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MEI-1/katanin is required for translocation of the meiosis I spindle to the oocyte cortex in C elegans.

In most animals, successful segregation of female meiotic chromosomes involves sequential associations of the meiosis I and meiosis II spindles with the cell cortex so that extra chromosomes can be deposited in polar bodies. The resulting reduction in chromosome number is essential to prevent the generation of polyploid embryos after fertilization. Using time-lapse imaging of living Caenorhabditis elegans oocytes containing fluorescently labeled chromosomes or microtubules, we have characterized the movements of meiotic spindles relative to the cell cortex. Spindle assembly initiated several microns from the cortex. After formation of a bipolar structure, the meiosis I spindle translocated to the cortex. When microtubules were partially depleted, translocation of the bivalent chromosomes to the cortex was blocked without affecting cell cycle timing. In oocytes depleted of the microtubule-severing enzyme, MEI-1, spindles moved to the cortex, but association with the cortex was unstable. Unlike translocation of wild-type spindles, movement of MEI-1-depleted spindles was dependent on FZY-1/CDC20, a regulator of the metaphase/anaphase transition. We observed a microtubule and FZY-1/CDC20-dependent circular cytoplasmic streaming in wild-type and mei-1 mutant embryos during meiosis. We propose that, in mei-1 mutant oocytes, this cytoplasmic streaming is sufficient to drive the spindle into the cortex. Cytoplasmic streaming is not the normal spindle translocation mechanism because translocation occurred in the absence of cytoplasmic streaming in embryos depleted of either the orbit/CLASP homolog, CLS-2, or FZY-1. These results indicate a direct role of microtubule severing in translocation of the meiotic spindle to the cortex.

Adenosine Triphosphatases↗

Crossed unilateral lesions of the medial forebrain bundle and either inferior temporal or frontal cortex impair object-reward association learning in Rhesus monkeys.

In an accompanying paper we showed that combined transection of the fornix, amygdala and temporal stem in monkeys produced dense amnesia, including an impairment in visual object-reward association learning. We proposed that this combined surgical section had its effect by isolating temporal cortex from the ascending projections of the basal forebrain and midbrain structures. To test this hypothesis, in the present experiment we disconnected the inferior temporal cortex from these basal forebrain and midbrain structures, while sparing cortical white matter, by crossed unilateral lesions of the medial forebrain bundle in one hemisphere and inferior temporal cortex in the opposite hemisphere. The aim of the medial forebrain bundle lesion was to section axons of cells, both those that project to the cortex via the medial forebrain bundle, and those which control the activity of these same structures. A single unilateral lesion alone had no effect on the ability to learn and remember visual object-reward associations, but the crossed unilateral lesions produced an impairment in this task which was equal in severity to the impairment seen earlier after bilateral section of the fornix, amygdala and temporal stem. The impairment was not an effect of interrupting fibres to the cortex from the ventromedial hypothalamus, or of unilateral sensory neglect. This supports the hypothesis that these midbrain and basal forebrain afferents to the inferior temporal cortex are important for new visual learning. Furthermore, an impairment of equal severity was demonstrated in a separate group of animals that received crossed unilateral lesions of the medial forebrain bundle in one hemisphere and of the frontal cortex in the opposite hemisphere. We propose that the frontal cortex acts to modulate basal forebrain activity which in turn reinforces object representations in the inferior temporal cortex during learning.

Animals↗

Relocation of specific visual functions following damage of mature posterior parietal cortex.

Many visual deficits have been reported following damage to specific cerebral sites within posterior parietal cortex. These deficits generally involve aspects of vision including spatial or motion perception and visuomotor control. One characteristic of many of these deficits is that they tend to attenuate over time. Presumably, other cortical regions possess adaptive neuroplastic mechanisms that allow them to accommodate functions that were previously dominated by the damaged region. This report summarizes a series of experiments that examined adaptive cortical plasticity following cerebral cortex damage sustained in maturity. Following bilateral lesions of posterior middle suprasylvian sulcal (pMSs) cortex in the cat, deficits were identified in both visual orienting and landmark discrimination tasks. However, the deficits on the visual orienting task were only profound for the first few days following the lesion and orienting abilities returned to normal levels within the first 2 weeks postlesion. In contrast, no such attenuation of the effect of the lesion was evident on the landmark discrimination task. Following recovery of function on the visual orienting task, individual cortical areas flanking the lesion were bilaterally deactivated with cooling. Reversible deactivation of anterior middle suprasylvian sulcal (aMSs) cortex, but none of the other adjacent cortices, yielded visual orienting deficits that are not found in intact animals during deactivation of aMSs cortex. Therefore, we concluded that the visual orienting functions normally mediated by pMSs cortex were able to relocate to aMSs cortex following lesion of pMSs cortex. Finally, bilateral lesion of both pMSs and aMSs cortices yielded visual orienting deficits that did not attenuate. Overall, this series of experiments demonstrates that certain visual functions may relocate to specific cortical loci following damage to discrete areas within posterior parietal cortex.

