bluuebunny/crossref_metadata_2025 huggingface dataset:
Minor Immunoreactivity in GDNF‐, BDNF‐, or NT‐3‐Treated Substantia Nigra Allografts
Authors: Shinoda Masaki , Hoffer Barry J. , Olson Lars
Published: March 2007

Glial‐cell‐line‐derived neurotrophic factor (GDNF) stimulates the survival of dopaminergic neurons. Little is known, however, about the possible immune sequelae of GDNF exposure or of exposure to other putative trophic factors. To address these questions, pieces of mesencephalic tissue, substantia nigra, from 15‐day‐old donor embryos were transplanted into the anterior chamber of the eye of adult male Sprague‐ Dawley recipient rats. At 5‐day intervals, an aliquot (0.5 µg) of GDNF, brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 (NT‐3), or cytochrome‐C (CC) was injected into the anterior chamber of the eye of the recipients, and the sizes of the transplants were measured. GDNF increased transplant survival and growth. On day 42, all rats were sacrificed, and the grafts were evaluated by cresyl‐violet staining and by immunohistochemistry using antibodies raised against neurofilament (NF), tyrosine hydroxylase, or glial fibrillary acidic
protein (GFAP), as well as the following monoclonai antibodies: OX‐38 anti‐CD4, OX‐8 anti‐CD8, OX‐18 anti‐MHC class I, OX‐6 anti‐ MHC class II, OX‐42 anti‐CD11b, R‐73 anti‐a and anti‐ß T‐cell receptor, and EDI raised against monocytes/macrophages. BDNF‐treated grafts showed only weak immunoreactivity, and even weaker reactions were seen in grafts treated with NT‐3, GDNF, or CC. No single immune system marker was significantly elevated in grafts from any treatment group. We used OX‐42 and EDI to study possible alterations of microglial components. Ramified microglial cells were found in GDNF‐treated grafts and to a lesser extent in NT‐3 and BDNF‐treated grafts. EDl‐labeled reactive microglial components were found in NT‐3‐ and BDNF‐treated grafts. Additionally, large and rounded OX‐42‐positive phagocytic cells were found in NT‐3‐treated grafts. Together with our previous finding that GDNF treatment of spinal cord transplants activates immune responses and leads to microglial activation, our data dempnstrate that although treatment with GDNF and to some degree with BDNF can enhance immune responses to immunogenic grafts, such as fetal spinal cord grafts, but the trophic factors per se do not elicit any marked response in non‐immunogenic grafts like substantia nigra.
CREB Activation Mediates Plasticity in Cultured Hippocampal Neurons
Authors: Segal Menahem , Murphy Diane D.
Published: March 2007

Activation of cyclic AMP dependent kinase is believed to mediate slow onset, long‐term potentiation (LTP) in central neurons. Cyclic‐
AMP activates a cascade of molecular events leading to phosphorylation of the nuclear cAMP responsive element binding protein (pCREB).
Whereas a variety of stimuli lead to activation of CREB, the molecular processes downstream of CREB, which may be relevant to neuronal
plasticity, are yet largely unknown. We have recently found that following exposure to estradiol, pCREB mediates the large increase in dendritic spine density in cultured rat hippocampal neurons. We now extend these observations to include other stimuli, such as
bicuculline, that cause the formation of new dendritic spines. Such stimuli share with estradiol the same mechanism of action in that both require activity‐dependent CREB phosphorylation. Our observations suggest that CREB phosphorylation is a necessary, but
perhaps not sufficient, step in the process leading to the generation of new dendritic spines and perhaps to functional plasticity as well.
Differential Emotional Experience Leads to Pruning of Dendritic Spines in the Forebrain of Domestic Chicks
Authors: Bock Jörg , Braun Katharina
Published: March 2007

