Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Wenhua Zhang
 -- 2158 2023-02-23 02:20:19 |
2 format correct
Jessie Wu
+ 2 word(s) 2160 2023-02-23 02:22:13 | |
3 format correct
Jessie Wu
-4 word(s) 2156 2023-02-23 02:23:43 | |
4 format correct
Jessie Wu
+ 2 word(s) 2158 2023-02-23 02:27:53 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Hu, P.; Lu, Y.; Pan, B.; Zhang, W. Amygdala Neuroinflammation and Psychiatric Disorders. Encyclopedia. Available online: https://encyclopedia.pub/entry/41565 (accessed on 08 July 2024).
Hu P, Lu Y, Pan B, Zhang W. Amygdala Neuroinflammation and Psychiatric Disorders. Encyclopedia. Available at: https://encyclopedia.pub/entry/41565. Accessed July 08, 2024.
Hu, Ping, Ying Lu, Bing-Xing Pan, Wen-Hua Zhang. "Amygdala Neuroinflammation and Psychiatric Disorders" Encyclopedia, https://encyclopedia.pub/entry/41565 (accessed July 08, 2024).
Hu, P., Lu, Y., Pan, B., & Zhang, W. (2023, February 23). Amygdala Neuroinflammation and Psychiatric Disorders. In Encyclopedia. https://encyclopedia.pub/entry/41565
Hu, Ping, et al. "Amygdala Neuroinflammation and Psychiatric Disorders." Encyclopedia. Web. 23 February, 2023.
Amygdala Neuroinflammation and Psychiatric Disorders
Edit
This entry is adapted from the peer-reviewed paper 10.3390/ijms231911076

Depression and anxiety disorder are the most common mental diseases affecting hundreds of millions of people worldwide. The comorbidity rate of anxiety disorder and depression is very high, with 74% of depressed patients having anxiety symptoms, while 61% of anxious patients have depression symptoms. Stress exposure is widely accepted as a critical contributing factor to psychological and neuropathological disorders. Especially during the COVID-19 pandemic, the high pressure of increasingly demanding work and life has led to a sharp rise in the incidence of mental diseases. Inflammation induces psychological and neuropathological disorders by influencing neuronal excitability, neurotransmitter release, receptor, and transporter expression through peripheral hormones and autonomic responses. A number of animal and human studies have revealed that the amygdala, ventral hippocampus, and medial prefrontal cortex (mPFC) are extensively involved in the occurrence of anxiety, depression, and related behavioral regulation. Among them, the amygdala, one of the kernel brain regions mediating stress-coping located in the deep temporal lobe, is considered the hub center for processing emotionally salient stimuli and implementing appropriate behavioral responses.

depression amygdala inflammation

1. Amygdala Inflammation and Anxiety Disorders

Numerous studies have implicated that inflammation-related anxiety disorders are associated with the aberrant activation of amygdala neurons. For example, studies have shown that in an inflammatory pain mouse model induced by complete Freund’s adjuvant (CFA) injection, the anxiety-like behavior in mice was markedly increased, which is associated with the upregulation of the excitatory postsynaptic receptors N-methyl-D-aspartate (NMDA) receptor and AMPA receptor in the basolateral amygdala (BLA), as well as the postsynaptic dense protein PSD95, while the expression of inhibitory receptors GABAA α2 and GABAA γ2 was significantly decreased [1]. However, opposite findings were reported, in that the levels of GABAA α2 and GABAA γ2 were dramatically increased in the BLA of CFA-treated mice [2]. In terms of synaptic transmission, CFA injection has been found to increase BLA excitatory synaptic transmission and decrease inhibitory synaptic transmission, as reflected by the increased frequency of spontaneous excitatory postsynaptic currents and the decreased frequency of spontaneous inhibitory postsynaptic currents [1]. While considering the neurotransmitters, CFA increased glutamate levels in the BLA and decreased GABA levels [3]. These findings suggest that the inflammation-induced disruption of the amygdala E/I balance is manifested by enhanced excitatory presynaptic release and upregulated excitatory postsynaptic receptors, together with the decreased inhibitory presynaptic release and reduced expression of inhibitory receptors, which may contribute to the hyperactivity of the amygdala and finally result in the occurrence of anxiety disorders [4]. However, researchers found that lipopolysaccharide (LPS) challenge mainly increases the excitatory synaptic transmission on BLA projection neurons but has no effect on inhibitory synaptic transmission [5]. The AMPA/NMDA ratio (a measure of postsynaptic changes in synaptic strength) also remained unaltered [5]. The exact reasons for these inconsistent results are not fully understood. One possible explanation is that the difference may be due to various factors, such as different models, experimental procedures, and the processing time involved. It should be noted that plantar injection of CFA induces not only an inflammatory response but also chronic pain, which is widely used as an animal model of chronic inflammatory pain. In contrast, i.p. injection of LPS mainly induces an inflammatory response. Interestingly, similar to the LPS-induced effects on the BLA, chronic stress also increased the excitatory synaptic transmission onto BLA PNs but had no obvious effect on the inhibitory synaptic transmission or NMDA/AMPA current ratio [6][7]. Given the concept that chronic stress induces amygdala inflammation, it is likely that amygdala inflammation may play a critical role in the chronic stress-induced functional remodeling of BLA PNs and anxiety-like behavior.