Animals↗

Effects of medial and dorsal cortex lesions on spatial memory in lizards.

In mammals and birds, the hippocampus is a major learning and memory center that plays a prominent role in spatial memory, the use of distal cues to guide navigation. The role of reptilian hippocampal homologues, the medial and dorsal cortex, in spatial memory has not been thoroughly investigated. The medial and dorsal cortex of reptiles is known to play a role in learning both tasks that are hippocampally dependent and tasks that are not hippocampally dependent in mammals and birds. In order to examine the specific role of the medial and dorsal cortex in spatial memory, we trained medial cortex, dorsal cortex, and sham lesioned Cnemidophorus inornatus lizards to locate the one heated rock of four identical rocks spaced evenly around the perimeter of a circular, sand filled, arena in a cool room. We used probe trials to examine the strategies used by lizards to locate the goal. Medial cortex lesions and dorsal cortex lesions slowed acquisition and altered the strategies used to locate the goal. However, none of the lizards adopted a spatial strategy to locate the goal suggesting that the dorsal cortex and medial cortex are involved in using non-spatial strategies for navigation.

Animals↗

Expression of brain-derived neurotrophic factor, neurotrophin-3 and their receptor messenger RNAs in monkey rhinal cortex.

The primate rhinal cortex, consisting of areas 36 and 35 of the perirhinal cortex and the entorhinal cortex (area 28), plays a crucial role in perception and memory. We investigated the expression of messenger RNAs for brain-derived neurotrophic factor and neurotrophin-3, as well as those for their respective tyrosine kinase receptors, TrkB and TrkC, in the monkey rhinal cortex. Results from in situ hybridization revealed that each of these messenger RNAs was expressed in neurons with distinct laminar and areal patterns of distribution. Brain-derived neurotrophic factor messenger RNA was principally detected in layers V/ VI of area 36, and layers II/III and V of the entorhinal cortex. Some of the messenger RNA-positive cells in the deep layers of the rhinal cortex were confirmed to exhibit a pyramidal cell-like morphology. Neurotrophin-3 messenger RNA expression was confined to layers II/III of the entorhinal cortex. In contrast, trkB and trkC messenger RNAs were expressed rather homogeneously and abundantly throughout the rhinal cortex. The laminar and cellular distributions of brain-derived neurotrophic factor and neurotrophin-3 messenger RNAs indicate the predominant expression of these neurotrophins in projection neurons. These results suggest that brain-derived neurotrophic factor and neurotrophin-3 regulate neuronal connectivities of forward and backward projections from the rhinal cortex and contribute to functional reorganization underlying the formation and maintenance of long-term memory in primates.

Animals↗

Horizontal or vertical optokinetic stimulation activates visual motion-sensitive, ocular motor and vestibular cortex areas with right hemispheric dominance. An fMRI study.