Auditory filial imprinting induces quantitative changes of synaptic density in the forebrain area mediorostral neostriatum/hyperstriatum ventrale of the domestic chick. The aim of the present study was to examine the time window and the extent and quality of experience that is required for the induction of these synaptic changes. We found that a brief (30 min) experience with the imprinting situation (tone stimulus + mother surrogate) is sufficient to induce spine elimination, which is detectable
on postnatal day 7, but not 80 min after the presentation of the imprinting stimuli. This synaptic reorganization requires the association of the acoustic imprinting tone with an emotional reward (mother surrogate); acoustic stimulation alone does not lead to detectable synaptic changes. The results of the present study provide further evidence that juvenile emotional learning events, such as filial imprinting, lead to a selective synaptic reorganization.
Consolidation of Memory After its Reactivation: Involvement of ß Noradrenergic Receptors in the Late Phase
Authors: Roullet Pascal , Sara Susan
Published: March 2007

Evidence is growing that the cAMP pathway through the cAMP responsive element binding protein (CREB) transcription factor plays an important role in long‐term memory formation (LTM). To study the role of ß‐noradrenergic receptors, positively linked to the cAMP secondmessenger system, in the dynamics of LTM processes, we used a memory‐reactivation paradigm because recent studies in our laboratory confirmed that reactivated memory is labile and undergoes an extended reconsolidation process. In an eight‐arm maze, rats were trained to choose the same three baited arms; 24 hr later, memory was reactivated and then the rats were injected intracerebroventricularly at 5 min, 30 min, 60 min, or 5 hr later with the ß‐antagonist timolol or with saline. The results showed that injection of timolol induced amnesia only at the 60 min post‐reactivation interval, whereas all control groups and groups that were timolol‐injected at other post‐reactivation intervals displayed optimal retention. The delayed amnesic action of timoloi suggests that ß noradrenergic receptors and the cAMP cascade are implicated in the late phase of reprocessing of a remembered event.
Integrated Regulation of Signal Coding and Plasticity by NMDA Receptors at a Central Synapse
Authors: D′Angelo Egidio , Rossi Paola
Published: March 2007

The role of NMDA and non‐NMDA glutamate receptors in long‐term potentiation has been intensely investigated, yet recent evidence on the dynamics of synaptic depolarization suggests that the original view should be extended. NMDA receptor‐mediated currents, apart from their Ca2+
permeability, show a marked voltage dependence, consisting of current increase and slowdown during membrane depolarization. During highfrequency synaptic transmission, NMDA current increase and slowdown are primed by non‐NMDA receptor‐dependent depolarization and proceed regeneratively. Thus, NMDA receptors make a decisive contribution to membrane depolarization and spike‐firing. From the data obtained at the mossy fiber‐ granule cell synapse of the cerebellum, we propose that the electrogenic role of NMDA receptors is functional to LTP induction. Moreover, during LTP, both NMDA and non‐ NMDA receptor currents are potentiated, thus establishing a feed‐forward mechanism that ultimately enhances spike firing. Thus, NMDA receptors exert an integrated control on signal coding and plasticity. This mechanism may have important implications for information processing at the cerebellar mossy fibergranule cell relay.
Fetal Spinal Cord Tissue in Mini‐Guidance Channels Promotes Longitudinal Axonal Growth after Grafting into Hemisected Adult Rat Spinal Cords
Authors: Bamber Norman I. , Li Huaying , Aebischer Patrick , Xu Xiao Ming
Published: March 2007