The specific mechanisms of how inflammation affects the BLA neuronal function and the occurrence of anxiety disorders are still vague. Such an effect may likely be related to the effect of cytokines on monoamine and glutamate. For example, studies showed that neonatal LPS treatment reduced TGF-β1 expression in the BLA during adulthood, which lead to the down-regulation of GABAARα2 subunit expression and GABA-induced current density, and ultimately caused the disruption of the E/I balance and the shift toward excitation, resulting in anxiety disorder [8]. Therefore, it is expected that anxiety-like behavior and the hyperactivity of the HPA axis induced by inflammation may be due to the increased neuron excitability caused by the decrease in the GABAergic inhibitory current in the BLA. Another study found that in LPS-induced anxiety models, IL33 expression was significantly upregulated in the BLA, while overexpression of IL33 in astrocytes inhibited BDNF expression through the NF-κB signaling pathway, affecting the synaptic transmission of GABA and causing anxiety disorders [9]. In addition, feeding on a chronic high-fat diet can promote anxiety-like behavior by increasing the expression of amygdala dopamine and pro-inflammatory cytokines TNF-α and IL-1β [10], while the local infusion of TNF-α-neutralizing antibody infliximab in the BLA reversed anxiety-like behavior in mice with persistent inflammatory pain [11]. In vitro patch-clamp recordings showed that TNF-α significantly enhanced AMPA receptor-mediated glutamate excitatory synaptic transmission and inhibited GABAA receptor-mediated BLA inhibitory synaptic transmission [11]. Furthermore, chemokine CXCL12, which has been considered a standard pro-inflammatory molecule for a long time, may also contribute to inflammatory-related anxiety as supported by the evidence that an LPS challenge induced chemokine CXCL12 production in the amygdala through astrocyte activation, while microinjection of CXCL12 into the amygdala is sufficient to induce anxious-like behavior in mice. In addition, CXCL12 enhances glutamatergic transmission by increasing the frequency of sEPSC in the BLA [12]. These findings provide direct evidence showing that pro-inflammatory molecules in the BLA contribute to the development of anxiety by systemic inflammatory stress, which also may be a potential therapeutic target for inflammatory anxiety.
The CeA also plays a vital role in regulating the immune stress response. The CeA was activated in male and female rats after LPS injection 14 days after birth [13]. CeA lesion significantly reduced the systemic injection of IL-1β-induced ACTH secretion, CRH in the hypothalamus, and c-Fos gene expression in oxytocin cells [14]. Similarly, bilateral CeA damage also attenuated the HPA axis response caused by HSV-1 infection, as well as fever, hyperactivity, and aggression [15]. It should be noted that different stress modes have distinct effects on CeA activation. For example, homeostasis disruption and systemic stressors (such as inflammatory stimulation and bleeding) activate the CeA [16][17], while psychological stressors such as restrain stress do not activate the CeA [14][18][19]. In contrast, the MeA is preferentially activated by psychological stressors. MeA damage reduced the IL1β response to restraint stress but not to homeostasis and systemic stressors [18].