The differential effects of optokinetic stimulation with and without fixation suppression were analysed in an fMRI study in 10 right-handed healthy subjects. Horizontal and vertical small-field optokinetic stimulation activated the same multiple visual, ocular motor and vestibular cortical and subcortical areas in both hemispheres. The extent of activation in each hemisphere was independent of the stimulus direction. All activated areas representing cortical (occipitotemporal cortex, posterior parietal cortex, precentral and posterior median frontal gyrus, prefrontal cortex, medial part of the superior frontal gyrus) and subcortical (caudate nucleus, putamen, globus pallidus and paramedian thalamus) ocular motor structures were activated during optokinetic stimulation as well as during fixation suppression of optokinetic nystagmus. However, the activation was significantly stronger with optokinetc nystagmus compared with fixation suppression. The only relatively increased activity during fixation suppression was seen in the medial part of the superior frontal gyrus (supplementary eye field) and the anterior cingulate gyrus. The anterior insula and the posterior insula (human homologue of the parieto-insular vestibular cortex) were activated during optokinetic nystagmus but not during fixation suppression. A significant right hemispheric predominance (regardless of stimulus direction) was found under both conditions in the visual motion-sensitive and ocular motor areas of the cortex, except the supplementary eye field and anterior cingulate gyrus. This was most prominent in the occipitotemporal cortex, but did not occur in the primary visual cortex and in subcortical ocular motor structures (putamen, globus pallidus and caudate nucleus). Thus, cortical and subcortical activation patterns did not differ for horizontal and vertical optokinetic stimulation, and there was distinct right-hemisphere dominance for visual motion-sensitive and cortical ocular motor areas and the thalamus. Fixation suppression of optokinetic nystagmus yielded four different results: (i) increased activation in the supplementary eye field and anterior cingulate gyrus; (ii) unchanged activation in the visual cortex; (iii) decreased activation in most of the ocular motor areas; and (iv) suppressed activation in the anterior and posterior insula and the thalamus. Activation of the parieto-insular vestibular cortex may be related to ocular motor function rather than self-motion perception.

Adult↗

Associative encoding in posterior piriform cortex during odor discrimination and reversal learning.

Recent proposals have conceptualized piriform cortex as an association cortex, capable of integrating incoming olfactory information with descending input from higher order associative regions such as orbitofrontal cortex and basolateral amygdala (ABL). If true, encoding in piriform cortex should reflect associative features prominent in these areas during associative learning involving olfactory cues. We recently reported that neurons in anterior piriform cortex (APC) in rats exhibited significant plasticity in their responses to odor cues during associative learning. Here, we have repeated this study, recording from neurons in posterior piriform cortex (PPC), a region of piriform cortex that receives much stronger input from ABL. If associative encoding in piriform cortex is driven by inputs from ABL, then we should see more plasticity in PPC neurons than we observed in APC. Consistent with this hypothesis, we found that PPC neurons were highly associative and appeared to be somewhat more likely than neurons recorded in APC to alter their responses to the odor cues after reversal of the odor-outcome associations in the task. Further, odor-selective PPC populations exhibited markedly different firing patterns based on the valence of the odor cue. These results suggest associative encoding in piriform cortex is represented in a topographical fashion, reflecting the stronger and more specific input from olfactory bulb concerning the sensory features of odors in anterior regions and stronger input from ABL concerning the meaning of odors in posterior regions.

Amygdala↗

Collapse of cortex expansion during germination of Bacillus megaterium spores.

When spores of Bacillus megaterium ATCC 12872 were incubated with CdCl2, they germinated without decomposition of the cortex. Moreover, the volume ratio of cortex to protoplast-plus-cortex, C/(P+C), of the CdCl2-germinated spores was reduced. Incubation of isolated cortex with the divalent compounds Cd2+, Ca2+, and Mg2+ reduced the gel volume to about 1/5 but incubation with a nonionic compounds, glucose, did not. The spores with reduced C/(P+C) were observed in the early period of glucose-induced germination. The time required for a 50% change in cortex morphology to occur was 2.5 min, which corresponds well with the time for 50% loss of heat resistance. This time was shorter than that necessary for release of peptidoglycan fragments and hydrolysis of cortex glycan chains. These data indicate that cortex hydrolysis is not related to the initiation of germination. 50% of the dipicolinic acid, calcium and magnesium were released at 3.4, 4.0, and 2.4 min, respectively. These results suggest that collapse of cortex expansion by the interaction of cortex with dipicolinic acid and cations released from the core, or exogenous ionic germinants is an important step in the initiation of germination.

Bacillus megaterium↗

Pain processing in four regions of human cingulate cortex localized with co-registered PET and MR imaging.

