Automated and quantitative image analysis of ischemic dendritic blebbing using in vivo 2-photon microscopy data

Ischemia induces a 'blebbing' of dendrites, a structural alteration where dendrites take on a 'beads on a string' appearance. We developed a toolkit program, BlebQuant, for quantitative automated bleb analysis to chart the morphology of dendrites labeled with GFP/YFP under normal conditions and after ischemia-induced damage. In vivo 2-photon data from mouse layer 5 neurons with apical dendritic tufts extending to the cortical surface were examined before, during, and after global ischemia. To quantify changes in dendritic structure, we used morphometric tools that exploit characteristic features of blebbing, distinguished as localized regions of spherical or ellipsoid swellings. By comparing acquired images during ischemia and reperfusion to a pre-ischemia reference image, our automated approach detected blebs based on defined eccentricity and area thresholds and quantified the percentage of blebbed dendrites based on a block-selection method. Our results indicate that the automated morphometric indices we employ yield results that correlate with manual assessment. The automated approach permits rapid and effective analysis of dendritic structure and may facilitate the study of ischemic dendritic damage.     

Cocultured,but not isolated,cortical explants display normal dendritic development: a long-term quantitative study

Dendritic growth has been studied in long-term organotypic neonatal rat occipital neocortex explants grown either apart as isolated explants or in tandem as cocultures. Quantitative light microscopic measurement of dendritic and axonal branching patterns within the cortical slice was accomplished using rapid Golgi stained materials. In both isolates and cocultures the overall cellular organization of the slice was maintained over 4 weeks in vitro with morphologically distinguishable pyramidal and nonpyramidal neurons located within the same layers and with the same orientations as observed in situ. Long-term increases in the total length of basal dendrites, apical dendrite and axons were observed only in cocultures and were similar to growth patterns reported for in situ materials. Dendritic growth was mainly due to elongation of terminal dendritic segments. Surprisingly, isolated explants showed no long-term increases in total (basal) dendrites, apical dendrites or axons with time in vitro. A transient decrease in the number of basal dendritic segments and increase in terminal segment lengths at the end of the first week in vitro, however, was observed in nonpyramidal neurons. It is hypothesized that (i) afferent inputs and/or efferent targets develop only in cocultures and provide a crucial condition for the continued growth of dendritic/axonal arborization for neocortical neurons in vitro, (ii) intrinsic interconnectivity within isolated explants is not sufficient to maintain long-term growth of neuritic arbors, and (iii) remodelling of dendritic arbors within isolated explants occurs at the same time as these explants are showing noticeable increases in the level of spontaneous bioelectric activity, which suggests that dendritic growth and network formation may be function dependent.     

Temporal pattern of survival and dendritic growth of fetal hippocampal cells transplanted into ischemic lesions of the adult rat hippocampus

Cell suspensions obtained from the fetal hippocampus were transplanted into the adult rat hippocampus at 1 or 4 weeks after transient forebrain ischemia. Only when the ischemia induced death of most of the CA1 pyramidal cells of the host hippocampus and transplantation was performed at 1 week after the ischemia, did a large number of transplanted cells survive and the most extensive dendritic growth was demonstrated by microtubule-associated protein 2 immunohistochemistry. The dendrites of the cells located in the ventral part were oriented ventrally, lining up similarly to the parallel arrangements of apical dendrites of normal CA1 pyramidal cells. These findings suggest that certain forms of trophic factors, which appear to occur in association with the presence of free terminals of afferent fibers during the earlier period after ischemic insult, are involved in the survival of and dendritic growth from transplanted hippocampal cells.     

Livin' on the edge: imaging dendritic spine turnover in the peri-infarct zone during ischemic stroke and recovery.

