Chronic nicotine exposure produces lateralized,age‐dependent dendritic remodeling in the rodent basolateral amygdala

This study investigated the dendritic morphology of neurons located in the right and left basolateral amygdala (BLA) and infralimbic (IL) cortex following chronic nicotine exposure during adolescence or adulthood. Sprague–Dawley rats were administered subcutaneous injections of nicotine (0.5 mg/kg; free base) or saline three times per week for 2 weeks (six total injections). The dose period began on either postnatal day (P) 32 (adolescent) or P61 (adult). Twenty days following the end of dosing, brains were processed for Golgi‐Cox staining, and dendrites from principal neurons in the BLA and pyramidal neurons in the IL were digitally reconstructed in three dimensions. Morphometric analysis revealed a contrasting pattern of BLA dendritic morphology between the adolescent and adult pretreatment groups. In the adult control group, basilar dendritic length did not differ with respect to hemisphere. Nicotine induced robust hemispheric asymmetry by increasing dendritic length in the right hemisphere only. In contrast, adolescent nicotine exposure did not produce significant alteration of basilar dendritic morphology. There was, however, an indication that nicotine eliminated a naturally existing hemispheric asymmetry in the younger cohort. At both ages, nicotine produced a reduction in complexity of the apical tree of principal neurons. Chronic nicotine did not affect the dendritic morphology of pyramidal neurons from the IL in either age group, indicating another dimension of anatomical specificity. Collectively, these data implicate the BLA as a target for lasting neuroplasticity associated with chronic nicotine exposure. Further, hemispheric differences in dendritic morphology were uncovered that depended on the age of nicotine exposure, a finding that underscores the importance of considering laterality when investigating neurodevelopmental effects of drug exposure. Synapse 64:754–764, 2010. © 2010 Wiley‐Liss, Inc.     

Dendritic structure alterations induced by hypothyroidism in pyramidal neurons of the rat visual cortex

In order to study the effect that neonatal hypothyroidism has on the whole morphology of pyramidal neurons of the cerebral cortex, the dendritic structure of these cells was defined by a set of 10 variables divided into two subsets, one composed of 7 variables defining the apical shaft and the other composed of 3 variables concerning the basal arborization. The canonical multivariate analysis applied to the measurements of these variables made on two groups of layer III pyramidal neurons belonging to 80-day-old control and thyroidectomized rats revealed that this disease only affects the development of the apical tuft region of those neurons. This result is in agreement with our previous finding concerning the effect of hypothyroidism on the dendritic densities of layer III pyramidal neurons (Dev. Brain Res., 28 (1986) 259-262).     

Pyramidal cortical cell morphology studied by multivariate analysis: effects of neonatal thyroidectomy, ageing and thyroxine-substitution therapy

The changes produced on the whole dendritic morphology of layer III cortical pyramidal neurons by neonatal hypothyroidism, induced in rats by thyroidectomy at 10 days of age (T), as well as those changes related to ageing, have been studied in rats at 40 and 80 days of age. For these purposes, the dendritic structure of these neurons was defined by a set of 10 variables whose measurements were analyzed using multivariate methods. The effect of tyroxine (T4) substitution therapies applied to T rats between 12-40 and 30-80 days of age has been further investigated with the same mathematical methodology. The results obtained from the analyses performed show that hypothyroidism affects both the apical tuft and the basal dendritic arborization of these neurons. The observed damage was similar: a decrease of the total length of the dendritic segments of the apical tuft and the basal arborization. This change, however, was detected in these two different subregions with a different timing. These results seem to reinforce our findings concerning the selective effect of T on different sites of these neurons. On the other hand, 3 morphological changes have been revealed regarding the development of the pyramidal neuron studied: (1) the total length of the apical tuft dendritic segments increases from 40 to 80 days of age; (2) the total length of the basal dendritic segments decreases from 40 to 80 days of age; and (3) the perimeter of the cell body decreases from 40 to 80 days of age. Finally, the results obtained did not allow us to detect any recovery of the damage induced by T, as a consequence of the T4 substitution therapies applied.     