Neurosurgical and positron emission tomography (PET) human studies and animal electrophysiological studies show that part of the anterior cingulate cortex (ACC) is nociceptive. Since the contribution of the ACC to pain processing is poorly understood, this study employed PET and magnetic resonance (MR) image co-registration in grouped and individual cases to locate regions of altered relative regional cerebral blood flow (rCBF). Seven right-handed, neurologically intact males were subjects; each received neuropsychological and pain threshold testing. Subjects were scanned during infusion of H2[15O]: four randomized scans during innocuous heat stimulation to the back of the left hand and four scans during noxious but bearable heat to the same place. The averaged rCBF values during innocuous stimuli were subtracted from those during noxious stimuli and statistical parametric maps (SPMs) for the group were computed to identify regions of altered relative rCBF. Finally, single-subject PET images of elevated and reduced rCBF were co-registered with MR images and projected onto reconstructions of the medial surface of the hemisphere. The SPM analysis of the group showed one site with elevated rCBF in the midcingulate cortex and one in the perigenual cortex predominantly contralateral to the side of stimulation. There were bilateral sites of reduced rCBF in the cingulofrontal transitional cortex and in the posterior cingulate cortex (PCC). Co-registered PET and MR images for individuals showed that only one case had a single, large region of elevated rCBF, while the others had a number of smaller regions. Six cases had at least one significant elevation of rCBF in the right hemisphere that primarily involved area 24b'; five of these cases also had an elevation in area 32', while the seventh case had elevated rCBF in these areas in the left hemisphere. The rostral site of elevated rCBF in the group was at the border of areas 24/24' and areas 32/32' although most cases had a site of elevation more rostral in the perigenual cingulate cortex. The ACC site of reduced rCBF was in areas 8 and 32 and that in the PCC included much of areas 29/30 in the callosal sulcus, areas 23b and 31 on the cingulate gyral surface and parietal area 7m. The localization of relative rCBF changes suggests different roles for the cingulate cortex in pain processing: (i) elevated rCBF in area 24' may be involved in response selection like nocifensive reflex inhibition; (ii) activation of the perigenual cortex may participate in affective responses to noxious stimuli like suffering associated with pain; and (iii) reduced rCBF in areas 8 and 32 may enhance pain perception in the perigenual cortex, while that in the PCC may disengage visually guided processes.

Adult↗

Voltage imaging of epileptiform activity in slices from rat piriform cortex: onset and propagation.

The piriform cortex is a temporal lobe structure with a very high seizure susceptibility. To investigate the spatiotemporal characteristics of epileptiform activity, slices of piriform cortex were examined by imaging electrical activity with a voltage-sensitive fluorescent dye. Discharge activity was studied for different sites of stimulation and different planes of slicing along the anterior-posterior axis. Epileptiform behavior was elicited either by disinhibition with a gamma-aminobutyric acid-A receptor antagonist or by induction with a transient period of spontaneous bursting in low-chloride medium. Control activity recorded with fluorescent dye had the same pharmacological and temporal characteristics as control activity reported previously with microelectrodes. Simultaneous optical and extracellular microelectrode recordings of epileptiform discharges showed the same duration, latency, and all-or-none character as described previously with microelectrodes. Under all conditions examined, threshold electrical stimulation applied throughout the piriform cortex evoked all-or-none epileptiform discharges originating in a site that included the endopiriform nucleus, a previously identified site of discharge onset. In induced slices, but not disinhibited slices, the site of onset also included layer VI of the adjoining agranular insular cortex and perirhinal cortex, in slices from anterior and posterior piriform cortex, respectively. These locations had not been identified previously as sites of discharge onset. Thus like the endopiriform nucleus, the deep agranular insular cortex and perirhinal cortex have a very low seizure threshold. Additional subtle differences were noted between the induced and disinhibited models of epileptogenesis. Velocity was determined for discharges after onset, as they propagated outward to the overlying piriform cortex. Propagation in other directions was examined as well. In most cases, velocities were below that for action potential conduction, suggesting that recurrent excitation and/or ephaptic interactions play a role in discharge propagation. Future investigations of the cellular and organizational properties of regions identified in this study should help clarify the neurobiological basis of high seizure susceptibility.

Animals↗

Hydrolysis of cortex peptidoglycan during bacterial spore germination.