2. Amygdala Inflammation and Depression

Although the vast majority of studies revealing the role of the amygdala in modulating emotional function have been focused on fear and anxiety, recent studies have shown that amygdala inflammation has an undoubtful function in depression. For example, intravenous or subcutaneous IL-1β injection increased depression-like behavior in mice and enhanced the expression of pro-inflammatory cytokines TNF-α and IL-6 in the amygdala, which is regulated by the CORT/GR system. Furthermore, serum corticosterone levels were markedly increased with IL-1β injection, while GR inhibitor RU486 reduced IL-1β-induced depression-like behavior and TNF-α and IL-6 expression [20]. In addition, chronic social stress (a combination of mild prenatal stress, mild maternal separation stress, and mild social frustration stress) induced depressive-like behavior, which is accompanied by the activation of amygdala microglia and increased expression of inflammatory factors IL-17, TNF-α, IL-1β, IL18, and IL-6. Interestingly, peripheral intraperitoneal injection of IL-17 antibody to block IL-17 activity inhibited stress-induced BLA microglia activation and alleviated depression-like behavior [21]. In addition, LPS-induced inflammation increases CeA activity in animals [22], which is associated with an increase in depressive-like behavior [22] and a reduction in certain social behaviors, such as grooming, sniffing, and close following with an interaction partner [23]. Blocking the activity in the amygdala by using a reversible lesion eliminates this inflammation-induced social withdrawal behavior [23].
In mammals, the downregulation of serotonin (5-HT) levels in the CNS has been implicated in the pathophysiology of depression. With the development of the cytokine theory of depression, it has been well documented that pro-inflammatory cytokines, including IL-1β, IFN, and TNF can reduce the bioavailability of neurotransmitters such as serotonin (5-HT) [24]. The synthetic precursor of 5-HT, tryptophan, is metabolized by the kynurenine pathway (KP) and 5-HT pathway [25]. Indeed, over 90% of tryptophan has been metabolized via the KP in mammals [26]. In the KP, indoleamine-2,3-dioxygenase (IDO) is a rate-limiting enzyme that catalyzes the decomposition and metabolism of tryptophan [25]. It should be noted that IDO is an inflammatory-inducible enzyme, which can be induced by a variety of inflammatory factors, such as IFNγ and TNFα [27][28]. Activation of the body’s immune system causes excessive secretion of cytokines, induces the activation of IDO, and increases the metabolism of tryptophan along the KP pathway, thereby competitively antagonizing the biosynthesis process of 5-HT and reducing the central 5-HT neurotransmission. Therefore, IDO plays an essential role in the cytokine theory of depression.
A large amount of evidence has shown that inflammatory response is accompanied by IDO dysfunction in depression [28][29]. Early-life stress from allergic dermatitis increases susceptibility to depression induced by systemic inflammation, which is accompanied by increased activation of microglia and cytokine expression in the amygdala, as well as upregulated expressions of IDO [30]. High IDO levels indicate that 5-HT metabolism may be accelerated, thus reducing the 5-HT level. The exact mechanism by which inflammation induces upregulation of IDO expression in the amygdala remains unclear. However, it should be noted that pro-inflammatory cytokines, such as IL-1β, can cross the BBB and trigger neuroinflammation by activating microglia. It has been reported that activated microglia release pro-inflammatory cytokines that reduce the synthesis of 5-HT, dopamine, and norepinephrine in the limbic system by activating IDO and mitogen-activated protein kinase (MAPK) in the inflammatory signaling pathway [31][32][33]. Interestingly, numerous studies have shown that inflammatory responses increase amygdala IL-1β expression and activate MAPK pathways (increased phosphorylation of JNK, ERK1/2, and P38).

3. Inflammation and the Amygdala Neural Circuit

The structural and functional connectivity between the amygdala and other emotion-related brain regions, such as the mPFC, hippocampus, and anterior cingulate cortex, play crucial roles in stress-induced anxiety and depressive behaviors [34][35][36]. Among them, the enhanced dmPFC-amygdala circuit has been widely shown to be implicated in inflammatory-related psychiatric disorders. For example, increased amygdala activity is associated with inflammation when exposed to social stress. Individuals who exhibit stronger coupling between the amygdala and dmPFC display higher inflammatory responses when faced with stressors [37]. The recent study demonstrated that LPS causes anxiety and depression-like behaviors accompanied by an enhanced activity of the dmPFC-BLA circuits [5]. In addition, allergic inflammation leads to enhanced functional connectivity within the mPFC-amygdala circuit, while disrupting the dynamic interactions of the mPFC-amygdala circuit may promote anxiety-related behaviors with asthma [38]. Furthermore, a recent study from the same lab showed that allergic inflammation induced an increase in neuronal activity, and functional connectivity of the ACC-BLA circuit was correlated with the level of anxiety [39]. Inflammation-associated mood change reduced the connectivity of sACC to the amygdala, which was modulated by peripheral IL-6 [40].
