scholarly journals Expression of α1-adrenergic receptors in rat prefrontal cortex: cellular co-localization with 5-HT2A receptors

2013 ◽  
Vol 16 (5) ◽  
pp. 1139-1151 ◽  
Author(s):  
Noemí Santana ◽  
Guadalupe Mengod ◽  
Francesc Artigas
Keyword(s):  
Prefrontal Cortex ◽  
Adrenergic Receptors ◽  
Antipsychotic Drugs ◽  
Pyramidal Neurons ◽  
Anterior Cingulate ◽  
Lower Percentage ◽  
Neuronal Populations ◽  
Cellular Expression ◽  
Behavioural Interactions

Abstract The prefrontal cortex (PFC) is involved in behavioural control and cognitive processes that are altered in schizophrenia. The brainstem monoaminergic systems control PFC function, yet the cells/networks involved are not fully known. Serotonin (5-HT) and norepinephrine (NE) increase PFC neuronal activity through the activation of α1-adrenergic receptors (α1ARs) and 5-HT2A receptors (5-HT2ARs), respectively. Neurochemical and behavioural interactions between these receptors have been reported. Further, classical and atypical antipsychotic drugs share nmin vitro affinity for α1ARs while having preferential affinity for D2 and 5-HT2ARs, respectively. Using double in situ hybridization we examined the cellular expression of α1ARs in pyramidal (vGluT1-positive) and GABAergic (GAD65/67-positive) neurons in rat PFC and their co-localization with 5-HT2ARs. α1ARs are expressed by a high proportion of pyramidal (59–85%) and GABAergic (52–79%) neurons. The expression in pyramidal neurons exhibited a dorsoventral gradient, with a lower percentage of α1AR-positive neurons in infralimbic cortex compared to anterior cingulate and prelimbic cortex. The expression of α1A, α1B and α1D adrenergic receptors was segregated in different layers and subdivisions. In all them there is a high co-expression with 5-HT2ARs (∼80%). These observations indicate that NE controls the activity of most PFC pyramidal neurons via α1ARs, either directly or indirectly, via GABAergic interneurons. Antipsychotic drugs can thus modulate the activity of PFC via α1AR blockade. The high co-expression with 5-HT2ARs indicates a convergence of excitatory serotonergic and noradrenergic inputs onto the same neuronal populations. Moreover, atypical antipsychotics may exert a more powerful control of PFC function through the simultaneous blockade of α1ARs and 5-HT2ARs.

scholarly journals Muscarinic Acetylcholine Receptor Localization on Distinct Excitatory and Inhibitory Neurons Within the ACC and LPFC of the Rhesus Monkey

2022 ◽  
Vol 15 ◽  
Author(s):  
Alexandra Tsolias ◽  
Maria Medalla
Keyword(s):  
Prefrontal Cortex ◽  
Muscarinic Receptors ◽  
Calcium Binding ◽  
Pyramidal Neurons ◽  
Muscarinic Acetylcholine Receptor ◽  
Anterior Cingulate ◽  
Inhibitory Neurons ◽  
Receptor Localization ◽  
Cortical Inputs ◽  
Almost All