Despite the most extreme dormancy and resistance properties among living systems, bacterial endospores retain an alert sensory mechanism to respond to the germinants and initiate germination. Although the molecular mechanism of the germination process is not completely described, current progress in the studies on the enzymes involved in the process gave us a somewhat clearer picture of the process of spore peptidoglycan (cortex) hydrolysis, a major biochemical event in germination. Germination-specific cortex-lytic enzymes require muramic acid d-lactam in their substrates. At least two types of enzymes are involved in the germination process: a spore cortex-lytic enzyme (SCLE) and a cortical fragment-lytic enzyme (CFLE). Except for their peptidoglycan-binding regions, the primary structures of SCLE and CFLE vary according species. Both enzymes differ in their hydrolytic bond-specificities and recognition of the substrates morphology. SCLE appears to initiate germination by uncrosslinking the intract cortex, and the CFLE further degrades the polysaccharide moiety of the SCLE-modified cortex. In vivo CFLE activity is likely regulated by its requirement for partially un-crosslinked cortex, while SCLE requires activation process. Clostridium perfringens SCLE is activated by a germination-specific serine protease during germination, but the activation mechanism of SCLE in Bacillus species is unknown. Cortex-lytic enzymes are expressed at the early stage of sporulation but the compartment of expression depends on proteins. However, all enzymes are located outside the cortex layer in dormant spores, suggesting that the hydrolysis process initiates at the exterior side of the cortex. The assembly of the germination apparatus is also discussed.

Hydrolysis↗

Neural associations of the frontal cortex.

Recent anatomical findings in the monkey indicate that the frontal cortex receives associative afferents from the visual, auditory, and somatosemsory areas of the cortex. The inferior parietal lobule and the inferior temporal cortex are important way-stations in these cortico-cortical afferent pathways. The olfactory system represents a fourth sensorium having access to the frontal cortex, namely, by way of substantial projections from the pirifom cortex and olfactory tubercle to the medial subdivision of the thalamic mediodorsal nucleus. Additional afferents to this nucleus originate from various fore- and midbrain structures implicated in the circuitry of the limbic system; such afferents could well be ediators of information related to the organism's internal milieu. On the efferent side, the frontal cortex is associated with the inferior parietal, temporal, cinguloparahippocampal cortex, and entorhinal area; it is the only cortical region known to project directly to the hypothalamus and hypothalamus-related structures in the paramedian midbrain tegmentum. The mosaic of origin and termination of the various connections indicates that the convexity of the frontal lobe (especially its caudal half) is reciprocally associated with the parietal and temporal cortex, while the major associations with the hippocampal mechanism originate from two separate areas, viz. the caudal orbitofrontal cortex and a region dorsal to the sulcus principalis, frontal fields from which also the major fronto-hypothalamic connections arise.

Animals↗

A microcolumnar structure of monkey cerebral cortex revealed by immunocytochemical studies of double bouquet cell axons.

Immunocytochemical methods were used to study 28,000 mol. wt calbindin and tachykinin immunoreactivity in the monkey cerebral cortex. Calbindin and tachykinin immunoreactivity give rise to a generally different pattern of staining of cell bodies and terminal-like puncta. However, the staining of long, vertically-oriented bundles of processes--identical to classical double bouquet cell axonal arborizations--is the most prominent feature of the pattern of both calbindin- and tachykinin-immunoreactive staining. These bundles form a widespread and regular columnar system descending from layer II to layers III-V. The bundles are most evident in layer III where, in tangential sections, they have a density of 7-15 bundles/10,000 microns 2 with a center-to-center spacing of 15-30 microns. The distribution of immunoreactive bundles through the cortex is not homogeneous; somatic sensory, auditory, and visual areas display a large number of calbindin-immunoreactive bundles while tachykinin-immunoreactive bundles are only numerous in the auditory areas and in area 18 of the visual cortex. In the motor cortex (area 4) few or no immunoreactive bundles are visualized with either antibody. Correlative light and electron microscope analysis of tachykinin immunoreactive bundles in the primary auditory cortex shows that the tachykinin-positive axons of the bundles form symmetrical synaptic contacts with dendritic shafts (57%) and spines (43%). Frequently, several immunoreactive boutons that arise from the same fiber are seen climbing along the surfaces of vertically-oriented, non-immunoreactive processes which include myelinated and unmyelinated axons and probably glial processes. The same ultrastructural features and a similar synaptic distribution were found in a previous study [DeFelipe et al. (1989) Brain Res. 503, 49-54] of calbindin-positive bundles in the somatic sensory cortex (areas 3a and 1). Despite the virtually identical morphological features of tachykinin- and calbindin-immunoreactive bundles, colocalization studies demonstrate little coexistence of the two antigens in somata and none in the axonal bundles of double bouquet cells. These data suggest that the double bouquet cell is a chemically heterogeneous, but ubiquitous morphological type of cortical interneuron, whose uniquely bundled axonal system, which is probably GABAergic, imposes a fundamental microcolumnar organization upon the cerebral cortex.

