Motoneuronal pools of muscles that subservepostural tasks contain dendrite bundles. Weinvestigated in the rat the development of thesebundles in the pools of the long back muscles andrelated this to postural development. Motoneuronsand their dendrites were retrogradelylabeled by injecting unconjugated cholera toxinsubunit B (CTB) into the muscles of 54 normalrats from birth until adulthood and into 18 ratsthat were vestibularly deprived from the 5thpostnatal day (P5). Dendrite bundles coursing ina transverse direction already occurred at P1.From P4, the first longitudinal bundles could beobserved, but the major spurt in developmentoccurred between P6 and P9, when conspicuousbundles developed coursing in rostro-caudal andtranverse directions. This is the age when ratsbecome able to stand freely and walk a few steps.Around P20, the dendrite bundles attained theiradult characteristics. Vestibular deprivation byplugging both semicircular horizontal canals didnot lead to a retarded development of dendritebundles nor to a changed morphology. Thisfinding is remarkable, as behavioral analysis showed a delay in postural development byabout 3 days. We hypothesize that dendritebundles in the pools of the long back musclesfunction to synchronize the motoneurons indifferent spinal cord segments.

Hildegard C. Geisler

Jos  IJkema-Paassen

Johan  Westerga

Albert  Gramsbergen

Vestibular Deprivation and the Development of Dendrite Bundles in the Rat

In this.study, we attempted to test whether
tyrosine hydroxylase (TH), the first ratelimiting
enzyme of catecholamine synthesis, is
confined to the perikarya of activated magnocellular
vasopressinergic (VPergic) neurons or
is also present in their distal axons in the
pituitary posterior lobe (PL). In addition, we
evaluated the possible correlation between TH
and VP turnover in the axons of rats drinking
2% NaCl for 1, 2, and 3 weeks. To this aim, we
examined the large swellings of VPergic axons,
the so-called Herring bodies, using the doubleimmunofluorescent
technique and the avidinbiotin
technique, combined with image analysis.
Here we have demonstrated for the first time a
colocalization of TH and VP in Herring bodies,
which is a strong argument in favor of TH
transport from the perikarya of VPergic
neurons via axons toward their terminals. THimmunoreactive
(IR) and VP-IR materials were distributed in Herring bodies with seeming
zonality. The number of VP-IR Herring bodies
decreased by a factor of four over the first week
of osmotic stimulation, remaining at almost the
same low level until the end of the experiment.
Conversely, the content of the VP-IR material
within the individual Herring bodies fell
gradually during the three weeks of saltloading.
The results suggest that VP depletion
from Herring bodies prevails in its transport
into these structures during the whole period of
osmotic stimulation. In contrast to VP-IR
Herring bodies, the number of TH-IR Herring
bodies and the content of TH-IR material
within the individual Herring bodies increased
progressively during the entire experiment. The
synchronization of the VP depletion and TH
accumulation in Herring bodies during longterm
osmotic stimulation raised the question
about a possible functional interaction between
both substances.

Marina Abramova

André Calas

Jean Thibault

Michael Ugrumov

Tyrosine Hydroxylase in Vasopressinergic Axons of the Pituitary Posterior Lobe of Rats Under Salt-Loading as a Manifestation of Neurochemical Plasticity

Synaptic response size in the CA1 region ofthe hippocampus in aged rats is reduced for agiven stimulus intensity, compared with thatelicited in young rats. Consistent with the in vitrofindings of reduced Schaffer collateral-evokedCA1 EPSPs in old rats, the population currentsevoked to iontophoretically applied AMPA arealso smaller relative to the presynaptic fiberpotential amplitude. On the other hand, the size ofthe presynaptic fiber potential and amplitude ofunitary intra-cellularly recorded EPSP responsesdo not change across age in the CA1 region. Theseelectrophysiological findings are consistent withthe hypothesis that old rats have fewer functionalsynaptic contacts per Schaffer collateral axonthan do young rats. The possibility that this agechange arises as a result of a differential tissuerecovery response to in vitro preparation wasexamined in the present study. CA1 presynapticfiber potential and EPSP amplitudes evoked bythe stimulation of Schaffer collateral afferentswere studied in intact, freely behaving youngand old rats. We confirmed in vivo the pattern of electrophysiophysiological results previouslyreported in vitro and found significantcorrelations between the synaptic responseamplitudes and the accuracy of spatial behaviorin the Morris swim task. The data suggest thatchanges in functional connectivity of old ratsmay be a significant contributor to cognitivechanges during aging.