Sex differences in dendritic response to differential experience in the rat visual cortex

Male and female hooded rats were raised from weaning in either a complex or an isolated environment. After one month, the visual cortex was Golgi—Cox-stained and layers III and V pyramidal and layer IV stellate neurons were quantified: (1) analyses of dendritic branch numbers and total dendritic length revealed that females exhibited smaller differences in response to the rearing environment than males in both apical oblique and basilar branches of layer III pyramidal neurons; (2) a similar but much weaker trend towards a sex by environment interaction was seen in layer IV stellate neurons, while in layer V pyramidal neurons the sexes showed equal amounts of dendritic response; (3) the terminal dendrites in every cell population were longer in the rats from the complex environment regardless of sex; (4) males had longer terminal branches in both environments in layer IV stellates and layer V lower apical oblique branches. Thus the sex differences that appeared across environments were small. The more prominent sex differences were seen when the rearing environment was varied, with females showing less susceptibility to environmental influences in some neuronal populations.     

The dendritic morphology of pyramidal neurons in the rat hippocampal CA3 area. I. Cell types

Pyramidal neurons from the hippocampal CA3 area of hooded rats were qualitatively and quantitatively described from Golgi-stained tissue. The most numerous of the pyramidal neurons, those with a single apical shaft, fell into two major categories. One category, termed short-shaft pyramidal neurons, is characterized by short apical shafts, a large number of thorny excrescences, and densely branched apical and basilar trees. The second category, long-shaft pyramidal neurons, is characterized by a long apical shaft, a small number of thorny excrescences and relatively less dendritic branching in both the apical and basilar trees. The somata of short-shaft pyramidal neurons tend to be located higher in stratum pyramidale than the somata of long-shaft neurons. Quantitative measurements, which included both analysis of dendritic branching and the distribution of dendritic material sampled at 10% intervals from the cell body, confirmed the qualitative observation that short-shaft neurons had more total dendritic length than long-shaft neurons. The difference in the total dendritic length observed between long- and short-shaft pyramidal neurons could be an indication that each type receives a different number of synapses per neuron. The less commonly observed variants of pyramidal neurons were briefly described but not quantified. This study demonstrates that CA3 pyramidal neurons are not a homogeneous group but that their heterogeneous characteristics fall into two major categories.     

Is there an optimal age for recovery from motor cortex lesions? II. behavioural and anatomical consequences of unilateral motor cortex lesions in perinatal, infant, and adult rats

Purpose: The purpose of this study was to compare the behavioural and anatomical effects of unilateral motor cortex ablation in neonatal, infant, and adult rats. Methods: Rats were given unilateral lesions of the motor cortex on the day of birth (P1), at ten days of age (P10), or in adulthood. They were trained on several motor tasks (skilled forelimb reaching, beam traversing, tongue extension), general motor activity, and a test of spatial learning (Morris water task). Results: Although all lesion groups were equally impaired at skilled reaching with the forelimb contralateral to the lesion, rats with P1 lesions also were impaired at traversing a narrow beam and at learning the Morris task. Gross anatomical analyses revealed that the P1 rats had smaller brains than the other groups, a result that may account for the larger behavioural deficits in the P1 group. Analysis of Golgi-Cox stained neurons showed that relative to control groups, all lesion groups showed an increase in dendritic length in the basilar dendrites of layer III pyramidal cells and, paradoxically a decrease in length of the apical dendrites of the same cells. Conclusions: The bilateral alterations in dendritic organization following the motor cortex lesions suggest that there has been a bilateral reor-ganization of intrinsic cortical connectivity following motor cortex lesions at any age. These alterations in connectivity are likely not identical in the young and adult animals, however, because relative to controls, both the young operated groups, but not the adult group, showed a bilat-eral drop in spine density in the basilar dendrites of layer V pyramidal cells. These findings are discussed with respect to the idea that there may be critical ages in development in which animals can use anatomical modifications to compensate for deficits produced by cortical injury.     