Solid fetal spinal cord (FSC) tissue, seeded into semipermeable mini‐guidance channels, was tested for the ability to promote axonal
growth across the gap created by a midthoracic (T8) hemisection in adult rats. Fetal thoracic spinal cords, at embryonic days 13 to
15, were harvested and gently aspirated into mini‐guidance channels (1.25 mm in diameter and 3.0 mm in length). Care was taken to
maintain the rostro‐caudal orientation of the FSC. In control rats, the FSC‐channel congraft struct was exposed to 5 freeze/thaw cycles to
produce non‐viable grafts before implantation into the hemisected cord. All cases revealed intact tissue cables of various diameters spanning the rostro‐caudal extent of the lesion cavity, with integration of host‐graft tissues at both interfaces. Immunofluorescence results
indicated that numerous neurofilament‐positive axons were present within the FSC tissue cable. Double‐labeling of a subpopulation of these axons with calcitonin generelated peptide indicated their peripheral nervous system (PNS) origin. Descending serotonergic and noradrenergic axons were found in the proximity of the rostral host‐graft interface, but were not observed to grow into the FSC‐graft. Anterograde tracing of propriospinal axons with Phaseolus vulgaris‐leucoagglutinin demonstrated that axons had regenerated into the FSC‐graft and had traveled longitudinally to the distal end of the channel. Few axons were observed to cross the distal host‐graft interface to enter the host spinal cord. Cross‐sectional analysis at the midpoint of the tissue cable stained with toluidine blue demonstrated a significant increase (P<0.01) in myelinated axons in viable FSC grafts (1455±663, mean±S.E.M.; n=6) versus freeze‐thaw control grafts (155±50; n=5). In addition to the myelinated axons, many unmyelinated axons were observed in the tissue cable at the electron microscopic level. Areas resembling the PNS with typical Schwann cells, as well as those resembling the central nervous system with neurons and central neuropil, were also seen. In freeze‐thaw control grafts, neither viable neurons nor central neuropil were observed. Retrograde tracing with Fast Blue and Diamidino Yellow demonstrated that neurons within the FSC graft extended axons into the host spinal cord at least for 2 mm from both the rostral and caudal host‐graft interfaces. We conclude that viable FSC grafts within semipermeable guidance channels may serve both as a permissive bridge for longitudinally directed axonal growth and a potential relay for conveying information across a lesion site in
the adult rat spinal cord.
Comparison of the Effects of Electrolytic and Chemical Destruction of the Red Nucleus on the Compensatory Capacity of Rats With Rubrospinal Tract Lesions
Authors: Fanardjian V. V. , Papoyan E. V. , Pogossian V. I. , Gevorkyan O. V.
Published: March 2007

Transection of the rubrospinal tract in rats, performed before lesion of the red nucleus, resulted in the facilitated recovery of motor
activity and operantly conditioned reflexes. Such facilitation was absent when the red nucleus is lesioned alone. This phenomenon is
explained by the switching of descending influences on the corticospinal tract through the participation of the following system: red nucleus—inferior olive—cerebellum—ventrolateral thalamic nucleus—cerebral cortex. The above mentioned facilitating influence on the recovery process was particularly prominent in rats with quinolinic acid‐induced lesion of the red nucleus. Under these conditions, the cerebellar ascending fibers to the ventrolateral thalamic nucleus were preserved. Decreased facilitated recovery following electrolytic lesion of the red nucleus suggests the existence of additional cerebello‐cortical pathways for the realization of the switching phenomenon.
Response Features Determining Spike Times
Authors: Richmond Barry J. , Oram Mike W. , Wiener Matthew C.
Published: March 2007

Interpreting messages encoded in single neuronal responses requires knowing which features of the responses carry information.
That the number of spikes is an important part of the code has long been obvious. In recent years, it has been shown that modulation of the
firing rate with about 25 ms precision carries information that is not available from the total number of spikes across the whole response. It
has been proposed that patterns of exactly timed (1 ms precision) spikes, such as repeating triplets or quadruplets, might carry information that is not available from knowing about spike count and rate modulation. A model using the spike count distribution, the low pass
filtered PSTH (bandwidth below 30 Hz), and, to a small degree, the interspike interval distribution predicts the numbers and types of
exactly‐timed triplets and quadruplets that are indistinguishable from those found in the data. From this it can be concluded that the coarse
(<30 Hz) sequential correlation structure over time gives rise to the exactly timed patterns present in the recorded spike trains. Because the coarse temporal structure predicts the fine temporal structure, the information carried by the fine temporal structure must be completely
redundant with that carried by the coarse structure. Thus, the existence of precisely timed spike patterns carrying stimulus‐related information does not imply control of spike timing at precise time scales.
Temporal Coding of Periodicity Pitch in the Auditory System: An Overview
Authors: Cariani Peter
Published: March 2007

