One week later, ibotenic acid or sham lesions were made in the mPFC centered on the prelimbic region (Brodmann's area 32) or the cingulate cortex (Brodmann's area 24). Mean EB conditioning deficits in the group with area 32 lesions occurred on the first and second days of each retraining period. These findings were interpreted to indicate that area 32, but not area 24, is involved in retrieval processes, rather than consolidation or storage, in that the animals were impaired at both retesting times, but were able to relearn the task.. 
Evidence for a decrease in primary and secondary basilar dendrites on pyramidal cells in area 32 of schizophrenic prefrontal cortex. Area fraction analysis showed a significant decrease in immunostaining in area nine layers III (58%) and V (44%), area 32 layers III (51%) and V (32%). We found a significant reduction in the density of immunopositive pyramidal cells in area 9 (11%) layer III, (20%) layer V, area 32 (16%) layer III and (17%) layer V with no difference in immunopositive interneurons.
Area 9 of the dorsolateral prefrontal cortex is involved in inductive reasoning and specific components of working memory processes, while area 32 of the medial prefrontal cortex has been implicated in theory of mind.
In contrast, projections from area 32 originated predominantly in layers 5-6 among PV inhibitory neurons. Axons from area 10 targeted CB and PV inhibitory neurons, whereas axons from area 32 targeted PV inhibitory neurons. The preferential association of the 2 prefrontal pathways with distinct classes of inhibitory neurons at their origin and termination may reflect the specialization of area 10 in working memory functions and area 32 in emotional communication.
We first verified afferent connections to the mPFC (Brodmann's area 32) from the VLTN, by injecting the retrograde tracer Flourogold(c) into area 32.
Analyses focused on the first part of the trial indicated that both groups showed activity in middle frontal (Brodmann areas 46 and 9) and anterior cingulate (Brodmann area 32) gyri.
Further analyses of glia-neuron ratios across frontal areas 4, 9L, 32, and 44 in a sample of humans, chimpanzees, and macaque monkeys showed that regions involved in specialized human cognitive functions, such as "theory of mind" (area 32) and language (area 44) have not evolved differentially higher requirements for metabolic support.
In area 32 there was a more modest reduction in both layers III (36%) and V (40%).
The theta power in area 9 (the medial prefrontal cortex) and area 32 (the rostral ACC) was gradually increased from a few seconds before the movement and reached a peak immediately after the movement.
Thirst caused activation in the anterior cingulate (Brodmann area 32) and the insula.
Projections from the parahippocampal cortex also extend to areas 10m, 10o, Iai, and rostral area 32, as well as to dorsolateral areas 9 and 46.
Electrolytic lesions were made in the medial prefrontal cortex (mPFC) centered on the prelimbic area (Brodmann's area 32), at five different intervals after training.
The percentages that WGA-HRP retrogradely labelled neurons composed of the projection neurons in individual layers of infralimbic (IL; area 25) prelimbic (PL; area 32), and dorsal anterior cingulate (ACd; area 24b) cortices were calculated.
The total number of neurons and glial cells in brains of 12 schizophrenia subjects and 14 comparison subjects were determined in two subdivisions of the prefrontal cortex: Brodmann's area 24, a part of the anterior cingulate cortex, and Brodmann's area 32 in the paracingulate cortex. RESULTS: The average total of bilateral glial cells in Brodmann's area 24 was 201 x 10(6 )in subjects with schizophrenia and 302 x 10(6 )in comparison subjects, a statistically significant difference of 33%, whereas there was a nonsignificant difference between the schizophrenia subjects and the comparison subjects in total number of glial cells in Brodmann's area 32. CONCLUSIONS: A selective reduction in glial cells in Brodmann's area 24 (but not in area 32) is seen in brains of subjects with schizophrenia relative to those of comparison subjects.
The most robust and consistent activation was observed in the dorsal anterior cingulate cortex (Brodmann area 32; x = 0 y = 16, z = 40).
The areas studied were the prelimbic (PL, area 32) and infralimbic (IL, area 25) cortices and the dorsal anterior agranular insular (AId) and regions of posterior insular cortex (PI-comprising the agranular, dysgranular and granular fields).
The theta power in the prefrontal area 9 and the prelimbic area 32 was higher in the S1-S2 interval than in the pre-S1 period.