Is there an optimal age for recovery from motor cortex lesions? II. behavioural and anatomical consequences of unilateral motor cortex lesions in perinatal, infant, and adult rats

Purpose: The purpose of this study was to compare the behavioural and anatomical effects of unilateral motor cortex ablation in neonatal, infant, and adult rats. Methods: Rats were given unilateral lesions of the motor cortex on the day of birth (P1), at ten days of age (P10), or in adulthood. They were trained on several motor tasks (skilled forelimb reaching, beam traversing, tongue extension), general motor activity, and a test of spatial learning (Morris water task). Results: Although all lesion groups were equally impaired at skilled reaching with the forelimb contralateral to the lesion, rats with P1 lesions also were impaired at traversing a narrow beam and at learning the Morris task. Gross anatomical analyses revealed that the P1 rats had smaller brains than the other groups, a result that may account for the larger behavioural deficits in the P1 group. Analysis of Golgi-Cox stained neurons showed that relative to control groups, all lesion groups showed an increase in dendritic length in the basilar dendrites of layer III pyramidal cells and, paradoxically a decrease in length of the apical dendrites of the same cells. Conclusions: The bilateral alterations in dendritic organization following the motor cortex lesions suggest that there has been a bilateral reor-ganization of intrinsic cortical connectivity following motor cortex lesions at any age. These alterations in connectivity are likely not identical in the young and adult animals, however, because relative to controls, both the young operated groups, but not the adult group, showed a bilat-eral drop in spine density in the basilar dendrites of layer V pyramidal cells. These findings are discussed with respect to the idea that there may be critical ages in development in which animals can use anatomical modifications to compensate for deficits produced by cortical injury.     

Morphology of neurons in area 4γ of the cat's cortex studied with intracellular injection of HRP

Neurons in laminae II, III, V, and VI of area 4γ of the cat motor cortex were studied following intracellular penetration with an HRP-filled microelectrode. Antidromic and synaptic responses produced by stimulation of the cerebral peduncles and/or of the ventrolateral nucleus of the thalamus were investigated. Horseradish peroxidase was then iontophoresed into the same neurons to allow examination of their detailed morphology. The morphology of pyramidal neurons whose somata were located in a particular lamina was similar but differed from that of pyramidal neurons in other laminae. The modified pyramidal neurons of lamina II had a truncated apical dendrite or did not possess an obvious apical dendrite, even though the ascending dendritic branches were longer and more extensive than the “basal” branches. As was the case for the pyramidal cells in other laminae, the axons of these lamina II modified pyramidal cells descended toward the white matter; their somata were generally pyramidal in shape; and their dendrites were spiny. All pyramidal neurons except some of lamina VI had ascending dendrites which terminated in a tuft in lamina I, subpially. No intracortical collaterals were seen originating from the axons of lamina II or of lamina VI pyramidal neurons. Lamina III pyramidal neurons had extensive short and long axon collaterals which contributed synaptic boutons to all laminae of the cortex. Pyramidal neurons of lamina V had fewer axon collaterals whose synaptic boutons were restricted to laminae V and VI. All somata of pyramidal tract neurons (PTNs), identified by antidromic responses from peduncular stimulation, were located in lamina V, except for one which was located in lamina VI. Recurrent collaterals of pyramidal neurons were activated by peduncular stimulation. Recurrent excitatory postsynaptic potentials (epsps) could be evoked in fast PTNs, slow PTNs, other pyramidal neurons of lamina V, and pyramidal neurons of lamina VI at latencies between 1.3 and 6.25 msec. In some slow PTNs, a recurrent inhibitory postsynaptic potential of long duration was the predominant response. Stimulation of the ventrolateral nucleus of the thalamus resulted in epsps in pyramidal neurons of lamina III, V, and VI at latencies between 1.0 and 5.0 msec.     

Ferret pyramidal cell dendritogenesis: changes in morphology and ganglioside expression during cortical development.