It is worth noting that many studies have shown that the abnormal activation of the mPFC-BLA-vHPC circuit contributes to chronic stress-induced anxiety [6][41][42][43], and depressive-like behavior [44]. Specifically, chronic stress increases the glutamate release from dmPFC presynaptic terminals in the BLA, which enhances the excitatory synaptic transmission efficiency of BLA neurons [6]. Interestingly, chronic stress-induced abnormal increase in BLA neuron activity only occurred in BLA neurons projected to the vHPC [42][43]. The specific mechanism of stress-induced changes in the amygdala circuit function remains unclear. Considering the effects of inflammatory cytokines on BLA neuronal function and connectivity, it is expected that chronic stress-induced functional remodeling of the BLA circuit may be due to the neuroinflammation caused by stress.
There is also evidence showing that changes within CeA circuit are implicated in inflammatory-related mental disease. For example, a recent study showed that in a mouse model of sepsis induced by intraperitoneal infection, the mice exhibited anxiety-like behavior and exaggerated fear memories, which are similar to anxiety and PTSD-like symptoms seen in human sepsis survivors [45]. It was found that sepsis induces the acute pathological activation of CeA-specific neuron types that project to the ventral BNST and transient and targeted silencing of this subpopulation using chemogenetic methods during the acute phase of sepsis can prevent the subsequent development of anxiety-related behaviors [45]. Considering inflammatory chronic pain increases the risk of depression, Zhou and colleagues identified a novel pathway involving 5-HT projections from the dorsal raphe nucleus to somatostatin-expressing interneurons in the CeA, and then to the lateral habenula for comorbid depressive symptoms in chronic pain [46]. In addition to the evidence that microglia-mediated synaptic engulfment in the CeA contributes to visceral pain [47], it is suggested that the CeA may act as a probable convergent point of chronic pain and depression. Interestingly, in addition to the well-established neuroendocrine-mediated pathway, by which stress regulates immune responses via the systemic release of neuroendocrine systemic mediators (CRH/ACTH/corticosterone), a recent study identified a direct descending neuronal circuit from the CeA and paraventricular CRH neurons into the spleen, which is activated in response to stress. Pharmacogenetic activation of this pathway increases plasma cell abundance after immunization [48]. This finding suggested a novel role of the amygdala in regulating the immune system.

References

  1. Yue, J.; Wang, X.S.; Guo, Y.Y.; Zheng, K.Y.; Liu, H.Y.; Hu, L.N.; Zhao, M.G.; Liu, S.B. Anxiolytic effect of CPEB1 knockdown on the amygdala of a mouse model of inflammatory pain. Brain Res. Bull. 2018, 137, 156–165.
  2. Wang, X.S.; Guan, S.Y.; Liu, A.; Yue, J.; Hu, L.N.; Zhang, K.; Yang, L.K.; Lu, L.; Tian, Z.; Zhao, M.G.; et al. Anxiolytic effects of Formononetin in an inflammatory pain mouse model. Mol. Brain 2019, 12, 36.
  3. Luo, L.; Sun, T.; Yang, L.; Liu, A.; Liu, Q.Q.; Tian, Q.Q.; Wang, Y.; Zhao, M.G.; Yang, Q. Scopoletin ameliorates anxiety-like behaviors in complete Freund’s adjuvant-induced mouse model. Mol. Brain 2020, 13, 15.
  4. McEwen, B.S. Protective and damaging effects of stress mediators. N. Engl. J. Med. 1998, 338, 171–179.
  5. Zheng, Z.H.; Tu, J.L.; Li, X.H.; Hua, Q.; Liu, W.Z.; Liu, Y.; Pan, B.X.; Hu, P.; Zhang, W.H. Neuroinflammation induces anxiety- and depressive-like behavior by modulating neuronal plasticity in the basolateral amygdala. Brain Behav. Immun. 2021, 92, 505–518.
  6. Liu, W.Z.; Zhang, W.H.; Zheng, Z.H.; Zou, J.X.; Liu, X.X.; Huang, S.H.; You, W.J.; He, Y.; Zhang, J.Y.; Wang, X.D.; et al. Identification of a prefrontal cortex-to-amygdala pathway for chronic stress-induced anxiety. Nat. Commun. 2020, 11, 2221.