RESULTS: 5-HT(2A) receptor binding was significantly increased after estrogen replacement therapy in the right prefrontal cortex (right precentral gyrus [ Brodmann's area 9], inferior frontal gyrus [ Brodmann's area 47], medial frontal gyrus [ Brodmann's area 6, 10] and the anterior cingulate cortex [ Brodmann's area 32]).
The growth of the frontal pole in humans has pushed area 25 and area 32pl, which corresponds to the prelimbic area 32 in Brodmann's monkey brain map, caudal and ventral to the genu of the corpus callosum. area 32ac, corresponding to the dorsal anterior cingulate area 32 in Brodmann's human brain map, is anterior and dorsal to the genu.
RESULTS: Within Brodmann's area 32, a glucose metabolism deficit in the depressed subjects on placebo day was observed by voxel-level analysis, but no volumetric deficit was found in the subgenual regions examined.
In separate experiments, pseudorabies virus (PRV) was injected into one of the three different cytoarchitectonic regions that comprise the medial prefrontal cortex: infralimbic (Brodmann area 25), prelimbic (Brodmann area 32), and cingulate (Brodmann area 24) cortical areas.
We recently demonstrated a schizophrenia-associated decrease in microtubule-associated protein 2 (MAP2) immunostaining in laminae III and V of medial prefrontal area 32 and interpreted that finding as suggestive of a loss of dendritic material. We now present data from medial prefrontal area 32 of 11 schizophrenics and 11 comparison subjects.
Immunocytochemical and ultrastructural evidence is presented indicating that direct inputs from the hippocampal CA1 field to prelimbic (area 32) and infralimbic (area 25) cortices in the rat, innervate not only 'spiny' (presumed pyramidal) neurons but also monosynaptically contact NADPH-diaphorase reactive cells and parvalbumin-containing local circuit neurons-the latter cell type is shown to be GABA immunoreactive.
area 32 exhibited a 31% reduction in layer V and a 36% reduction in layer III.
mPFC lesions of prelimbic cortex (Brodmann's area 32) retarded EB conditioning in the trace but not the delay paradigm.
As for mPFC ablation, the lesioned area involved the agranular precentral region (Brodmann's area 8), the anterior cingulate cortex (Brodmann's area 24) and the prelimbic area (Brodmann's area 32).
Abuse memories were associated with alterations in blood flow in medial prefrontal cortex, with decreased blood flow in subcallosal gyrus (area 25), and a failure of activation in anterior cingulate (area 32).
Projections from medial temporal memory-related cortices subdivided medial cortices into different sectors, by targeting preferentially caudal medial areas (area 24, caudal 32 and 25), to a lesser extent rostral medial areas (rostral area 32, areas 14 and 10), and sparsely area 9. Projections from unimodal sensory cortices reached preferentially specific medial cortices, including a projection from visual cortices to area 32/24, from somatosensory cortices to area 9, and from olfactory cortices to area 14.
In temporal and prefrontal association cortex (Brodmann's areas 21 and 46) and in cingulofrontal transition cortex (area 32), specific GAT-1 immunoreactivity (ir) was localized to numerous puncta and fibers in all cortical layers.
The latter comparisons and correlation analysis indicated a wide range of active regions including bilateral prefrontal, inferior parietal and premotor cortices and thalamic responses, contralateral hippocampus, insula and primary somatosensory cortex and ipsilateral perigenual cingulate cortex (area 24) and medial frontal cortex (area 32).
The results indicated that ventral precallosal and subcallosal areas 14 and 25, and the ventral, subcallosal part of area 32, all receive projections from the mediodorsal portion of the magnocellular division of the medial dorsal nucleus (MDmc). The dorsal, precallosal part of area 32 receives projections mainly from the dorsal portion of the parvocellular division of the medial dorsal nucleus (MDpc), which also provides some input to area 14.
As in the earlier study, the dorsal prefrontal cortex and anterior cingulate area 32 were activated during new learning, but not during automatic performance.
In this immunocytochemical study of rat prelimbic cortex (area 32), a gradient of CN immunolabelling was found in the somata and processes of pyramidal cells and in interneurones.
Electron microscopical examination of 120 labelled boutons in area 32 (60 in layer 2 and 60 in layer 5) indicated that 116 (97%) established asymmetrical synaptic contacts with dendritic spines and 4 (3%) were in synaptic contact with small dendritic shafts.
Using the affected arm, AHD cases showed significant overactivity of contralateral prefrontal, lateral premotor cortex, rostral supplementary motor area, anterior cingulate area 32, bilateral sensorimotor cortex (SMC) and insula, mesial parietal cortex, and ipsilateral cerebellum.