Pyramidal cell ontogenesis and basilar dendritic differentiation were evaluated concomitantly with ganglioside expression and distribution in ferret cerebral cortex. Layer V neurons began basilar dendritogenesis on postnatal day 1 (P1) with a peak in dendritic arborization occurring at P21. Layer II/III neurons, in contrast, were in early stages of basilar dendritic differentiation at P14, resulting in a complex dendritic arbor at P28. High performance thin-layer chromatography showed numerous changes in ganglioside expression during cortical development, including a decline of GM2 in the mature cortex. The temporal expression and cellular distribution of GM2, GD2, GM1, GD3, and GM3 gangliosides in developing cerebral cortex were determined by immunocytochemistry. GM2 immunoreactivity (IR) was most prominent in layer V neurons between P1 and P21 and in layer II/III neurons between P14 and P28 with staining diminishing to near absent levels in the adult. GM2-IR appeared as punctate structures within the somatodendritic domain and by electron microscopy was shown to be membrane-bound vesicles often in close proximity to the plasmalemma. Expression of GM2, but not of other gangliosides studied, followed two well-documented developmental neurogenic gradients: ventrolateral to dorsomedial and radial (inside-first outside-last). Onset of significant GD2 expression in layer II/III and V pyramidal cells was delayed until P14 and persisted in adult neocortex. GD3 was localized most prominently to glial-like cells, whereas GM1 was primarily localized to white matter. The close temporal and spatial concordance of GM2-IR in cortical pyramidal neurons undergoing dendritogenesis is consistent with its proposed role as a modulator of dendritic differentiation.     

A Golgi study of the early postnatal development of the visual cortex of the hooded rat

Although neuroanatomical plasticity has been demonstrated in the rat visual cortex, no systematic data on the dendritic development of the area are available. In the present study, the visual cortex of hooded rats at 1, 3, 5, 7, 10 and 15 postnatal days of age (P1-P15) was impregnated with the rapid Golgi method. The cortex was divided into the superficial layers, II-IV, and the middle layer V. At P1, pyramidal neurons had apical shafts and the beginning of the apical terminal arch. Analysis of both basilar and oblique dendritic number showed that pyramidal neurons of the middle layer developed more quickly than those in the superficial layers. The number of lower order basilar dendritic branches reached asymptote over the examined time period, whereas the higher order branches were still increasing in number but at a decelerating rate by P15. Dendrites at all ages exhibited varicosities which were especially prominent on the thin dendritic branches of the earlier ages. Some thin, filamentous processes, termed protospines, were found on dendrites and cell bodies at P1 to P5. They seemed to decrease by P7, when a few mature spines appeared. Spines increased in number on days P10 and P15. A comparison of the data from this study with quantified Golgi studies in adult rats indicates that by P10 and P15 the number of basilar branches is in the range seen in the adult.     

Does prenatal nicotine exposure alter the brain's response to nicotine in adolescence? A neuroanatomical analysis

This study examined changes in dendritic morphology and spine density in multiple brain regions [Zilles' areas: (i) the Cg3 region of the anterior cingulate cortex or the medial prefrontal cortex, layer III (Cg3); (ii) the dorsal agranular insular cortex, layer III (AID); (iii) the PAR I region of the parietal cortex, layer III (Par1) and (iv) the nucleus accumbens (NAc)]of Long–Evans rats following exposure to nicotine prenatally, in late adolescence, or both prenatally and in adolescence. Prenatal nicotine exposure induced enduring changes in neuroanatomical organisation that varied between male and female offspring, with males exhibiting increased dendritic complexity of neurons in AID and NAc whereas females experienced increased dendritic complexity in Par1 but decreased dendritic complexity of neurons in NAc. Similarly, nicotine given in late adolescence dramatically reorganised neural circuitry of both male and female offspring, with males exhibiting decreased dendritic complexity of neurons in Par1 and Cg3 but increased dendritic complexity in AID, and females exhibiting decreased dendritic complexity in Cg3 and NAc but increased complexity in AID. Exposure to nicotine both prenatally and in adolescence produced few neuroanatomical parameters that demonstrated a prenatal experience × adolescent drug administration interaction. Females showed additive effects in Par1, Cg3 and NAc whereas males demonstrated additive effects only in AID. Thus, the timing of nicotine exposure produced differential effects on cerebral organisation in a regionally specific manner.     