The spontaneous recovery of sensory, motor, and cognitive functions after stroke is thought to be mediated primarily through the reorganization and rewiring of surviving brain circuits. Given that dendritic spine turnover underlies rewiring during normal development and plasticity, this process is likely to play a key role in mediating functional changes that occur during and after stroke. Recently, a new approach has been taken using two-photon microscopy to monitor, in real time, the temporal and spatial progression of dendritic plasticity in the living animal, both while it is experiencing the initial ischemic episode as well as during long-term recovery from stroke damage. Here, we highlight recent evidence showing that stroke can trigger extensive changes in the relatively hardwired adult brain. For example, when dendrites are challenged by acute ischemia, they can disintegrate within minutes of ischemia and rapidly reassemble during reperfusion. Over longer time scales, dendrites in the surviving peri-infarct zone show heightened levels of spine turnover for many weeks after stroke, thereby raising the possibility that future stroke therapies may be able to facilitate or optimize dendritic rewiring to improve functional recovery.     

Dynamic changes in CA1 dendritic spines associated with ischemic tolerance

Hippocampal CA1 neurons are particularly vulnerable to 5-10 min durations of global ischemia. These cells can develop tolerance to ischemia through prior exposure to brief episodes of ischemia (ischemic preconditioning, IP). Dendritic spines are implicated in various forms of neuroplasticity including memory and recovery of function. Here we characterized the changes in hippocampal CA1 dendritic spines during the development of ischemic tolerance and the subsequent postischemic recovery period. Gerbils received 5 min, bilateral carotid artery occlusions preceded by two 1.5 min occlusions each of which were 24 h apart (tolerance groups). Spine densities were calculated from CA1 apical and basilar dendrites in tolerant animals that survived 3 (IP3), 10 (IP10) or 30 (IP30) days as well as sham-operated animals and those that received only the two preconditioning episodes (PO). Habituation to a novel open-field was assessed 3, 7, 10 and 30 days after ischemia to gauge CA1 functional integrity. Dendritic spines were quantified from Golgi-Cox stained sections of the CA1 subfield. IP10, IP30 and PO animals had significantly higher CA1 basilar and apical spine densities than all other groups. Tolerant animals initially displayed open-field habituation impairments at a time when spine densities were reduced. Behavioral impairments gradually subsided over time in coincidence with an increase in CA1 spine densities. These findings suggest that dendritic spines may play a role in recovery of function associated with ischemic tolerance and stroke.     

In vivo reversible regulation of dendritic patterning by afferent input in bipolar auditory neurons

Afferent input regulates neuronal dendritic patterning locally and globally through distinct mechanisms. To begin to understand these mechanisms, we differentially manipulate afferent input in vivo and assess effects on dendritic patterning of individual neurons in chicken nucleus laminaris (NL). Dendrites of NL neurons segregate into dorsal and ventral domains, receiving excitatory input from the ipsilateral and contralateral ears, respectively, via nucleus magnocellularis (NM). Blocking action potentials from one ear, by either cochlea removal or temporary treatment with tetrodotoxin (TTX), leads to rapid and significant retraction of affected NL dendrites (dorsal ipsilaterally and ventral contralaterally) within 8 h compared with the other dendrites of the same neurons. The degree of retraction is comparable with that induced by direct deafferentation resulting from transection of NM axons. Importantly, when inner ear activity is allowed to recover from TTX treatments, retracted NL dendrites regrow to their normal length within 48 h. The retraction and growth involve elimination of terminal branches and addition of new branches, respectively. Examination of changes in NL dendrites at 96 h after unilateral cochlea removal, a manipulation that induces cell loss in NM and persistent blockage of afferent excitatory action potentials, reveals a significant correlation between cell death in the ipsilateral NM and the degree of dendritic retraction in NL. These results demonstrate that presynaptic action potentials rapidly and reversibly regulate dendritic patterning of postsynaptic neurons in a compartment specific manner, whereas long-term dendritic maintenance may be regulated in a way that is correlated with the presence of silent presynaptic appositions.     