  7. Qin, X.; He, Y.; Wang, N.; Zou, J.X.; Zhang, Y.M.; Cao, J.L.; Pan, B.X.; Zhang, W.H. Moderate maternal separation mitigates the altered synaptic transmission and neuronal activation in amygdala by chronic stress in adult mice. Mol. Brain 2019, 12, 111.
  8. Zhong, H.; Rong, J.; Yang, Y.; Liang, M.; Li, Y.; Zhou, R. Neonatal inflammation via persistent TGF-beta1 downregulation decreases GABAAR expression in basolateral amygdala leading to the imbalance of the local excitation-inhibition circuits and anxiety-like phenotype in adult mice. Neurobiol. Dis. 2022, 169, 105745.
  9. Zhuang, X.; Zhan, B.; Jia, Y.; Li, C.; Wu, N.; Zhao, M.; Chen, N.; Guo, Y.; Du, Y.; Zhang, Y.; et al. IL-33 in the basolateral amygdala integrates neuroinflammation into anxiogenic circuits via modulating BDNF expression. Brain Behav. Immun. 2022, 102, 98–109.
  10. Akter, S.; Uddin, K.R.; Sasaki, H.; Shibata, S. Gamma oryzanol alleviates high-fat diet-induced anxiety-like behaviors through downregulation of dopamine and inflammation in the amygdala of mice. Front. Pharmacol. 2020, 11, 330.
  11. Chen, J.; Song, Y.; Yang, J.; Zhang, Y.; Zhao, P.; Zhu, X.J.; Su, H.C. The contribution of TNF-alpha in the amygdala to anxiety in mice with persistent inflammatory pain. Neurosci. Lett. 2013, 541, 275–280.
  12. Yang, L.; Wang, M.; Guo, Y.Y.; Sun, T.; Li, Y.J.; Yang, Q.; Zhang, K.; Liu, S.B.; Zhao, M.G.; Wu, Y.M. Systemic inflammation induces anxiety disorder through CXCL12/CXCR4 pathway. Brain Behav. Immun. 2016, 56, 352–362.
  13. Doenni, V.M.; Song, C.M.; Hill, M.N.; Pittman, Q.J. Early-life inflammation with LPS delays fear extinction in adult rodents. Brain Behav. Immun. 2017, 63, 176–185.
  14. Xu, Y.; Day, T.A.; Buller, K.M. The central amygdala modulates hypothalamic-pituitary-adrenal axis responses to systemic interleukin-1beta administration. Neuroscience 1999, 94, 175–183.
  15. Weidenfeld, J.; Itzik, A.; Goshen, I.; Yirmiya, R.; Ben-Hur, T. Role of the central amygdala in modulating the pituitary-adrenocortical and clinical responses in experimental herpes simplex virus-1 encephalitis. Neuroendocrinology 2005, 81, 267–272.
  16. Sawchenko, P.E.; Li, H.Y.; Ericsson, A. Circuits and mechanisms governing hypothalamic responses to stress: A tale of two paradigms. Prog. Brain Res. 2000, 122, 61–78.
  17. Thrivikraman, K.V.; Su, Y.; Plotsky, P.M. Patterns of Fos-Immunoreactivity in the CNS Induced by Repeated Hemorrhage in Conscious Rats: Correlations with Pituitary-Adrenal Axis Activity. Stress 1997, 2, 145–158.
  18. Dayas, C.V.; Buller, K.M.; Day, T.A. Neuroendocrine responses to an emotional stressor: Evidence for involvement of the medial but not the central amygdala. Eur. J. Neurosci. 1999, 11, 2312–2322.
  19. Prewitt, C.M.; Herman, J.P. Hypothalamo-Pituitary-Adrenocortical Regulation Following Lesions of the Central Nucleus of the Amygdala. Stress 1997, 1, 263–280.
  20. Zhang, Y.P.; Wang, H.Y.; Zhang, C.; Liu, B.P.; Peng, Z.L.; Li, Y.Y.; Liu, F.M.; Song, C. Mifepristone attenuates depression-like changes induced by chronic central administration of interleukin-1beta in rats. Behav. Brain Res. 2018, 347, 436–445.
  21. Kim, J.; Suh, Y.H.; Chang, K.A. Interleukin-17 induced by cumulative mild stress promoted depression-like behaviors in young adult mice. Mol. Brain 2021, 14, 11.