Functional classes of cortical projection neurons develop dendritic distinctions by class-specific sculpting of an early common pattern.

We demonstrate in rat neocortex that the distinct laminar arrangements of the apical dendrites of two classes of layer 5 projection neurons, callosal and corticotectal, do not arise de novo, but are generated later in development from a common tall pyramidal morphology. Neurons of each class initially elaborate an apical dendrite in layer 1. Layer 5 callosal neurons later lose the segments of their apical dendrite superficial to layer 4, generating their characteristic short pyramidal morphology. The apical dendrite of layer 5 callosal neurons later lose the segments of their apical dendrite superficial to layer 4, generating their characteristic short pyramidal morphology. The apical dendrite of layer 5 callosal neurons is actively eliminated, rather than passively displaced, as superficial cortical layers expand. Corticotectal neurons and callosal neurons superficial to layer 5 maintain their apical dendrite to layer 1. Therefore, this selective dendritic loss occurs in a neuron class-specific manner and, within the callosal population, in a lamina-specific manner. Based on our additional observations and other studies, this phenomenon can be extended to other types of cortical projection neurons. These findings show that selective dendritic elimination plays a major role in shaping the functional architecture characteristic of the adult cortex.     

Effect of the environment on the dendritic morphology of the rat auditory cortex

The present study aimed to identify morphological correlates of environment‐induced changes at excitatory synapses of the primary auditory cortex (A1). We used the Golgi‐Cox stain technique to compare pyramidal cells dendritic properties of Sprague‐Dawley rats exposed to different environmental manipulations. Sholl analysis, dendritic length measures, and spine density counts were used to monitor the effects of sensory deafness and an auditory version of environmental enrichment (EE). We found that deafness decreased apical dendritic length leaving basal dendritic length unchanged, whereas EE selectively increased basal dendritic length without changing apical dendritic length. On the contrary, deafness decreased while EE increased spine density in both basal and apical dendrites of A1 Layer 2/3 (LII/III) neurons. To determine whether stress contributed to the observed morphological changes in A1, we studied neural morphology in a restraint‐induced model that lacked behaviorally relevant acoustic cues. We found that stress selectively decreased apical dendritic length in the auditory but not in the visual primary cortex. Similar to the acoustic manipulation, stress‐induced changes in dendritic length possessed a layer‐specific pattern displaying LII/III neurons from stressed animals with normal apical dendrites but shorter basal dendrites, while infragranular neurons (Layers V and VI) displayed shorter apical dendrites but normal basal dendrites. The same treatment did not induce similar changes in the visual cortex, demonstrating that the auditory cortex is an exquisitely sensitive target of neocortical plasticity, and that prolonged exposure to different acoustic as well as emotional environmental manipulation may produce specific changes in dendritic shape and spine density. Synapse 64:97–110, 2010. © 2009 Wiley‐Liss, Inc.     

The pyramidal neurons in layer III of cat primary auditory cortex (AI)