Electron microscopic investigation of the cerebral cortex after cerebral ischemia and reperfusion in the gerbil

Prompt dendritic damage has been observed in the hippocampus of the gerbil brain after transient cerebral ischemia. In the present study, we studied the frontoparietal cortex of the gerbil brain electron microscopically after brief bilateral carotid occlusion to assess the vulnerability of dendritic processes. After ischemia for 5 min, there was swelling of the periphery of dendrites accompanied by swelling of mitochondria, cytoplasmic vacuolation and disintegration of microtubules in layer I, which spread to layer III after ischemia for 20 min. After reperfusion for 3-24 h following ischemia for 20 min, swelling in the periphery of dendrites and of mitochondria inside receded but vacuole formation and disintegration of microtubules propagated proximally. In neuronal perikarya, polyribosomal disaggregation was observed after ischemia for 20 min and persisted thereafter, while fragmentation of rough endoplasmic reticulum (ER) and microvacuolation occurred after reperfusion for 3 h. Electron-dense clumping of neuronal perikarya was observed after reperfusion for 6 h particularly in layers III and Vb, which increased in number for up to 72 h. The observed progressive damage in dendrites may be common to neurons vulnerable to cerebral ischemia and may significantly contribute to development of delayed neuronal death.     

Protein aggregation after focal brain ischemia and reperfusion.

Two hours of transient focal brain ischemia causes acute neuronal death in the striatal core region and a somewhat more delayed type of neuronal death in neocortex. The objective of the current study was to investigate protein aggregation and neuronal death after focal brain ischemia in rats. Brain ischemia was induced by 2 hours of middle cerebral artery occlusion. Protein aggregation was analyzed by electron microscopy, laser-scanning confocal microscopy, and Western blotting. Two hours of focal brain ischemia induced protein aggregation in ischemic neocortical neurons at 1 hour of reperfusion, and protein aggregation persisted until neuronal death at 24 hours of reperfusion. Protein aggregates were found in the neuronal soma, dendrites, and axons, and they were associated with intracellular membranous structures during the postischemic phase. High-resolution confocal microscopy showed that clumped protein aggregates surrounding nuclei and along dendrites were formed after brain ischemia. On Western blots, ubiquitinated proteins (ubi-proteins) were dramatically increased in neocortical tissues in the postischemic phase. The ubi-proteins were Triton-insoluble, indicating that they might be irreversibly aggregated. The formation of ubi-protein aggregates after ischemia correlated well with the observed decrease in free ubiquitin and neuronal death. The authors concluded that proteins are severely damaged and aggregated in neurons after focal ischemia. The authors propose that protein damage or aggregation may contribute to ischemic neuronal death.     

Target-specific differences in somatodendritic morphology of layer V pyramidal neurons in rat motor cortex

Dendritic geometry has been shown to be a critical determinant of information processing and neuronal computation. However, it is not known whether cortical projection neurons that target different subcortical nuclei have distinct dendritic morphologies. In this study, fast blue retrograde tracing in combination with intracellular Lucifer yellow injection and diaminobenzidine (DAB) photoconversion in fixed slices was used to study the morphological features of corticospinal, corticostriatal, and corticothalamic neurons in layer V of rat motor cortex. Marked differences in the distribution of soma, somal size, and dendritic profiles were found among the three groups of pyramidal neurons. Corticospinal neurons were large, were located in deep layer V, and had the most expansive dendritic fields. The apical dendrites of corticospinal pyramidal neurons were thick, spiny, and branched. In contrast, nearly all corticostriatal neurons were small cells located in superficial layer V. Their apical dendritic shafts were significantly more slender, though spiny like those of corticospinal neurons. Corticothalamic neurons, which were located in superficial layer V and in layer VI, had small or medium-sized soma, slender apical dendritic shafts, and dendrites that were largely spine free. This study indicates that, in layer V of rat motor cortex, each population of projection neurons has a unique somatodendritic morphology and suggests that distinct modes of cortical information processing are operative in corticospinal, corticostriatal, and corticothalamic neurons.     