Animals↗

Layer V neurons bear the majority of mRNAs encoding the five distinct dopamine receptor subtypes in the primate prefrontal cortex.

In situ hybridization histochemistry was used to determine the laminar distribution of D1, D2, D3, D4, and D5 dopamine receptor mRNAs in the primate prefrontal cortex and to compare striatal and cortical levels of these messages within the same tissue sections. All five subtypes of dopamine receptor mRNA are present in both the monkey striatum and the cerebral cortex but in different proportions within each structure. Thus, levels of D1 and D2 mRNAs are noticeably stronger in the striatum than in the cortex, whereas D4 and D5 expression is clearly higher in the cortex. The D3 transcripts appear nearly equivalent in the striatum and the cortex. A major finding is that, within the prefrontal cortex, mRNAs encoding all dopamine receptor subtypes are expressed most strongly in layer V. This laminar pattern of mRNA distribution does not hold in all cortical regions. The relatively high levels of mRNAs encoding known dopamine receptor subtypes in the primate cerebral cortex, including the D4 receptor, underscore the importance of this structure as a target for therapeutic actions of antipsychotic drugs. Further, their prominence in layer V of the prefrontal cortex, which contains the corticostriatal and corticotectal projection neurons, provides a neural basis for dopaminergic regulation of the descending control systems.

Animals↗

Thalamic projections to sensorimotor cortex in the macaque monkey: use of multiple retrograde fluorescent tracers.

We used several fluorescent dyes (Fast Blue, Diamidino Yellow, Rhodamine Latex Microspheres, Evans Blue, and Fluoro-Gold) in each of eight macaques, to examine the patterns of thalamic input to the sensorimotor cortex of macaques 12 months or older. Inputs to different zones of motor, premotor, and postarcuate cortex, supplementary motor area, and areas 3b/1 and 2/5 in the postcentral cortex, were examined. Coincident labeling of thalamocortical neuron populations with different dyes (1) increased the precision with which their soma distributions could be related within thalamic space, and (2) enabled the detection by double labeling, of individual thalamic neurons that were common to the thalamic soma distributions projecting to separate, dye-injected cortical zones. Double-labeled thalamic neurons projecting to sensorimotor cortex were rarely seen in mature macaques, even when the injection sites were only 1-1.5 mm apart, implying that their terminal arborizations were quite restricted horizontally. By contrast, separate neuron populations in each thalamic nucleus with input to sensorimotor cortex projected to more than one cytoarchitecturally distinct cortical area. In ventral posterior lateral (oral) (VPLo), for example, separate populations of cells sent axons to precentral medial, and lateral area 4, medial premotor, and postarcuate cortex, as well as to supplementary motor area. Extensive convergence of thalamic input even to the smallest zones of dye uptake in the cortex (approximately 0.5 mm3) characterized the sensorimotor cortex. The complex forms of these projection territories were explored using 3-dimensional reconstructions from coronal maps. These projection territories, while highly ordered, were not contained by the cytoarchitectonic boundaries of individual thalamic nuclei. Their organization suggests that the integration of the diverse information from spinal cord, cerebellum, and basal ganglia that is needed in the execution of complex sensorimotor tasks begins in the thalamus.

Afferent Pathways↗

Patterns of connectivity in the cat sensory-motor cortex: a light and electron microscope analysis of the projection arising from area 3a.

Through its complex network of interconnections, each of the functionally specialized subdivisions in the cat primary somatosensory cortex may provide the motor cortex with different input and thus play a unique role in motor behavior. Areas 2 and 3a receive separate peripheral information. Cells in both regions project directly to the cat motor cortex but are thought to target different populations of neurons. In this study the morphology and distribution patterns of the area 3a projection to the motor cortex were compared to previous findings on the projection from area 2. Also, details of the projection from area 3a to area 2 were studied. Injections of Phaseolus vulgaris leucoagglutinin were made into area 3a and fixed brain tissue was processed for immunohistochemical staining of this anterograde tracer. Tissue was examined with the light microscope to determine the patterns of the 3a projections to area 2 and motor cortex, area 4. Axons arising from cells in area 3a terminated in multiple column-like clusters in both motor cortex and area 2. The small number of cells labeled at the injection sites suggested that multiple foci of the 3a fibers are formed by collateral axonal branches of the same neurons. The topography of the projection from area 3a to the motor cortex was more clearly defined than that from area 3a to area 2. Electron microscope analysis determined the laminar distribution and types of synapses formed between area 3a efferents and their target neurons. A high proportion of synapses was found in layer III in both target regions. However, unlike in area 4, labeled terminals were sparse in laminae I and II of area 2. Axospinous synapses were slightly more numerous than axodendritic synapses, but both were distributed similarly throughout the thickness of the cortex. In area 2 the axospinous synapses accounted for 63% of synapses and in area 4 for 57% of synapses. No axosomatic synapses were detected.