The neuronal architecture of pyramidal cells in layer III of the primary auditory cortex (AI) of adult cats was examined as a prelude to connectional and fine structural studies; in a further paper, the results of parallel studies of non-pyramidal layer III cells are presented. Layer III is about 400 micron thick, comprises about one-quarter of the thickness of AI, and lies some 400-800 micron deep to the pial surface. It is distinguished in Nissl, fiber, and Golgi preparations from layers II and IV, and also on connectional grounds, since its neurons are one of the principal inputs to the contralateral AI. Layer III may be divided into two roughly equal tiers on the basis of its neuronal and cytoarchitecture. Layer IIIa is populated by small cells with oval somata and many tiny pyramidal cells; the fiber architecture is dominated by radial bundles of medium-sized axons interspersed among columns of apical dendrites arising from deeper-lying pyramidal cells. In layer IIIb medium-sized and large pyramidal cells are more numerous, and the fiber architecture has a different, much denser texture, including extensive lateral components which invade layer IV, and large contingents of descending, probably corticofugal, axons. Five kinds of pyramidal neurons occur in Golgi preparations. Most numerous are the small, medium-sized, and large pyramidal cells; the two types of star pyramidal neurons are less common. The small pyramidal cell has a limited dendritic field and rather delicate dendrites; all but the apical one usually end in layer III. The medium-sized pyramidal cell is the most common neurons, and its rich basilar dendritic arbors are conspicuous, with their many dendritic appendages, in the layer III neuropil; their distal dendrites spread into layer IV. The largest pyramidal cells lie mainly in layer IIIb, and their lateral dendrites often mark the layer IIIb-IVa border. The apical dendrites of medium-sized and large pyramidal cells often extend to layer Ib, where they branch obliquely. The axons of these cells branch laterally after descending through layer III and toward the white matter. Often secondary or tertiary branches reascend to layer IV and more superficially; there is considerable stereotypy in this branching pattern. These numerous secondary branches contribute heavily to the layer IIIb-IVa lateral fiber plexus. The fourth variety of pyramidal cell has a round soma and a stellate dendritic field whose distal branches extend from layer V to layer I, but whose axon is chiefly in layer III. Finally, a star pyramidal cell with long lateral basilar arbors but rather smooth dendrites completes the picture.(ABSTRACT TRUNCATED AT 400 WORDS)     

Exposure to excess glucocorticoids alters dendritic morphology of adult hippocampal pyramidal neurons.

We have used Golgi-impregnated tissue to demonstrate that exposure to excess glucocorticoids alters dendritic morphology in a specific population of neurons in the adult rat hippocampus. Daily injection of 10 mg of corticosterone for 21 days resulted in decreased numbers of apical dendritic branch points and decreased total apical dendritic length measured in a 100-microns-thick section in CA3 pyramidal cells compared to sham-injected and non-injected controls. In contrast, no changes were observed in CA3 pyramidal cell basal dendritic morphology. Furthermore, no changes were observed in the dendritic morphology of CA1 pyramidal cells or granule cells of the dentate gyrus. Cross-sectional cell body area of any of the 3 cell types examined in this study was unaffected by corticosterone treatment. Finally, qualitative analysis of Nissl-stained tissue from the same brains revealed increased numbers of darkly staining, apparently shrunken CA3 pyramidal cells in corticosterone treated compared to control brains. The changes in dendritic morphology we have observed may be indicative of neurons in the early stages of degeneration, as prolonged exposure to high levels of corticosterone has been shown by others to result in a loss of CA3 pyramidal cells. Additionally, these results suggest possible structural alterations which may occur under physiological conditions in which corticosterone levels are chronically elevated such as in aged animals.     

Nerve growth factor stimulates growth of cortical pyramidal neurons in young adult rats

The cytoarchitectonics of pyramidal neurons in the cerebral cortex of non-lesioned rats can be re-modeled by i.c.v. infusions of nerve growth factor (NGF). 4 months after the application of NGF, the pyramidal neurons in layers III and V of the motor cortex and layer V of the anterior cingulate cortex were analyzed and compared with pyramidal neurons from vehicle-treated rats. NGF-treated brains showed: (1) significant increase in dendritic branching in the basilar fields of the layer V, but not layer III, neurons; and (2) a significant increase in spine density in the terminal, but not proximal, dendritic branches. These findings indicated that, besides its known effects on forebrain cholinergic neurons, NGF produces a very generalized synaptic re-modeling involving the cells responsible for the major output of the cerebral cortex in the intact adult brain. © 1979 Elsevier Science B.V. All rights reserved.     

EFFECTS OF PRENATAL EXPOSURE TO ETHANOL ON THE MATURATION OF THE PYRAMIDAL NEURONS IN THE CEREBRAL CORTEX OF THE GUINEA-PIG: A QUANTITATIVE GOLGI STUDY

The effects of chronic ethanol consumption during gestation on the development of layer V pyramidal cells was studied quantitatively in the somatosensory cerebral cortex of the newborn guinea-pig. The spread of the basilar dendritic arborizations and counts of dendritic spines on the apical dendrite of neurons that had been processed with the rapid Golgi method were compared with those found in age-matched controls receiving an isocaloric diet without alcohol. There were significant differences in the number of primary basilar dendrites (P less than 0.05) and dendritic ramifications at a distance of 25 micron from the soma (P less than 0.01) between the alcohol-exposed and control animals. There also were significant differences in the number of dendritic spines on the apical dendrite (P less than 0.001). This experimental model further illustrates developmental anomalies in the cerebral cortex following prenatal ethanol exposure.     