Immunohistochemical localization of a membrane-associated, 4.1-like protein in the rat visual cortex during postnatal development

Expression and localization of a membrane-associated protein, an analog of erythrocyte protein 4.1, in the visual cortex were immunohistochemically studied in the rat, ranging in age from newborn to adult. In the adult, dendrites and somas of layer V pyramidal cells were stained by the antiprotein 4.1 antibody. In most of these immunoreactive neurons, the plasma membrane seemed to be preferentially stained. Neurons located in layers II and III of the cortex were only faintly stained, and those in layers IV and VI were not stained. At birth, the immunoreactivity was already present in pyramidal cells located in the upper part of the cortical subplate. Immature neurons located in the cortical plate were not stained by the antibody, suggesting that the 4.1-like protein is expressed only in the neurons that have differentiated or are differentiating. At postnatal days 2-8, immunoreactive neurons were dramatically increased in layers V and VI and intense labeling was seen at the apical dendrites of layer V pyramidal cells. Most of the stained processes of these and other neurons showed a sign of rapid dendritic growth, i.e., growth cones and filopidia. At days 10-17, the basal dendrites of pyramidal cells in layers II and III became detectable, although still slender. At days 20-37, these dendrites in layers II, III, and V became intensely immunoreactive, and dendritic spines were visualized by the antibody. Throughout all the ages, axons of neurons and neuroglia were not stained by the antibody. Also, most of the neurons in layer IV of the cortex were not immunoreactive. These results suggest that the 4.1-like protein is abundantly expressed in growing parts of the dendrites and spines. A hypothesis that this protein may play a role in synaptic plasticity in the developing visual cortex is discussed.     

Interlaminar connections and pyramidal neuron organisation in the visual cortex,area 17, of the Macaque monkey

The patterns of arborisation of apical dendrites of different varieties of pyramidal neurons in area 17 differ and are characteristic for each cell type. They appear to serve as a means of collating within one neuron information derived directly from several different laminae. These different patterns of apical dendrite arborisation provide dendritic links which relate closely to the laminar distribution of axons of the spiny stellate neurons as well as the pyramidal neurons themselves. The axons of spiny stellate neurons lying in laminae IVCβ and IVA (Lund, '73)—Which receive information from parvocellular geniculate layers — project heavily to the lower half of lamina III (IIIB) and to a narrow zone at the top of lamina V (VA); laminae IIIB and VA are in turn linked by a specific variety of pyramidal neuron, with basal dendritic field in lamina VI, whose apical dendrite has marked lateral branching only in laminae VA and IIIB (where it terminates). Pyramidal neurons with basal dendritic field in laminae VA (with vestigial apical dendrite) or in IIIB have recurrent axon projections to lamina IIIA and above (the descending axon projection of lamina IIIB pyramids is principally to lamina VA itself). The pyramidal neurons of laminae IIIA and above have axons which distribute in the same upper laminae as their dendtritic fields and a descending axon projection to lamina VB. Pyramidal neurons with basal dendritic field on lamina VB have an apical dendrite which, if not vestigal, arborises in IIIA or above; their axons in some cases project to the superior colliculus or may be exclusively, or in addition, recurrent, distributing collaterals within laminae VB, VI and in IIIA or above; one variety of pyramidal neuron with basal dentritic field in lamina VI makes a dentritic link with these same regions, its apical dendrite arborising first within lamina VB and then in lamina IIIA and above. Axons of spiny stellate neurons of lamina IVCα (which receives the projection of the magnocellular layers of the lateral geniculate nucleus) as well as distributing widely within lamina IVCα also contribute to laminae IVB and VA; a link is again made by a specific variety of pyramidal neuron, with basal dendtritic field in lamina VI, which shows branching to its apical dendtrite only in laminae VA and as a terminal arborisation in IVCα. Another variety of pyramidal neuron with basal dendtric field in lamina VI has apical dendritic arborisation only in lamina IVB. The pyramidal neurons with basal dendritic field in lamina IVB and apical dendrite arborising in lamina IIIB and above, also contribute axonal collatetrals to lamina IIIA and above; their horizontal axon collaterals, together with the axons of spiny stellate neurons of laminae IVCα and IVB, form the horizontal fiber band of lamina IVB (to which the axons of laminae III and II pyramidal neurons do not contribute. The descending axon projection of the spiny stellate and pyramidal neurons of lamina IVB appears to be principally to lamina VI. The pattern of branching of pyramidal neuron apical dendrites is therefore neither random nor a continuum of one basic pattern; instead it is a series of separate patterns, each spatially distributed in a highly specific and unique fashion relating to the patterns of projection of afferent information through the 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.     