  22. Frenois, F.; Moreau, M.; O’Connor, J.; Lawson, M.; Micon, C.; Lestage, J.; Kelley, K.W.; Dantzer, R.; Castanon, N. Lipopolysaccharide induces delayed FosB/DeltaFosB immunostaining within the mouse extended amygdala, hippocampus and hypothalamus, that parallel the expression of depressive-like behavior. Psychoneuroendocrinology 2007, 32, 516–531.
  23. Marvel, F.A.; Chen, C.C.; Badr, N.; Gaykema, R.P.; Goehler, L.E. Reversible inactivation of the dorsal vagal complex blocks lipopolysaccharide-induced social withdrawal and c-Fos expression in central autonomic nuclei. Brain Behav. Immun. 2004, 18, 123–134.
  24. Miller, A.H. Norman cousins lecture. mechanisms of cytokine-induced behavioral changes: Psychoneuroimmunology at the translational interface. Brain Behav. Immun. 2009, 23, 149–158.
  25. Modoux, M.; Rolhion, N.; Mani, S.; Sokol, H. Tryptophan metabolism as a pharmacological target. Trends Pharmacol. Sci. 2021, 42, 60–73.
  26. O’Mahony, S.M.; Clarke, G.; Borre, Y.E.; Dinan, T.G.; Cryan, J.F. Serotonin, tryptophan metabolism and the brain-gut-microbiome axis. Behav. Brain Res. 2015, 277, 32–48.
  27. Robinson, C.M.; Hale, P.T.; Carlin, J.M. The role of IFN-gamma and TNF-alpha-responsive regulatory elements in the synergistic induction of indoleamine dioxygenase. J. Interferon Cytokine Res. 2005, 25, 20–30.
  28. O’Connor, J.C.; Andre, C.; Wang, Y.; Lawson, M.A.; Szegedi, S.S.; Lestage, J.; Castanon, N.; Kelley, K.W.; Dantzer, R. Interferon-gamma and tumor necrosis factor-alpha mediate the upregulation of indoleamine 2,3-dioxygenase and the induction of depressive-like behavior in mice in response to bacillus Calmette-Guerin. J. Neurosci. 2009, 29, 4200–4209.
  29. O’Connor, J.C.; Lawson, M.A.; Andre, C.; Moreau, M.; Lestage, J.; Castanon, N.; Kelley, K.W.; Dantzer, R. Lipopolysaccharide-induced depressive-like behavior is mediated by indoleamine 2,3-dioxygenase activation in mice. Mol. Psychiatry 2009, 14, 511–522.
  30. Hashimoto, O.; Kuniishi, H.; Nakatake, Y.; Yamada, M.; Wada, K.; Sekiguchi, M. Early life stress from allergic dermatitis causes depressive-like behaviors in adolescent male mice through neuroinflammatory priming. Brain Behav. Immun. 2020, 90, 319–331.
  31. Miller, A.H.; Maletic, V.; Raison, C.L. Inflammation and its discontents: The role of cytokines in the pathophysiology of major depression. Biol. Psychiatry 2009, 65, 732–741.
  32. Zhu, C.B.; Blakely, R.D.; Hewlett, W.A. The proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha activate serotonin transporters. Neuropsychopharmacology 2006, 31, 2121–2131.
  33. Moron, J.A.; Zakharova, I.; Ferrer, J.V.; Merrill, G.A.; Hope, B.; Lafer, E.M.; Lin, Z.C.; Wang, J.B.; Javitch, J.A.; Galli, A.; et al. Mitogen-activated protein kinase regulates dopamine transporter surface expression and dopamine transport capacity. J. Neurosci. 2003, 23, 8480–8488.
  34. Duval, E.R.; Javanbakht, A.; Liberzon, I. Neural circuits in anxiety and stress disorders: A focused review. Ther. Clin. Risk Manag. 2015, 11, 115–126.
  35. Tovote, P.; Fadok, J.P.; Luthi, A. Neuronal circuits for fear and anxiety. Nat. Rev. Neurosci. 2015, 16, 317–331.
  36. Kim, M.J.; Loucks, R.A.; Palmer, A.L.; Brown, A.C.; Solomon, K.M.; Marchante, A.N.; Whalen, P.J. The structural and functional connectivity of the amygdala: From normal emotion to pathological anxiety. Behav. Brain Res. 2011, 223, 403–410.