Hemispheric differences in basilar dendrites and spines of pyramidal neurons in the rat prelimbic cortex: activity- and stress-induced changes

Pyramidal neurons of the rat medial prefrontal cortex have been shown to react to chronic stress by retracting their apical dendrites and by spine loss. We extended these findings by focusing on the basilar dendritic tree of layer III pyramidal neurons in both hemispheres of the rat prelimbic cortex. Animals were subjected to daily restraint stress for 1 week (6 h/day), during either the resting or the activity period. The morphology of basilar dendrites and spines of Golgi–Cox-stained neurons in the left and right hemispheres was digitally reconstructed and analyzed. We observed the following: (i) there was an inherent hemispheric asymmetry in control rats during the resting period: the number of spines on proximal dendrites was higher in the left than in the right hemisphere; (ii) basal dendrites in controls displayed a diurnal variation: there was more dendritic material during the resting period than in the activity period; (iii) chronic stress reduced the length of basal dendrites in only the right prelimbic cortex; (iv) chronic stress reduced spine density on proximal basal dendrites; (v) restraint stress during the activity period had more pronounced effects on the physiological stress parameters than restraint stress during the resting period. Our results show dynamic hemisphere-dependent structural changes in pyramidal neurons of the rat prelimbic cortex that are tightly linked to periods of resting and activity. These morphological alterations reflect the capacity of the neurons to react to external stimuli and mirror presumptive changes in neuronal communication.     

Morphological heterogeneity of CA1 pyramidal neurons in response to ischemia

We have found, based on the electrophysiological properties, two subtypes of CA1 pyramidal neurons in the CA1 region of the normal hippocampus, late postsynaptic potential (L-PSP) neurons and non-L-PSP neurons. In addition, our previous study has shown that the electrophysiological properties of these two subtypes of pyramidal neurons were differentially modified after ischemia. In the present study, we hypothesized that ischemia might also induce different morphological alterations in these two subtypes of neuron. To test the hypothesis, we compared the changes in the dendritic arborization and soma volume of these two subtypes of neurons in rats subjected to transient global ischemia. We found a significant decrease in the basal dendritic length of L-PSP neurons at 12 hr after reperfusion, resulting mainly from a significant decrease in the dendrite terminal length. The apical dendritic length of L-PSP neurons markedly increased at 24 hr after ischemia, resulting mainly from an increase in the number of branching arbors in the middle part of the apical dendritic trees. The soma size of L-PSP neurons was significantly reduced at 12 hr, but they became slightly larger at 24 hr and 48 hr after reperfusion. In contrast to L-PSP neurons, non-L-PSP neurons showed slight modifications in the dendritic arborization but had persistent swelling of their soma after ischemia. These results indicate that pathological changes in these two subtypes of neurons are different after ischemia.     

Aberrant dendritic development in the human agyric cortex: a quantitative and qualitative Golgi study of two cases

A quantitative and qualitative Golgi comparison of the visual cortex from two agyric brains and of two age-matched controls is reported. In the camera lucida drawings, most pyramidal cells were oriented vertically to the pial surface in the external cellular layer, frequently with their apical dendrites directed toward the deep layers (inverted pyramidal neurons). The deep cellular layer contained pyramidal and polymorphic neurons normally found in the second to fourth cortical layers. In quantitative analysis of the agyric cortex of a ten-month-old patient, relative immaturity of basal dendritic arborization was apparent together with a bipolar configuration of dendritic development of the pyramidal neurons. The 3-year-old patient had a significant delay in apical dendritic arborization (shorter branch length, decreased number of dendritic intersections) compared with his age-matched normal control. The pathogenesis of the abnormal dendritic development in agyria is discussed.