This paper outlines a taxonomy of neural pulse codes and reviews neurophysiological evidence for interspike interval‐based representations for pitch and timbre in the auditory nerve and cochlear nucleus. Neural pulse codes can be divided into channel‐based codes, temporal‐pattern codes, and time‐of‐arrival codes. Timings of discharges in auditory nerve fibers reflect the time structure of
acoustic waveforms, such that the interspike intervals that are produced precisely convey information concerning stimulus periodicities.
Population‐wide inter‐spike interval distributions are constructed by summing together intervals from the observed responses of many single Type I auditory nerve fibers. Features in such distributions correspond closely with pitches that are heard by human listeners. The most common all‐order interval present in the auditory nerve array almost invariably corresponds to the pitch frequency, whereas the relative fraction of pitchrelated intervals amongst all others qualitatively corresponds to the strength of the pitch. Consequently, many diverse aspects of pitch perception are explained in terms of such temporal representations. Similar stimulus‐driven temporal discharge patterns are observed in major neuronal populations of the cochlear nucleus. Population‐interval distributions constitute an alternative time‐domain strategy for representing sensory information that complements spatially organized sensory maps. Similar autocorrelation‐like representations are possible in other sensory systems, in which neural discharges are time‐locked to stimulus waveforms.
Intrinsic and Extrinsic Neuronal Mechanisms in Temporal Coding: A Further Look at Neuronal Oscillations
Authors: Lestienne Rémy
Published: March 2007

Many studies in recent years have been devoted to the detection of fast oscillations in the Central Nervous System (CNS), interpreting
them as synchronizing devices. We should, however, refrain from associating too closely the two concepts of synchronization and oscillation. Whereas synchronization is a relatively well‐defined concept, by contrast oscillation of a population of neurones in the
CNS looks loosely defined, in the sense that both its frequency sharpness and the duration of the oscillatory episodes vary widely from
case to case. Also, the functions of oscillations in the brain are multiple and are not confined to synchronization. The paradigmatic instantiation of oscillation in physics is given by the harmonic oscillator, a device particularly suited to tell the time, as in clocks. We will thus examine first the case of oscillations or cycling discharges of neurones, which provide a clock or impose a “tempo” for various kinds of information processing. Neuronal oscillators are rarely just clocks clicking at a fixed frequency. Instead, their frequency is often adjustable and controllable, as in the example of the “chattering cells” discovered in the superficial layers of the visual cortex. Moreover, adjustable frequency oscillators are suitable for use in “phase locked loops” (PLL) networks, a device that can convert time coding to frequency coding; such PLL units have been found in the somatosensory cortex of guinea pigs. Finally, are oscillations stricto sensu necessary to induce synchronization in the discharges of downstream neurones? We know that this is not the case, at least not for local populations of neurones. As a contribution to this question, we propose that repeating patterns in neuronal discharges production may be looked at as one such alternative solution in relation to the processing of information. We review here the case of precisely repeating triplets, detected in the discharges of olfactory mitral cells of a freely breathing rat under odor stimulation.
Pretreatment With Fragments of Substance‐P or With Cholecystokinin Differentially Affects Recovery From Sub‐Total Nigrostriatal 6‐Hydroxydopamine Lesion
Authors: Nikolaus S. , Huston J. P. , Schwarting R. K. W.
Published: March 2007