Patients with idiopathic torsion dystonia showed significant overactivity in the contralateral lateral premotor cortex, rostral supplementary motor area, Brodmann area 8, anterior cingulate area 32, ipsilateral dorsolateral prefrontal cortex, and bilateral lentiform nucleus.
Data from both brain lesion and brain stimulation experiments suggest that area 32 of the medial prefrontal cortex (prelimbic area) participates in the acquisition and/or expression of conditioned bradycardia. Thus, multiple- and single-unit activity was recorded from area 32 in rabbits during Pavlovian heart rate (HR) conditioning. In the first experiment, neuronal discharge recorded from chronically implanted multiple-unit electrodes in the superficial and deep layers of area 32 increased systematically in response to the presentation of tone conditioned stimuli (CS) paired with paraorbital electric shock as the unconditioned stimulus (US). These findings suggest that the CS-evoked increase in neuronal activity in area 32 was associatively produced. A second experiment examined the CS-evoked response of single units (n = 98) in area 32 during differential Pavlovian conditioning, in which one tone (CS+) was consistently followed by the paraorbital shock US and a second tone (CS-) was not. However, a major difference between the present findings and those of our previous studies of areas 8 and 24 is that in several instances changes in CS-evoked activity in area 32 were significantly greater in response to the CS- than to the CS+, suggesting that some cells in the prelimbic region may code the absence of aversive stimulation, that is, a period of relative "safety.".
Electrical stimulation of area 24 and area 32 of the medial prefrontal cortex (mPFC) in rabbits elicited increases in respiration rate and decreases in heart rate (HR) and blood pressure. Administration of an alpha-adrenergic receptor antagonist eliminated the pressor response and bradycardiac response produced by area 25 stimulation but it had no effect on the bradycardia elicited by stimulation of area 24 or area 32. Lesions centered on area 32 of the mPFC greatly attenuated the conditioned bradycardiac response elicited by paired tone and paraorbital shock presentations.
However, only areas 24 and the more dorsal portions of area 32 projected to the superior colliculus. Area 25 and the ventral portions of area 32 also showed a bilateral projection to the parabrachial nuclei and dorsal and ventral medulla. The dorsal portions of area 32, and all of area 24 were, however, devoid of these projections.
When a comparison of the rCBF response to the free selection task with that to the stereotyped task was performed between the two groups of subjects, ALS patients showed significantly impaired (P < 0.01) activation of the rostral anterior cingulate cortex (area 32), medial prefrontal cortex (area 10), left parahippocampal gyrus and retrosplenial cortex.
In primary motor (area 4) and temporal (area 21) cortex, binding in the outer half of the cortical ribbon was denser than that in the inner half and a distinct band was apparent in temporal and cingulate (area 32) in the lower portion of layer III.
The mediodorsal regions included portions of medial area 32 and the caudal part of dorsal area 8. The cells of origin were located in rostromedial visual cortices after injection of retrograde tracers in area 32 and in more caudal medial and dorsolateral visual areas after injection in caudal area 8. Orbital area 12 seemed to be a major target of projections from somatosensory cortices and the rostral portion of medial area 32 received substantial projections from auditory cortices. The least architectonically differentiated areas (orbital area 11 and medial area 32) had more widespread corticocortical connections, including strong links with limbic cortices.(ABSTRACT TRUNCATED AT 400 WORDS).
In control rats, HRP-positive neurons were distributed in layer Vb throughout motor area 4, rostral motor area 6/8, dorsal somatosensory area 3, caudal somatosensory area 2, and various "association" regions including parietal areas 14, 39, and 40, occipital areas 18a and 18b, cingulate areas 24a and 24b, and prefrontal area 32.
Intracranial self-stimulation (ICSS) was obtained from 3 areas of anteromedial cortex: the prelimbic area (Brodman's area 32), the anterior cingulate area and the posterior cingulate area.
The deep supragenual dopaminergic field was already present at birth like the dopaminergic innervation of the prefrontal cortex area 32. The innervation of the superficial and deep layers of the rat anterior cingulate cortex by two distinct dopaminergic subpopulations, one of them closely related to that of prefrontal cortex area 32, could be compared with other laminar differences.
The results indicate that the rostralmost part of the cingulate gyrus (area 32) sends projections to the lateral prefrontal and midorbitofrontal cortex and to the rostral portion of the superior temporal gyrus.
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