Acetylcholine (ACh) can act on pre- and post-synaptic muscarinic receptors (mAChR) in the cortex to influence a myriad of cognitive processes. Two functionally-distinct regions of the prefrontal cortex—the lateral prefrontal cortex (LPFC) and the anterior cingulate cortex (ACC)—are differentially innervated by ascending cholinergic pathways yet, the nature and organization of prefrontal-cholinergic circuitry in primates are not well understood. Using multi-channel immunohistochemical labeling and high-resolution microscopy, we found regional and laminar differences in the subcellular localization and the densities of excitatory and inhibitory subpopulations expressing m1 and m2 muscarinic receptors, the two predominant cortical mAChR subtypes, in the supragranular layers of LPFC and ACC in rhesus monkeys (Macaca mulatta). The subset of m1+/m2+ expressing SMI-32+ pyramidal neurons labeled in layer 3 (L3) was denser in LPFC than in ACC, while m1+/m2+ SMI-32+ neurons co-expressing the calcium-binding protein, calbindin (CB) was greater in ACC. Further, we found between-area differences in laminar m1+ dendritic expression, and m2+ presynaptic localization on cortico-cortical (VGLUT1+) and sub-cortical inputs (VGLUT2+), suggesting differential cholinergic modulation of top-down vs. bottom-up inputs in the two areas. While almost all inhibitory interneurons—identified by their expression of parvalbumin (PV+), CB+, and calretinin (CR+)—expressed m1+, the localization of m2+ differed by subtype and area. The ACC exhibited a greater proportion of m2+ inhibitory neurons compared to the LPFC and had a greater density of presynaptic m2+ localized on inhibitory (VGAT+) inputs targeting proximal somatodendritic compartments and axon initial segments of L3 pyramidal neurons. These data suggest a greater capacity for m2+-mediated cholinergic suppression of inhibition in the ACC compared to the LPFC. The anatomical localization of muscarinic receptors on ACC and LPFC micro-circuits shown here contributes to our understanding of diverse cholinergic neuromodulation of functionally-distinct prefrontal areas involved in goal-directed behavior, and how these interactions maybe disrupted in neuropsychiatric and neurological conditions.

scholarly journals Morphology of Pyramidal Neurons in the Rat Prefrontal Cortex: Lateralized Dendritic Remodeling by Chronic Stress

2007 ◽  
Vol 2007 ◽  
pp. 1-14 ◽  
Author(s):  
Claudia Perez-Cruz ◽  
Jeanine I. H. Müller-Keuker ◽  
Urs Heilbronner ◽  
Eberhard Fuchs ◽  
Gabriele Flügge
Keyword(s):  
Prefrontal Cortex ◽  
Pyramidal Neurons ◽  
Right Hemisphere ◽  
Anterior Cingulate ◽  
Chronic Restraint Stress ◽  
Hemispheric Difference ◽  
Infralimbic Cortex ◽  
Dendritic Length ◽  
The Right ◽  
Apical Dendrites

The prefrontal cortex (PFC) plays an important role in the stress response. We filled pyramidal neurons in PFC layer III with neurobiotin and analyzed dendrites in rats submitted to chronic restraint stress and in controls. In the right prelimbic cortex (PL) of controls, apical and distal dendrites were longer than in the left PL. Stress reduced the total length of apical dendrites in right PL and abolished the hemispheric difference. In right infralimbic cortex (IL) of controls, proximal apical dendrites were longer than in left IL, and stress eliminated this hemispheric difference. No hemispheric difference was detected in anterior cingulate cortex (ACx) of controls, but stress reduced apical dendritic length in left ACx. These data demonstrate interhemispheric differences in the morphology of pyramidal neurons in PL and IL of control rats and selective effects of stress on the right hemisphere. In contrast, stress reduced dendritic length in the left ACx.

scholarly journals Synaptophysin gene expression in schizophrenia

2000 ◽  
Vol 176 (3) ◽  
pp. 236-242 ◽  
Author(s):  
Sharon L. Eastwood ◽  
Nigel J. Cairns ◽  
Paul J. Harrison
Keyword(s):  
Gene Expression ◽  
Cerebral Cortex ◽  
Prefrontal Cortex ◽  
Messenger Rna ◽  
Regional Distribution ◽  
Anterior Cingulate ◽  
Cortical Areas ◽  
Dorsolateral Prefrontal ◽  
Synaptic Pathology

BackgroundDecreased expression of proteins such as synaptophysin in the hippocampus and prefrontal cortex in schizophrenia is suggestive of synaptic pathology. However, the overall profile of changes is unclear.AimsTo investigate synaptophysin gene expression in the cerebral cortex in schizophrenia.MethodThe dorsolateral prefrontal (Brodmann area [BA] 9/46), anterior cingulate (BA 24), superior temporal (BA 22) and occipital (BA 17) cortex were studied in two series of brains, totalling 19 cases and 19 controls. Synaptophysin was measured by immunoautoradiography and immunoblotting. Synaptophysin messenger RNA (m RNA) was measured using in situ hybridisation.ResultsSynaptophysin was unchanged in schizophrenia, except for a reduction in BA 17 of one brain series. Synaptophysin mRNA was decreased in BA 17, and in BA 22 in the women with schizophrenia. No alterations were seen in BA 9/46.ConclusionsSynaptophysin expression is decreased in some cortical areas in schizophrenia. The alterations affect the mRNA more than the protein, and have an unexpected regional distribution. The characteristics of the implied synaptic pathology remain to be determined.