The neuropeptide substance P is known to have mnemogenic and reinforcing actions and can exert neurotrophic and regenerative
effects in vitro as well as in vivo. Furthermore, our previous work in the rat showed that either pre‐ or post‐lesion treatment with
substance P can promote functional recovery in cases of partial nigrostriatal dopamine lesions. Other work has provided evidence that the effects of substance P might be differentially encoded by its C‐ and N‐terminal fragments. The C‐terminal fragment was found to be reinforcing, whereas the mnemogenic as well as neurotrophic properties have been ascribed to the N‐terminal sequences. Given these relations, we asked here whether pre‐lesion treatment with either a C‐ or an N‐terminal fragment of substance P might differentially affect the behavioral and neurochemical outcome of nigrostriatal dopamine lesions. Therefore, either substance
P1−7 or substance P5−11
(37 nmol/kg each) was administered intraperitoneally daily for eight consecutive days before unilateral 6‐hydroxy‐dopamine lesions of the substantia nigra. Control rats received prelesion treatment with vehicle. Furthermore, we investigated the effects of pre‐treatment with Boc‐cholecystokinin‐4 (0.91 nmol/kg), as we had found an increase in dopamine metabolism in animals that were pre‐treated with cholecystokinin‐8 in a former study. In accordance with our previous work, drug treatment effects were observed when excluding animals with most severe dopamine lesions: In animals with partial lesions (residual neostriatal dopamine levels of more than 10%), lesion‐dependent asymmetries in turning behavior were observed in animals that were pre‐treated with vehicle‐, substance P1−7
, or Boc‐cholecysto‐kinin–4,. whereas turning after pre‐treatment with substance P5−11
was not significantly asymmetrical. Furthermore, the ipsi‐ and contra‐lateral neostriatal dopamine levels did not differ significantly in this group. Moreover, pre treatment with substance
P5−11
affected dopamine metabolism in the neostriatum and in the venral striatum, as indicated by increased ratios of dihydroxyphenyllic acid to dopamine. The data provide the first evidence that the promotive effects of substance‐P treatment in the unilateral dopamine lesion
model might be mediated by its C‐terminal and might depend on actions on residual dopamine mechanisms.
Long‐Lasting Effects of GABA Infusion Into the Cerebral Cortex of the Rat
Authors: Montiel Teresa , Almeida Daniel , Arango Iván , Calixto Eduardo , Casasola César , Brailowsky Simón
Published: March 2007

In electrophysiological terms, experimental
models of durable information storage in the
brain include long‐term potentiation (LTP),
long‐term depression, and kindling. Protein
synthesis correlates with these enduring
processes. We propose a fourth example of
long‐lasting information storage in the brain,
which we call the GABA‐withdrawal syndrome
(GWS). In rats, withdrawal of a chronic
intracortical infusion of GABA, a ubiquitous
inhibitory neurotransmitter, induced epileptogenesis
at the infusion site. This overt GWS lasted
for days. Anisomycin, a protein synthesis
inhibitor, prevented the appearance of GWS
in vivo. Hippocampal and neocortical slices
showed a similar post‐GABA hyperexcitability
in vitro and an enhanced susceptibility to LTP
induction. One to four months after the epileptic
behavior disappeared, systemic administration
of a subconvulsant dose of pentylenetetrazol
produced the reappearance of paroxysmal
activity. The long‐lasting effects of tonic
GABAA
receptor stimulation may be involved
in long‐term information storage processes at
the cortical level, whereas the cessation of
GABAA
receptor stimulation may be involved in chronic pathological conditions, such as
epilepsy. Furthermore, we propose that GWS
may represent a common key factor in the
addiction to GABAergic agents (for example,
barbiturates, benzodiazepines, and ethanol).
GWS represents a novel form of neurono‐glial
plasticity. The mechanisms of this phenomenon
remain to be understood.
Alleviation of Brain Injury‐Induced Cerebral Metabolic Depression by Amphetamine: A Cytochrome Oxidase Histochemistry Study
Authors: Sutton Richard L. , Hovda David A. , Chen Michael J. , Feeney Dennis M.
Published: March 2007