Animals↗

Frontal granular cortex input to the cingulate (M3), supplementary (M2) and primary (M1) motor cortices in the rhesus monkey.

Although frontal lobe interconnections of the primary (area 4 or M1) and supplementary (area 6m or M2) motor cortices are well understood, how frontal granular (or prefrontal) cortex influences these and other motor cortices is not. Using fluorescent dyes in rhesus monkeys, we investigated the distribution of frontal lobe inputs to M1, M2, and the cingulate motor cortex (area 24c or M3, and area 23c). M1 received input from M2, lateral area 6, areas 4C and PrCO, and granular area 12. M2 received input from these same areas as well as M1; granular areas 45, 8, 9, and 46; and the lateral part of the orbitofrontal cortex. Input from the ventral part of lateral area 6, area PrCO, and frontal granular cortex targeted only the ventral portion of M1, and primarily the rostral portion of M2. In contrast, M3 and area 23c received input from M1, M2; lateral area 6 and area 4C; granular areas 8, 12, 9, 46, 10, and 32; as well as orbitofrontal cortex. Only M3 received input from the ventral part of lateral area 6 and areas PrCO, 45, 12vl, and the posterior part of the orbitofrontal cortex. This diversity of frontal lobe inputs, and the heavy component of prefrontal input to the cingulate motor cortex, suggests a hierarchy among the motor cortices studied. M1 receives the least diverse frontal lobe input, and its origin is largely from other agranular motor areas. M2 receives more diverse input, arising primarily from agranular motor and prefrontal association cortices. M3 and area 23c receive both diverse and widespread frontal lobe input, which includes agranular motor, prefrontal association, and frontal limbic cortices. These connectivity patterns suggest that frontal association and frontal limbic areas have direct and preferential access to that part of the corticospinal projection which arises from the cingulate motor cortex.

Animals↗

Neurophysiological mechanisms of recovery from visual cortex damage in cats: properties of lateral suprasylvian visual area neurons following behavioral recovery.

Damage to visual cortical areas 17, 18, and 19 in the cat produces severe and long-lasting deficits in performance of form and pattern discriminations. However, with extensive retraining the animals are able to recover their ability to discriminate form and pattern stimuli. Recent behavioral experiments from this laboratory have shown that a nearby region of cortex, the lateral suprasylvian visual area (LS area), plays an important role in this recovery (Wood et al., 1974; Baumann and Spear, 1977b). The present experiment investigated the underlying neurophysiological mechanisms of the recovery by recording from single neurons in the LS area of cats which had recovered from long-term visual cortex damage. Five adult cats received bilateral removal of areas 17, 18, and 19. They were then trained to criterion on two-choice brightness, form, and pattern discriminations. Recording from LS area neurons was carried out after the behavioral training, from 3 to 7 months after the visual cortex lesions. The properties of these neurons were compared to those of LS area neurons in normal cats (Spear and Baumann, 1975) and in cats with acute or short-term visual cortex damage and no behavioral recovery (Spear and Baumann, 1979). The results showed that all of the changes from normal which were produced by acute visual cortex damage were also present after the behavioral recovery. Moreover, all of the response properties of LS area neurons which remain after acute visual cortex damage were present in similar form after the behavioral recovery. There was no evidence for any functional reorganization in the LS area concomitant with its role in the behavioral recovery. These results suggest that functional reorganization plays little or no role in recovery from visual cortex damage in adult cats. Rather, the recovery of form and pattern discrimination ability appears to be based upon the functioning of residual neural processes in the LS area which remain after the visual cortex damage.

Animals↗