, and dendrites of neurons in the CeA and has been found in neurons that project to the PAG (Tay et al, 1989).…”

Section: Downloaded Frommentioning

confidence: 68%

Effect of the μ Opioid on Excitatory and Inhibitory Synaptic Inputs to Periaqueductal Gray-Projecting Neurons in the Amygdala

Finnegan

Chen

Pan

2004

J Pharmacol Exp Ther

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Opioids are potent analgesics, but the sites of their action and cellular mechanisms are not fully understood. The central nucleus of the amygdala (CeA) is important for opioid analgesia through the projection to the periaquaductal gray (PAG). In this study, we examined the effects of opioid receptor stimulation on inhibitory and excitatory synaptic inputs to PAG-projecting CeA neurons retrogradely labeled with a fluorescent tracer injected into the ventrolateral PAG of rats. Whole-cell voltageclamp recordings were performed on labeled CeA neurons in brain slices. The specific opioid receptor agonist, [D-Ala 2 ,NMe-Phe 4 ,Gly 5 -ol]-enkephalin (DAMGO, 1 M), significantly reduced the frequency of miniature inhibitory postsynaptic currents (mIPSCs) without altering the amplitude and decay constant of mIPSCs in 47.6% (10 of 21) of cells tested. DAMGO also significantly decreased the peak amplitude of evoked IPSCs in 69% (9 of 13) of cells examined. However, DAMGO did not significantly alter the frequency of miniature excitatory postsynaptic currents (EPSCs) and the amplitude of evoked EPSCs in 69% (9 of 13) and 83% (10 of 12) of labeled cells, respectively. The IPSCs were blocked by the GABA A receptor antagonist bicuculline, whereas the EPSCs were largely abolished by the non-N-methyl-D-aspartate antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. The immunoreactivity of opioid receptors was colocalized with synaptophysin, a presynaptic marker, in close appositions to labeled CeA neurons. These results suggest that activation of opioid receptors on presynaptic terminals primarily attenuates GABAergic synaptic inputs to PAG-projecting neurons in the CeA.

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Section: Downloaded Frommentioning

confidence: 68%

Effect of the μ Opioid on Excitatory and Inhibitory Synaptic Inputs to Periaqueductal Gray-Projecting Neurons in the Amygdala

Finnegan

Chen

Pan

2004

J Pharmacol Exp Ther

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“…Our laboratory had demonstrated that NT stimulates proliferation of cultured human microglia and triggers secretion of proinflammatory cytokines and chemokines through activation of NTR3/sortilin (24). NT receptors in the human brain transiently increase after birth (71) and are more concentrated in the amygdala (72).…”

Section: Discussionmentioning

confidence: 99%

IL-37 is increased in brains of children with autism spectrum disorder and inhibits human microglia stimulated by neurotensin

Tsilioni

Patel

Pantazopoulos

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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Autism spectrum disorder (ASD) does not have a distinct pathogenesis or effective treatment. Increasing evidence supports the presence of immune dysfunction and inflammation in the brains of children with ASD. In this report, we present data that gene expression of the antiinflammatory cytokine IL-37, as well as of the proinflammatory cytokines IL-18 and TNF, is increased in the amygdala and dorsolateral prefrontal cortex of children with ASD as compared to non-ASD controls. Gene expression of IL-18R, which is a receptor for both IL-18 and IL-37, is also increased in the same brain areas of children with ASD. Interestingly, gene expression of the NTR3/sortilin receptor is reduced in the amygdala and dorsolateral prefrontal cortex. Pretreatment of cultured human microglia from normal adult brains with human recombinant IL-37 (1 to 100 ng/mL) inhibits neurotensin (NT)-stimulated secretion and gene expression of IL-1β and CXCL8. Another key finding is that NT, as well as the proinflammatory cytokines IL-1β and TNF increase IL-37 gene expression in cultured human microglia. The data presented here highlight the connection between inflammation and ASD, supporting the development of IL-37 as a potential therapeutic agent of ASD.

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“… 52 We reported that the peptides NT 53 and CRH 9 secreted under stress were increased in the serum of young children with ASD, as compared with normal controls. 53 The highest expression of NT receptors in the human brain is in the amygdala, 54 hypothalamus and area of Broca, 55 which regulate emotions and language, respectively. Stress can activate MCs through CRH leading to increased BBB permeability.…”

Section: Maternal Health Prematurity and Low Birth Weight Are Linkedmentioning

confidence: 99%

Atopic diseases and inflammation of the brain in the pathogenesis of autism spectrum disorders

et al. 2016

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Autism spectrum disorders (ASDs) affect as many as 1 in 45 children and are characterized by deficits in sociability and communication, as well as stereotypic movements. Many children also show severe anxiety. The lack of distinct pathogenesis and reliable biomarkers hampers the development of effective treatments. As a result, most children with ASD are prescribed psychopharmacologic agents that do not address the core symptoms of ASD. Autoantibodies against brain epitopes in mothers of children with ASD and many such children strongly correlate with allergic symptoms and indicate an aberrant immune response, as well as disruption of the blood–brain barrier (BBB). Recent epidemiological studies have shown a strong statistical correlation between risk for ASD and either maternal or infantile atopic diseases, such as asthma, eczema, food allergies and food intolerance, all of which involve activation of mast cells (MCs). These unique tissue immune cells are located perivascularly in all tissues, including the thalamus and hypothalamus, which regulate emotions. MC-derived inflammatory and vasoactive mediators increase BBB permeability. Expression of the inflammatory molecules interleukin (IL-1β), IL-6, 1 L-17 and tumor necrosis factor (TNF) is increased in the brain, cerebrospinal fluid and serum of some patients with ASD, while NF-kB is activated in brain samples and stimulated peripheral blood immune cells of other patients; however, these molecules are not specific. Instead the peptide neurotensin is uniquely elevated in the serum of children with ASD, as is corticotropin-releasing hormone, secreted from the hypothalamus under stress. Both peptides trigger MC to release IL-6 and TNF, which in turn, stimulate microglia proliferation and activation, leading to disruption of neuronal connectivity. MC-derived IL-6 and TGFβ induce maturation of Th17 cells and MCs also secrete IL-17, which is increased in ASD. Serum IL-6 and TNF may define an ASD subgroup that benefits most from treatment with the natural flavonoid luteolin. Atopic diseases may create a phenotype susceptible to ASD and formulations targeting focal inflammation of the brain could have great promise in the treatment of ASD.

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Neurotensin receptors in the human amygdaloid complex. Topographical and quantitative autoradiographic study

Cited by 10 publications

References 62 publications

Effect of the μ Opioid on Excitatory and Inhibitory Synaptic Inputs to Periaqueductal Gray-Projecting Neurons in the Amygdala

Effect of the μ Opioid on Excitatory and Inhibitory Synaptic Inputs to Periaqueductal Gray-Projecting Neurons in the Amygdala

IL-37 is increased in brains of children with autism spectrum disorder and inhibits human microglia stimulated by neurotensin

Atopic diseases and inflammation of the brain in the pathogenesis of autism spectrum disorders

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