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.
Age‐Related Decrease in the Schaffer Collateral‐Evoked EPSP in Awake, Freely, Behaving Rats
Authors: Barnes C. A. , Rao G. , Orr G.
Published: March 2007

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.
Vestibular Deprivation and the Development of Dendrite Bundles in the Rat
Authors: Geisler Hildegard C. , IJkema-Paassen Jos , Westerga Johan , Gramsbergen Albert
Published: March 2007

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.
GABA Withdrawal Modifies Network Activity in Cultured Hippocampal Neurons
Authors: Golan H. , Mikenberg K. , Greenberger V. , Segal M.
Published: March 2007

Dissociated hippocampal neurons, grown
in culture for 2 to 3 weeks, tended to fire
bursts of synaptic currents at fairly regular
intervals, representing network activity. A
brief exposure of cultured neurons to GABA
caused a total suppression of the spontaneous
network activity. Following a washout of
GABA, the activity was no longer clustered in
bursts and instead, the cells fired at a high
rate tonic manner. The effect of removing
GABA could be seen as long as 1 to 2 days
after GABA withdrawal and is expressed as
an increase in the number of active cells in a
network, as well as in their firing rates. Such
striking effects of GABA removal may
underlie part of the GABA withdrawal
syndrome seen elsewhere.
Effects of the Novel NMDA Receptor Antagonist Gacyclidine on Recovery From Medial Frontal Cortex Contusion Injury in Rats
Authors: Smith Jeffrey S. , Fulop Zoltan L. , Levinsohn Steven A. , Darrell Richard S. , Stein Donald G.
Published: March 2007

Gacyclidine, a novel, noncompetitive NMDA receptor antagonist, was injected (i.v.) into rats at three different doses to determine if the drug could promote behavioral recovery and reduce the behavioral and anatomical impairments that occur after bilateral contusions of the medial frontal cortex (MFC). In the Morris water maze,contused rats treated with gacyciidine at a dosage of 0.1 mg/kg performed better than their vehicle‐treated conspecifics. Rats given gacyclidine at either 0,3 or 0.03 mg/kg performed better than brain‐injured controls, but not as well as those treated with 0.1 mg/kg. Counts of surviving neurons in the nucleus basalis magnoceilularis (NBM) and the medial dorsal nucleus (MDN) of the thalamus were used to determine whether gacyclidine treatment attenuated secondary cell death. In both the NBM and the MDN, the counts revealed fewer surviving neurons in untreated contused rats than in gacyclidine‐treated rats. Increases in the size and number of microglia and astrocytes were observed in the striatum of gacyclidinetreated contused brains. Although most consequences of MFC contusions were attenuated, we still observed increases in ventricle dilation and thinning of the cortex. In fact, the ventricles of rats treated with 0.1 mg/kg of gacyclidine were larger than those of their vehicle treated counterparts, although we observed no behavioral impairment.
The GABA‐Withdrawal Syndrome: A Model of Local Status Epilepticus
Authors: Silva-Barrat Carmen , Champagnat Jean , Menini Christian
Published: March 2007

The GABA‐withdrawal syndrome (GWS)
is a model of local status epilepticus following
the interruption of a chronic GABA infusion
into the rat somatomotor cortex. GWS is
characterized by focal epileptic electroencephalographic
discharges and associated contralateral
myoclonus. In neocorticai slices obtained
from GWS rats, most neurons recorded in the
GABA‐infused area are pyramidal neurons
presenting bursting properties. The bursts are
induced by white‐matter stimulation and/or
intracellular depolarizing current injection
and correlate with a decrease of cellular
sensitivity to GABA, caused by its prolonged
infusion. This effect is related to a calcium
influx that may reduce the GABAA
receptormediated
inward current and is responsible
for the bursting properties. Here we present
evidence for the involvement of calcium‐ and
NMDA‐induced currents in burst genesis. We
also report modulatory effects of noradrenaline
appearing as changes on firing patterns of
bursting and nonbursting cells. Complementary
histochemical data reveal the existence of a
local noradrenergic hyperinnervation and an
ectopic expression of tyrosine hydroxylase
mRNAs in the epileptic zone.
Intracerebral Transplants and Memory Dysfunction: Circuitry Repair or Functional Level Setting?
Authors: Will Bruno , Kelche Christian , Cassel Jean-Christophe
Published: March 2007