Persistent astroglial swelling accompanies rapid reversible dendritic injury during stroke-induced spreading depolarizations

Spreading depolarizations are a key event in the pathophysiology of stroke, resulting in rapid dendritic beading, which represents acute damage to synaptic circuitry. The impact of spreading depolarizations on the real‐time injury of astrocytes during ischemia is less clear. We used simultaneous in vivo 2‐photon imaging and electrophysiological recordings in adult mouse somatosensory cortex to examine spreading depolarization‐induced astroglial structural changes concurrently with signs of neuronal injury in the early periods of focal and global ischemia. Astrocytes in the metabolically compromised ischemic penumbra‐like area showed a long lasting swelling response to spontaneous spreading depolarizations despite rapid dendritic recovery in a photothrombotic occlusion model of focal stroke. Astroglial swelling was often facilitated by recurrent depolarizations and the magnitude of swelling strongly correlated with the total duration of depolarization. In contrast, spreading depolarization‐induced astroglial swelling was transient in normoxic healthy tissue. In a model of transient global ischemia, the occurrence of a single spreading depolarization elicited by a bilateral common carotid artery occlusion coincided with astroglial swelling alongside dendritic beading. With immediate reperfusion, dendritic beading subsides. Astroglial swelling was either transient during short ischemic periods distinguished by a short‐lasting spreading depolarization, or persistent during severe ischemia characterized by a long‐lasting depolarization with the ultraslow negative voltage component. We propose that persistent astroglial swelling is initiated and exacerbated during spreading depolarization in brain tissue with moderate to severe energy deficits, disrupting astroglial maintenance of normal homeostatic function thus contributing to the negative outcome of ischemic stroke as astrocytes fail to provide neuronal support. © 2012 Wiley Periodicals, Inc.     

The dendritic architecture of prefrontal pyramidal neurons in schizophrenic patients

Despite a considerable number of investigations revealing the prefrontal cortex (PFC) to be a major site of pathological changes in schizophrenia, the neuronal basis of these alterations is still unknown. We used a 3-D image analysis technique to investigate the dendritic arborization of Golgi-impregnated prefrontal pyramidal neurons in schizophrenic patients and controls. While the apical dendrites were found to be unchanged in schizophrenics, the basilar dendritic systems were markedly reduced in the patient group. A segment analysis showed that the observed alterations were mainly confined to distal dendritic segments. The dendritic changes are likely to be associated with specific dysfunctions of prefrontal circuitry and point to the pathogenetical relevance of pre- and perinatal disturbances of PFC maturation in schizophrenic patients.     

Effects of early postnatal receptor damage on dendritic development in gustatory recipient zones of the rostral nucleus of the solitary tract.