scholarly journals Reduced ribosomal DNA transcription in the prefrontal cortex of suicide victims: consistence of new molecular RT-qPCR findings with previous morphometric data from AgNOR-stained pyramidal neurons

2021 ◽  
Author(s):  
Marta Krzyżanowska ◽  
Krzysztof Rębała ◽  
Johann Steiner ◽  
Michał Kaliszan ◽  
Dorota Pieśniak ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Ribosomal Dna ◽  
Pyramidal Neurons ◽  
Quantitative Polymerase Chain Reaction ◽  
Anterior Cingulate ◽  
Rdna Transcription ◽  
Relative Level ◽  
Prefrontal Cortical ◽  
Dorsolateral Cortex ◽  
Cortical Regions

AbstractPrefrontal cortical regions play a key role in behavioural regulation, which is profoundly disturbed in suicide. The study was carried out on frozen cortical samples from the anterior cingulate cortex (dorsal and ventral parts, ACd and ACv), the orbitofrontal cortex (OFC), and the dorsolateral cortex (DLC) obtained from 20 suicide completers (predominantly violent) with unknown psychiatric diagnosis and 21 non-suicidal controls. The relative level of ribosomal RNA (rRNA) as a marker of the transcriptional activity of ribosomal DNA (rDNA) was evaluated bilaterally in prefrontal regions mentioned above (i.e. in eight regions of interest, ROIs) by reverse transcription and quantitative polymerase chain reaction (RT-qPCR). The overall statistical analysis revealed a decrease in rDNA activity in suicide victims versus controls, particularly in male subjects. Further ROI-specific post hoc analyses revealed a significant decrease in this activity in suicides compared to non-suicides in five ROIs. This effect was accentuated in the ACv, where it was observed bilaterally. Our findings suggest that decreased rDNA transcription in the prefrontal cortex plays an important role in suicide pathogenesis and corresponds with our previous morphometric analyses of AgNOR-stained neurons.

scholarly journals α2-Adrenergic Receptors Modify Dendritic Spike Generation Via HCN Channels in the Prefrontal Cortex

2008 ◽  
Vol 99 (1) ◽  
pp. 394-401 ◽  
Author(s):  
Albert M. I. Barth ◽  
E. Sylvester Vizi ◽  
Tibor Zelles ◽  
Balazs Lendvai
Keyword(s):  
Prefrontal Cortex ◽  
Adrenergic Receptors ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Hcn Channels ◽  
Transient Activation ◽  
Dendritic Spikes ◽  
Dendritic Spike ◽  
Frequency Threshold

Although dendritic spikes are generally thought to be restricted to the distal apical dendrite, we know very little about the possible modulatory mechanisms that set the spatial limits of dendritic spikes. Our experiments demonstrated that high-frequency trains of backpropagating action potentials avoided filtering in the apical dendrite and initiated all-or-none dendritic Ca2+ transients associated with dendritic spikes in layer 5 pyramidal neurons of the prefrontal cortex. The block of hyperpolarization-activated currents ( Ih) by ZD7288 could shift the frequency threshold and decreased the number of action potentials required to produce the all-or-none Ca2+ transient. Activation of α2-adrenergic receptors could also shift the frequency domain of spike induction to lower frequencies. Our data suggest that noradrenergic activity in the prefrontal cortex influences dendritic Ih and extends the zone of dendritic spikes in the apical dendrite via α2-adrenergic receptors. This mechanism might be one cellular correlate of the α2-receptor–mediated actions on working memory.

scholarly journals The behavioral variant of Alzheimer's disease does not show a selective loss of Von Economo and phylogenetically related neurons in the anterior cingulate cortex

