Parvalbumin, but not calretinin, neurons express high levels of α1-containing GABAA receptors, α7-containing nicotinic acetylcholine receptors and D2-dopamine receptors in the basolateral amygdala of the rat

Równiak, Maciej; Kolenkiewicz, Małgorzata; Kozłowska, Anna

doi:10.1016/j.jchemneu.2017.08.002

Cited by 15 publications

(18 citation statements)

References 105 publications

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“…As was observed in previous studies in the rodent amygdala 15 , 49 , 71 , 72 in both mouse lines, DA 1 + and DA 2 + signal was mainly observed in soma and immunoreactive puncta, although some clearly depicted fibers were also present (Fig. 4 ).…”

Section: Resultssupporting

confidence: 84%

“…Finally, in rodents, reduced oestrogen signalling due to oestrogen receptor β (ERβ) knock-out increases anxiety in females (but not in males) 6 , 7 , while ERβ agonists usually induce severe anxiolytic actions 8 . It is generally known that one of the most important structure responsible for overall regulation of emotional behaviour, especially in the processing of fear and anxiety is the amygdala 9 , 10 and oestrogens reduce neuronal excitability in this brain structure 11 – 13 through their receptors 14 , 15 , thereby reduced oestrogen signalling as a result of ERβ knock-out is anxiogenic. It was noted that the function of this brain structure is always impaired in anxiety disorders 16 .…”

Section: Introductionmentioning

confidence: 99%

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Dopaminergic and cholinergic modulation of the amygdala is altered in female mice with oestrogen receptor β deprivation

Kalinowski

Bogus‐Nowakowska

Kozłowska

et al. 2023

Sci Rep

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The amygdala is modulated by dopaminergic and cholinergic neurotransmission, and this modulation is altered in mood disorders. Therefore, this study was designed to evaluate the presence/absence of quantitative alterations in the expression of main dopaminergic and cholinergic markers in the amygdala of mice with oestrogen receptor β (ERβ) knock-out which exhibit increased anxiety, using immunohistochemistry and quantitative methods. Such alterations could either contribute to increased anxiety or be a compensatory mechanism for reducing anxiety. The results show that among dopaminergic markers, the expression of tyrosine hydroxylase (TH), dopamine transporter (DAT) and dopamine D2-like receptor (DA2) is significantly elevated in the amygdala of mice with ERβ deprivation when compared to matched controls, whereas the content of dopamine D1-like receptor (DA1) is not altered by ERβ knock-out. In the case of cholinergic markers, muscarinic acetylcholine type 1 receptor (AChRM1) and alpha-7 nicotinic acetylcholine receptor (AChRα7) display overexpression while the content of acetylcholinesterase (AChE) and vesicular acetylcholine transporter (VAChT) remains unchanged. In conclusion, in the amygdala of ERβ knock-out female the dopaminergic and cholinergic signalling is altered, however, to determine the exact role of ERβ in the anxiety-related behaviour further studies are required.

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Section: Resultssupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

Dopaminergic and cholinergic modulation of the amygdala is altered in female mice with oestrogen receptor β deprivation

Kalinowski

Bogus‐Nowakowska

Kozłowska

et al. 2023

Sci Rep

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“…In addition, this inhibition is significantly decreased when dopamine is released during heightened emotional states ( Mcdonald et al, 1996 ; Dallman et al, 2003 ; Pinto and Sesack, 2008 ). The modulation of emotional responses by the BLA is mainly determined by the balance of excitatory and inhibitory inputs to its dominated neurons which are tightly controlled by GABAergic interneurons ( Równiak et al, 2017 ). As mentioned above, the GABAergic neurons of the amygdala modulate activation of the CeA via projections from the BLA ( Nuss, 2015 ).…”

Section: Gabaergic Control Of the Amygdalamentioning

confidence: 99%

Stress in Regulation of GABA Amygdala System and Relevance to Neuropsychiatric Diseases

et al. 2018

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The amygdala is an almond-shaped nucleus located deep and medially within the temporal lobe and is thought to play a crucial role in the regulation of emotional processes. GABAergic neurotransmission inhibits the amygdala and prevents us from generating inappropriate emotional and behavioral responses. Stress may cause the reduction of the GABAergic interneuronal network and the development of neuropsychological diseases. In this review, we summarize the recent evidence investigating the possible mechanisms underlying GABAergic control of the amygdala and its interaction with acute and chronic stress. Taken together, this study may contribute to future progress in finding new approaches to reverse the attenuation of GABAergic neurotransmission induced by stress in the amygdala.

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“…The primary antibodies used in the study were carefully chosen. The specificity of the primary antisera used in this study was shown by various researchers using these products in previous immunohistochemical studies [ 27 , 56 , 57 , 58 , 59 , 60 ]. The rabbit antibody against neuron-specific nuclear protein NeuN (ABN78) was positively validated by the manufacturer using Western blotting in mouse brain extracts, showing bands ~48/42 kDa.…”

Section: Methodsmentioning

confidence: 89%

Expression of Calbindin, a Marker of Gamma-Aminobutyric Acid Neurons, Is Reduced in the Amygdala of Oestrogen Receptor β-Deficient Female Mice

Kalinowski

Bogus‐Nowakowska

Kozłowska

et al. 2022

JCM

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Oestrogen receptor β (ERβ) knock-out female mice display increased anxiety and decreased threshold for synaptic plasticity induction in the basolateral amygdala. This may suggest that the γ-aminobutyric acid (GABA) inhibitory system is altered. Therefore, the immunoreactivity of main GABAergic markers—i.e., calbindin, parvalbumin, calretinin, somatostatin, α1 subunit-containing GABAA receptor and vesicular GABA transporter—were compared in the six subregions (LA, BL, BM, ME, CE and CO) of the amygdala of adult female wild-type and ERβ knock-out mice using immunohistochemistry and quantitative methods. The influence of ERβ knock-out on neuronal loss and glia was also elucidated using pan-neuronal and astrocyte markers. The results show severe neuronal deficits in all main amygdala regions in ERβ knock-out mice accompanied by astroglia overexpression only in the medial, basomedial and cortical nuclei and a decrease in calbindin-expressing neurons (CB+) in the amygdala in ERβ knock-out mice compared with controls, while other markers of the GABAergic system remain unchanged. Concluding, the lack of ERβ led to failure in the structural integrity of the CB+ subpopulation, reducing interneuron firing and resulting in a disinhibitory effect over pyramidal function. This fear-promoting excitatory/inhibitory alteration may lead to the increased anxiety observed in these mice. The impact of neuronal deficits and astroglia overexpression on the amygdala functions remains unknown.

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Parvalbumin, but not calretinin, neurons express high levels of α1-containing GABAA receptors, α7-containing nicotinic acetylcholine receptors and D2-dopamine receptors in the basolateral amygdala of the rat

Cited by 15 publications

References 105 publications

Dopaminergic and cholinergic modulation of the amygdala is altered in female mice with oestrogen receptor β deprivation

Dopaminergic and cholinergic modulation of the amygdala is altered in female mice with oestrogen receptor β deprivation

Stress in Regulation of GABA Amygdala System and Relevance to Neuropsychiatric Diseases

Expression of Calbindin, a Marker of Gamma-Aminobutyric Acid Neurons, Is Reduced in the Amygdala of Oestrogen Receptor β-Deficient Female Mice

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