The rostral gustatory zone of the nucleus of the solitary tract (NST) exhibits extensive anatomical development during the first 3 weeks of postnatal life, and this development requires the presence of intact gustatory receptors during a critical period. We have previously shown that unilateral damage induced to fungiform papillae of the anterior tongue at postnatal day 2 (P2) alters normal migration and ramification of chorda tympani (CT) axons in the rostral NST. In addition to alterations of axonal development, P2 receptor damage decreases the intraneuronal distance between neurons that project axons to the second-order central gustatory relay, located in the caudal parabrachial nucleus (PBN). This observation suggested that P2 receptor damage may alter both axonal development and dendritic development in the rostral gustatory NST. The present study evaluated potential changes in dendritic development of PBN projection neurons following either P2 or P10 receptor damage. Morphological studies were first conducted to quantitatively define somatic characteristics of neurons that project axons to the PBN. Independent experiments used fluorescent labeling combined with subsequent Golgi-impregnation to study dendritic architecture of identified PBN projection neurons. Results confirmed that P2 receptor damage alters dendritic development of PBN projection neurons located in CT terminal fields. Anterior tongue receptor damage at P2 (1) reduces planar length of first- and second-order dendritic branches, (2) reduces the mean number of second-order branches per neuron, and (3) reduces the density of spine processes on second-order dendritic branches. A critical period exists for these effects, similar to that reported for axonal development, insofar as P2 receptor damage alters dendritic development of PBN projection neurons, whereas P10 receptor damage does not. Dendrites of identified PBN projection neurons located in regions of the NST that receive primary afferent axons from the glossopharyngeal nerve are not affected by anterior tongue damage at P2. These results show that early postnatal receptor damage influences both pre- and postsynaptic development in the rostral gustatory NST. These anatomical changes are undoubtedly related to alterations in taste-guided behaviors that are observed following P2 receptor damage.     

Transneuronally altered dendritic processing of tangle-free neurons in Alzheimer's disease

In Alzheimer's disease (AD), changes in dendritic morphology can be regarded as a result of an inherent disease-specific process associated with the formation of neurofibrillary tangles. Using three-dimensional morphometrical techniques and neuropatholologically staged tissue (Braak classification) of 32 cases, we demonstrate alterations in the dendritic length, branch order and number of segments of a tangle-free neuronal population in the AD-afflicted hippocampus, i.e. parvalbumin-containing cells of the fascia dentata. These alterations occurred primarily on the apical dendritic tree, the target of the entorhinal input. Mean of relative dendritic length, branch order and number of dendritic segments of apical dendrites decreased significantly, by 40-70% comparing stage V to stages 0 or I. In contrast, basal dendrites receiving no entorhinal input did not show significant changes. Entorhinal neurons projecting to the hippocampus are the first to be affected in AD and the first to die, resulting in hippocampal deafferentation. Therefore, this input-specific dendritic alteration of tangle-free neurons suggests that AD is confounded with a transneuronal component resulting from deafferentation. Experiments showed that deafferentation results in altered dendritic geometry causing an impaired signal integration. Thus, transneuronally altered dendritic signal integration might occur in neurons devoid of the major intraneuronal hallmark of AD, i.e. the neurofibrillary tangle.     

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.     

Longitudinal in vivo imaging reveals balanced and branch-specific remodeling of mature cortical pyramidal dendritic arbors after stroke

The manner in which fully mature peri-infarct cortical dendritic arbors remodel after stroke, and thus may possibly contribute to stroke-induced changes in cortical receptive fields, is unknown. In this study, we used longitudinal in vivo two-photon imaging to investigate the extent to which brain ischemia can trigger dendritic remodeling of pyramidal neurons in the adult mouse somatosensory cortex, and to determine the nature by which remodeling proceeds over time and space. Before the induction of stroke, dendritic arbors were relatively stable over several weeks. However, after stroke, apical dendritic arbor remodeling increased significantly (dendritic tip growth and retraction), particularly within the first 2 weeks after stroke. Despite a threefold increase in structural remodeling, the net length of arbors did not change significantly over time because dendrite extensions away from the stroke were balanced by the shortening of tips near the infarct. Therefore, fully mature cortical pyramidal neurons retain the capacity for extensive structural plasticity and remodel in a balanced and branch-specific manner.