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Vogt B.A.,Cingulum NeuroSciences Institute | Vogt B.A.,Boston University | Vogt B.A.,Julich Research Center
Neurogastroenterology and Motility | Year: 2013

The article by Agostini et al. (2013) in this issue of Neurogastroenterology and Motility evaluated patients with Crohn's disease (CD) for volumetric changes throughout the brain. They observed decreased gray matter volumes in dorsolateral prefrontal cortex and anterior midcingulate cortex (aMCC) and disease duration was negatively correlated with volumes in subgenual anterior cingulate (sACC), posterior MCC (pMCC), ventral posterior cingulate (vPCC), and parahippocampal cortices. As all patients were in remission and suffered from ongoing abdominal pain, this study provides a critical link between forebrain changes and abdominal pain experience independent of active disease and drug treatment. The aMCC has a role in feedback-mediated decision making and there are specific cognitive tasks that differentiate aMCC and pMCC that can be used to evaluate defects in CD. The sACC is an important area as it has impaired functions in major depression. As depressive symptoms are a feature in a subset of patients with active inflammatory diseases including IBD, treatment targeting this subregion should prove efficacious. Finally, vPCC has a role in ongoing self-monitoring of the personal relevance of sensory stimuli including visceral signals via sACC. This pathway may be interrupted by vPCC atrophy in CD. Cingulate atrophy in CD leads to targeting chronic pain and psychiatric symptoms via cingulate-mediated therapies. These include psychotherapy, guided imagery and relaxation training, analgesic dosages of morphine or antidepressants, and hypnosis. Thus, a new generation of novel treatments may emerge from drug and non-traditional therapies for CD in this formative area of research. © 2013 Blackwell Publishing Ltd.

Vogt B.A.,Cingulum NeuroSciences Institute | Vogt B.A.,Boston University
Brain Structure and Function | Year: 2015

The rabbit cingulate cortex is highly differentiated in contrast to rodents and numerous recent advances suggest the rabbit area map needs revision. Immunohistochemistry was used to assess cytoarchitecture with neuron-specific nuclear binding protein (NeuN) and neurocytology with intermediate neurofilament proteins, parvalbumin and glutamic acid decarboxylase. Key findings include: (1) Anterior cingulate cortex (ACC) area 32 has dorsal and ventral divisions. (2) Area 33 is part of ACC. (3) Midcingulate cortex (MCC) has anterior and posterior divisions and this was verified with extensive quantitative analysis and a horizontal series of sections. (4) NeuN, also known as Fox-3, is not limited to somata and formed nodules, granular clusters and striations in the apical dendrites of pyramidal neurons. (5) Area 30 forms a complex of anterior and posterior parts with further medial and lateral divisions. (6) Area 29b has two divisions and occupies substantially more volume than in rat. (7) Area 29a begins with a subsplenial component and extends relatively further caudal than in rat. As similar areal designations are often used among species, direct comparisons were made of rabbit areas with those in rat and monkey. The dichotomy of MCC is of particular interest to studies of pain as anterior MCC is most frequently activated in human acute pain studies and the rabbit can be used to study this subregion. Finally, the area 30 complex is not primarily dysgranular as in rat and is more differentiated than in any other mammal including human. The large and highly differentiated rabbit cingulate cortex provides a unique model for assessing cingulate cortex, pain processing and RNA splicing functions. © 2015 Springer-Verlag Berlin Heidelberg

Vogt B.A.,Cingulum NeuroSciences Institute | Vogt B.A.,Boston University | Paxinos G.,University of New South Wales
Brain Structure and Function | Year: 2014

A gulf exists between cingulate area designations in human neurocytology and those used in rodent brain atlases with a major underpinning of the former being midcingulate cortex (MCC). The present study used images extracted from the Franklin and Paxinos mouse atlas and Paxinos and Watson rat atlas to demonstrate areas comprising MCC and modifications of anterior cingulate (ACC) and retrosplenial cortices. The laminar architecture not available in the atlases is also provided for each cingulate area. Both mouse and rat have a MCC with neurons in all layers that are larger than in ACC and layer Va has particularly prominent neurons and reduced neuron densities. An undifferentiated ACC area 33 lies along the rostral callosal sulcus in rat but not in mouse and area 32 has dorsal and ventral subdivisions with the former having particularly large pyramidal neurons in layer Vb. Both mouse and rat have anterior and posterior divisions of retrosplenial areas 29c and 30, although their cytology is different in rat and mouse. Maps of the rodent cingulate cortices provide for direct comparisons with each region in the human including MCC and it is significant that rodents do not have a posterior cingulate region composed of areas 23 and 31 like the human. It is concluded that rodents and primates, including humans, possess a MCC and this homology along with those in ACC and retrosplenial cortices permit scientists inspired by human considerations to test hypotheses on rodent models of human diseases. © 2012 Springer-Verlag Berlin Heidelberg.

Shyu B.-C.,Academia Sinica, Taiwan | Sikes R.W.,Northeastern University | Vogt L.J.,Cingulum NeuroSciences Institute | Vogt L.J.,New York University | And 2 more authors.
Journal of Neurophysiology | Year: 2010

Although the cingulate cortex is frequently activated in acute human pain studies, postsynaptic responses are not known nor are links between nociceptive afferents, neuronal responses, and outputs to other structures. Intracellular potentials were recorded from neurobiotin-injected, pyramidal neurons in anterior cingulate area 24b following noxious stimulation of the sciatic nerve in anesthetized rabbits. Layer IIIc pyramids had extensive and horizontally oriented basal dendrites in layer IIIc where nociceptive afferents terminate. They had the longest excitatory postsynaptic potentials (EPSPs; 545 ms) that were modulated with hyperpolarizing currents. Pyramids in layer V had an intermediate tuft of oblique apical dendrites in layer IIIc that were 150-350 μm from somata in layer Va and 351-550 μm in layer Vb. Although average EPSP durations were short in layers II-IIIab (222 ± 31), Va (267 ± 65), and Vb (159 ± 31), there were five neurons in layers IIIab-Va that had EPSP durations lasting >300 ms (548 ± 63 ms). Neurons in layers IIIc, Va, and Vb had the highest amplitude EPSPs (6.25, 6.84 ± 0.58, and 6.4 ± 0.47 mV, respectively), whereas those in layers II-IIIab were 5 ± 0.56 mV. Nociceptive responses in layer Vb were complex and some had initial inhibitory postsynaptic potentials with shorter-duration EPSPs. Layers II-IIIab had dye-coupled pyramids and EPSPs in these layers had short durations (167 ± 33 ms) compared with those in layers IIIc-Va (487 ± 28 ms). In conclusion there are two populations of anterior cingulate cortex pyramids with EPSPs of significantly different durations, although their dendritic morphologies do not predict EPSP duration. Short-duration EPSPs are thalamic-mediated, nociceptive responses lasting ≤200 ms. Longer, "integrative" EPSPs are >350 ms and are likely modulated by intracortical axon collateral discharges. These findings suggest that links between nociception and projections to cortical and motor systems are instantaneous because nociceptive responses are generated directly by pyramidal projection neurons in all layers. Copyright © 2010 The American Physiological Society.

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