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.
Neural Compensations After Lesion of the Cerebral Cortex
Authors: Kolb Bryan , Brown Russell , Witt-Lajeunesse Alane , Gibb Robbin
Published: March 2007

Functional improvement after cortical
injury can be stimulated by various factors
including experience, psychomotor stimulants,
gonadal hormones, and neurotrophic factors.
The, timing of the administration of these
factors may be critical, however. For example,
factors such as gonadal hormones, nerve growth
factor, or psychomotor stimulants may act to
either enhance or retard recovery, depending
upon the timing of administration. Nicotine, for
instance, stimulates recovery if given after an
injury but is without neuroprotective effect and
may actually retard recovery if it is given only
preinjury. A related timing problem concerns
the interaction of different treatments. For
example, behavioral therapies may act, in part,
via their action in stimulating the endogenous
production of trophic factors. Thus, combining
behavioral therapies with pharmacological
administration of compounds to increase the
availability of trophic factors enhances functional
outcome. Finally, anatomical evidence suggests
that the mechanism of action of many treatments
is through changes in dendritic arborization,
which presumably reflects changes in synaptic
organization. Factors that enhance dendritic
change stimulate functional compensation,
whereas factors that retard or block dendritic
change block or retard compensation.
Magnetoencephalographic Signals Identify Stages in Real‐Life Decision Processes
Authors: Braeutigam Sven , Stins John F. , Rose Steven P. R. , Swithenby Stephen J. , Ambler Tim
Published: March 2007

We used magnetoencephalography (MEG)
to study the dynamics of neural responses in
eight subjects engaged in shopping for day‐to‐day
items from supermarket shelves. This
behavior not only has personal and economic
importance but also provides an example of an
experience that is both personal and shared
between individuals. The shopping experience
enables the exploration of neural mechanisms
underlying choice based on complex memories.
Choosing among different brands of closely
related products activated a robust sequence of
signals within the first second after the presentation
of the choice images. This sequence
engaged first the visual cortex (80‐100 ms),
then as the images were analyzed, predominantly
the left temporal regions (310‐340 ms).
At longer latency, characteristic neural activetion
was found in motor speech areas (500‐520
ms) for images requiring low salience choices
with respect to previous (brand) memory, and
in right parietal cortex for high salience choices
(850‐920 ms). We argue that the neural
processes associated with the particular brand‐choice
stimulus can be separated into identifiable
stages through observation of MEG responses
and knowledge of functional anatomy.
People With Cerebral Palsy:Effects of and Perspectives for Therapy
Authors: Mayston Margaret J.
Published: March 2007

The movement disorder of cerebral palsy (CP) is expressed in a variety of ways and to varying degrees in each individual. The condition has become more complex over the last 20 years with the increasing survival of children born at less than 28 to 30 weeks gestationai age. Impairments present in children with CP as a direct result of the brain injury or occurring indirectly to compensate for underlying problems include abnormal muscle tone; weakness and lack of fitness; limited variety of muscle synergies; contracture and altered biomechanics, the net result being limited functional ability. Other contributors to the motor disorder include sensory, cognitive and perceptual impairments. In recent years understanding of the motor problem has increased, but less is known about effects of therapy. Evidence suggests that therapy can improve functional possibilities for children with cerebral palsy but is inconclusive as to which approach might be most beneficial. The therapist requires an understanding of the interaction of all systems, cognitive/perceptual, motor, musculoskeletal, sensory and behavioral, in the context of the development and plasticity of the CNS. It is necessary to understand the limitations of the damaged immature nervous system, but important to optimize the child′s functional possibilities.
Changes in Muscles and Tendons Due to Neural Motor Disorders:Implications for Therapeutic Intervention
Authors: Hof A. L.
Published: March 2007