C. A. Barnes

G.  Rao

G.  Orr

Age-Related Decrease in the Schaffer Collateral-Evoked EPSP in Awake, Freely, Behaving Rats

In this study we investigate the capability of
lesions, performed between embryonic day E18
and postnatal day P6, to provoke glial reaction.
Two different lesion types were applied: ‘severe’
lesion (tissue defect) and ’light’ lesion (stab
wound). The glial reaction was detected with
immunostain[ng against glial fibrillary acidic
protein. When performed as early as P0, severe
lesions could result in reactive gliosis, which
persisted even after a month. The glial reaction
was detected at P6/P7 and became strong by P8,
regardless of the age when the animals were
lesioned between P0 and P5. Namely, a strict
limit could be estimated for the age when
reactive glia were already found rather than for
the age when glial reaction-provoking lesions
could occur. After prenatal lesions, no glial
reaction developed, but the usual glia limitans
covered the deformed brain, surface. Light
lesions provoked glial reactions when
performed at P6. In conclusion, three scenarios
were found, depending on the age of the animal
at injury: (i) healing without glial reaction,
regardless of the remaining deformation; (ii) depending on the size of the lesion, either healing without residuum or with remaining
tissue defect plus reactive gliosis; and (iii) healing always with reactive gliosis. The age limits between them were at P0 and P5. The glial reactivity seemingly appears after the end of the neuronal migration and just precedes the massive transformation of the radial glia into astrocytes. Estimating the position of the appearance of glial reactivity among the events of cortical maturation can help to adapt the experimental results to humans.

Mihály Kálmán

Béla M. Ajtai

Jon Håvard Sommernes

Characteristics of Glial Reaction in the Perinatal Rat Cortex: Effect of Lesion Size in the ‘Critical Period’

Amy F. T. Arnsten

Through the Looking Glass: Differential Noradenergic Modulation of Prefrontal Cortical Function

Robert T. Knight

Neural Mechanisms of Attention: The Northern California Years

Measurements of oxidative metabolic
capacity following the ablation of rat sensorimotor
cortex and ,he administration of amphetamine
were examined to determine their
effects on the metabolic dysfunction that
follows brain injury. Twenty-four hours after
surgery, rats sustaining either sham operations
or unilateral cortical ablation were administered
a single injection of D-amphetamine (2 mg/kg;
i.p.) or saline and then sacrificed 24 h later.
Brain tissue was processed for cytochrome
oxidase histochemistry, and 12 bilateral cerebral
areas were measured, using optical density as
an index of the relative amounts of the
enzyme. Compared with that of the control
groups, cytochrome oxidase in the injured
animals was significantly reduced throughout
the cerebral cortex and in 5 of II subcortical
structures. This injury-induced depression of
oxidative capacity was most pronounced in
regions of the hemisphere ipsilateral to the
ablation. Animals given D-amphetamine had less depression of oxidative capacity, which
was most pronounced bilaterally in the cerebral
cortex, red nucleus, and superior colliculus;
and in the nucleus accumbens, caudateputamen,
and globus pallidus ipsilaterai to the
ablation. The ability of D-amphetamine to
alleviate depressed cerebral oxidative metabolism
following cortical injury may be one mechanism
by which drugs increasing noradrenaline
release accelerate functional recovery in both
animals and humans.

Richard L. Sutton

David A. Hovda

Michael J. Chen

Dennis M. Feeney

Alleviation of Brain Injury-Induced Cerebral Metabolic Depression by Amphetamine: A Cytochrome Oxidase Histochemistry Study

Intracerebral grafting techniques of fetal
neural cells have been used essentially with
two main types of lesion paradigms, namely
damage to long projection systems, in which
the source and the target are clearly separate,
and damage to neurons that are involved in
local circuits within a small (sub)region of the
brain. With the’first lesion paradigm, grafts
placed homotopically (in the source) are not
appropriate because their fibers grow poorly
through the host parenchyma and fail to reach
their normal target. To be successful, the
grafts must be placed ectopically in the target
region of the damaged projection systems,
where generally they work as level-setting
systems. Conversely, with the second paradigm,
the grafts are supposed to compensate for a
local loss of neurons and must be placed
homotopically to induce functional effects that
are based on the reconstruction of a point-to-point
circuitry. By inserting a biological or
artificial bridging-substrate between the source
and the target of long projection systems, it
might be possible to combine the positive
effects of both homotopic and ectopic grafting
by achieving both target reinnervation and
normal control of the grafted neurons within
the source area. These issues are illustrated
and discussed in this review.

Bruno Will

Christian Kelche

Jean-Christophe Cassel

Intracerebral Transplants and Memory Dysfunction: Circuitry Repair or Functional Level Setting?

About this journal

Neural Plasticity is an interdisciplinary journal dedicated to the publication of articles related to all aspects of neural plasticity, with special emphasis on its functional significance as reflected in behavior and in psychopathology.

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Chief Editor, Professor Baudry, is currently University Professor at Western University of Health Sciences in Pomona, CA. His research focuses on understanding the molecular/cellular mechanisms of learning and memory and neurodegeneration.

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Neural Plasticity - Table of contents 2000

title

Neural Plasticity is an interdisciplinary journal dedicated to the publication of articles related to all aspects of neural plasticity, with special emphasis on its functional significance as reflected in behavior and in psychopathology.

Neural Plasticity