  37. Muscatell, K.A.; Dedovic, K.; Slavich, G.M.; Jarcho, M.R.; Breen, E.C.; Bower, J.E.; Irwin, M.R.; Eisenberger, N.I. Greater amygdala activity and dorsomedial prefrontal-amygdala coupling are associated with enhanced inflammatory responses to stress. Brain Behav. Immun. 2015, 43, 46–53.
  38. Dehdar, K.; Mahdidoust, S.; Salimi, M.; Gholami-Mahtaj, L.; Nazari, M.; Mohammadi, S.; Dehghan, S.; Jamaati, H.; Khosrowabadi, R.; Nasiraei-Moghaddam, A.; et al. Allergen-induced anxiety-like behavior is associated with disruption of medial prefrontal cortex—Amygdala circuit. Sci. Rep. 2019, 9, 19586.
  39. Gholami-Mahtaj, L.; Mooziri, M.; Dehdar, K.; Abdolsamadi, M.; Salimi, M.; Raoufy, M.R. ACC-BLA functional connectivity disruption in allergic inflammation is associated with anxiety. Sci. Rep. 2022, 12, 2731.
  40. Harrison, N.A.; Brydon, L.; Walker, C.; Gray, M.A.; Steptoe, A.; Critchley, H.D. Inflammation causes mood changes through alterations in subgenual cingulate activity and mesolimbic connectivity. Biol. Psychiatry 2009, 66, 407–414.
  41. Qin, X.; Pan, H.Q.; Huang, S.H.; Zou, J.X.; Zheng, Z.H.; Liu, X.X.; You, W.J.; Liu, Z.P.; Cao, J.L.; Zhang, W.H.; et al. GABAA(δ) receptor hypofunction in the amygdala-hippocampal circuit underlies stress-induced anxiety. Sci. Bull. 2022, 67, 97–110.
  42. Zhang, J.Y.; Liu, T.H.; He, Y.; Pan, H.Q.; Zhang, W.H.; Yin, X.P.; Tian, X.L.; Li, B.M.; Wang, X.D.; Holmes, A.; et al. Chronic stress remodels synapses in an amygdala circuit-specific manner. Biol. Psychiatry 2019, 85, 189–201.
  43. Zhang, W.H.; Liu, W.Z.; He, Y.; You, W.J.; Zhang, J.Y.; Xu, H.; Tian, X.L.; Li, B.M.; Mei, L.; Holmes, A.; et al. Chronic stress causes projection-specific adaptation of amygdala neurons via small-conductance calcium-activated potassium channel downregulation. Biol. Psychiatry 2019, 85, 812–828.
  44. Ma, H.; Li, C.; Wang, J.; Zhang, X.; Li, M.; Zhang, R.; Huang, Z.; Zhang, Y. Amygdala-hippocampal innervation modulates stress-induced depressive-like behaviors through AMPA receptors. Proc. Natl. Acad. Sci. USA 2021, 118, e2019409118.
  45. Bourhy, L.; Mazeraud, A.; Costa, L.H.A.; Levy, J.; Rei, D.; Hecquet, E.; Gabanyi, I.; Bozza, F.A.; Chretien, F.; Lledo, P.M.; et al. Silencing of amygdala circuits during sepsis prevents the development of anxiety-related behaviours. Brain 2022, 145, 1391–1409.
  46. Zhou, W.; Jin, Y.; Meng, Q.; Zhu, X.; Bai, T.; Tian, Y.; Mao, Y.; Wang, L.; Xie, W.; Zhong, H.; et al. A neural circuit for comorbid depressive symptoms in chronic pain. Nat Neurosci 2019, 22, 1649–1658.
  47. Yuan, T.; Orock, A.; Greenwood-Van Meerveld, B. Amygdala microglia modify neuronal plasticity via complement C1q/C3-CR3 signaling and contribute to visceral pain in a rat model. Am. J. Physiol. Gastrointest. Liver Physiol. 2021, 320, G1081–G1092.
  48. Zhang, X.; Lei, B.; Yuan, Y.; Zhang, L.; Hu, L.; Jin, S.; Kang, B.; Liao, X.; Sun, W.; Xu, F.; et al. Brain control of humoral immune responses amenable to behavioural modulation. Nature 2020, 581, 204–208.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Biology; Immunology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Ping Hu
,
Ying Lu
,
Bing-Xing Pan
,
Wen-Hua Zhang
View Times: 777
Revisions: 4 times (View History)
Update Date: 23 Feb 2023
Table of Contents
    1000/1000
    Hot Most Recent
    Video Production Service
    Feedback