2021 ◽  
Author(s):  
Ellen Singleton ◽  
Yolande A.L. Pijnenburg ◽  
Priya Gami-Patel ◽  
Baayla D.C. Boon ◽  
Femke Bouwman ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Anterior Cingulate Cortex ◽  
Pyramidal Neurons ◽  
Neuronal Loss ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Von Economo Neurons ◽  
Neuronal Populations ◽  
Selective Loss

Background: The neurobiological origins of the early and predominant behavioral changes seen in the behavioral variant of Alzheimer's disease (bvAD) remain unclear. A selective loss of Von Economo Neurons (VENs) and phylogenetically related neurons have been observed in behavioral variant frontotemporal dementia (bvFTD) and several psychiatric diseases. Here, we assessed whether these specific neuronal populations show a selective loss in bvAD. Methods: VENs and GABA receptor subunit theta (GABRQ)-immunoreactive pyramidal neurons of the anterior cingulate cortex (ACC) were quantified in post-mortem tissue of patients with bvAD (n=9) and compared to typical AD (tAD, n=6), bvFTD due to frontotemporal lobar degeneration based on TDP-43 pathology (FTLD, n=18) and controls (n=13) using ANCOVAs adjusted for age and Bonferroni corrected. In addition, ratios of VENs and GABRQ-immunoreactive (GABRQ-ir) pyramidal neurons over all Layer 5 neurons were compared between groups to correct for overall Layer 5 neuronal loss. Results: The number of VENs or GABRQ-ir neurons did not differ significantly between bvAD (VENs: 26.0±15.3, GABRQ-ir pyramidal: 260.44±87.13) and tAD (VENs: 32.0±18.1, p=1.00, GABRQ-ir pyramidal: 349.83±109.64, p=0.38) and controls (VENs: 33.5±20.3, p=1.00, GABRQ-ir pyramidal: 339.38±95.88, p=0.37). Compared to bvFTD, patients with bvAD showed significantly more GABRQ-ir pyramidal neurons (bvFTD: 140.39±82.58, p=0.01) and no significant differences in number of VENs (bvFTD: 10.9±13.8, p=0.13). Results were similar when assessing the number of VENs and GABRQ-ir relative to all neurons of Layer 5. Discussion: VENs and phylogenetically related neurons did not show a selective loss in the ACC in patients with bvAD. Our results suggest that, unlike in bvFTD, the clinical presentation in bvAD may not be related to the loss of VENs and related neurons in the ACC.

Age differences in ventromedial prefrontal cortex functional connectivity during socioemotional content processing

2020 ◽  
Vol 48 (7) ◽  
pp. 1-19
Author(s):  
Ryan T. Daley ◽  
Holly J. Bowen ◽  
Eric C. Fields ◽  
Angela Gutchess ◽  
Elizabeth A. Kensinger
Keyword(s):  
Prefrontal Cortex ◽  
Functional Connectivity ◽  
Inferior Frontal Gyrus ◽  
Age Groups ◽  
Emotional Content ◽  
Ventromedial Prefrontal Cortex ◽  
Anterior Cingulate ◽  
Supramarginal Gyrus ◽  
Age Related ◽  
Content Processing

Self-relevance effects are often confounded by the presence of emotional content, rendering it difficult to determine how brain networks functionally connected to the ventromedial prefrontal cortex (vmPFC) are affected by the independent contributions of self-relevance and emotion. This difficulty is complicated by age-related changes in functional connectivity between the vmPFC and other default mode network regions, and regions typically associated with externally oriented networks. We asked groups of younger and older adults to imagine placing emotional and neutral objects in their home or a stranger's home. An age-invariant vmPFC cluster showed increased activation for self-relevant and emotional content processing. Functional connectivity analyses revealed age × self-relevance interactions in vmPFC connectivity with the anterior cingulate cortex. There were also age × emotion interactions in vmPFC functional connectivity with the anterior insula, orbitofrontal gyrus, inferior frontal gyrus, and supramarginal gyrus. Interactions occurred in regions with the greatest differences between the age groups, as revealed by conjunction analyses. Implications of the findings are discussed.

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