Patients with an upper motor neurone syndrome (CP) suffer from many disabling primary symptoms: spasms, weakness, and loss of dexterity. These primary ‘neurogenic’ symptoms often lead to secondary disabilities, muscle contractures, and tertiary effects, bone deformations. A common symptom of CP is hypertonia, with. the consequence that the involved muscles remain in an excessively shortened length for most of the time. As a normal reaction of the muscle tissue, the number of sarcomeres is reduced and the muscle fibers shorten permanently: a contracture develops. A possible second type of contracture is that normal muscle lengthening along with bone growth is affected. Current treatments for the secondary effects include (1) reduction of muscle force, (2)lengthening of the muscle fibers by serial plaster casts, and (3)surgical lengthening of tendons or aponeurosis. The choice of treatment depends on the cause of the functional deficit. Bone tissue also adapts itself to abnormal forces, especially in the growth period. The hypertonias or contractures of CP so may give rise to bone malformations that interfere with function (e.g. femur endorotation) or may reduce the action of muscles by changing the lever arm (e.g. ankle varus). Although prevention should always be preferred, a timely surgical intervention cannot always be avoided. The differences in treatment for the various groups require and justify an extensive laboratory investigation, including EMG recordings in gait, measurement of passive elastic properties, and long‐term observation of the hypertonia.
Spinal Cord Lesion: Effects of and Perspectives for Treatment
Authors: Dietz V.
Published: March 2007

Following central motor lesions, two forms
of adaptation can be observed which lead to
improved mobility: (1) the development of spastic
muscle tone, and (2) the activation of spinal
locomotor centers induced by specific treadmill
training. Tension development during spastic
gait is different from that during normal gait
and appears to be independent of exaggerated
monosynaptic stretch reflexes. Exaggerated
stretch reflexes are associated with an absence
or reduction of functionally essential polysynaptic
reflexes. When supraspinal control of spinal
reflexes is impaired, the inhibition of monosynaptic
reflexes is missing in addition to a
reduced facilitation of polysynaptic reflexes.
Therefore, overall leg muscle activity becomes
reduced and less well modulated in patients with
spasticity. Electrophysiologicai and histological
studies have shown that a transformation of
motor units takes place following central motor
lesions with the consequence that regulation of
muscle tone is achieved at a lower level of
neuronal organization which in turn enables the
patient to walk. Based on observations of the
locomotor capacity of the spinal cat, recent
studies have indicated that spinal locomotor
centers can be activated and trained in patients
with complete or incomplete paraplegia when
the body is partially unloaded. However, the
level of electromyographic activity in the
gastrocnemius (the main antigravity muscle
during gait) is considerably lower in the patients
compared to healthy subjects. During the course
of a daily locomotor training program, the
amplitude of gastrocnemius, electromyographic
activity increases significantly during the stance
phase, while inappropriate tibialis anterior
activation decreases. Patients with incomplete
paraplegia benefit from such training programs
such that their walking ability on a stationary
surface improves. The pathophysiology and
functional significance of spastic muscle tone and
the effects of treadmill training on the locomotor
pattern underlying new attempts to improve the
mobility of patients with paraplegia are reviewed.
Physiology and Pathophysiology of the Swallowing Area of Human Motor Cortex
Authors: Hamdy S. , Aziz Q. , Thompson D. G. , Rothwell J. C.
Published: March 2007

Swallowing problems can affect as many as one in three patients in the period immediately after stroke. Despite this, in the majority of cases, recovery usually occurs to a safe level after a month or two. In this review, we show. how the organization of the cortical projections to swallowing nuscles can account for many of the clinical observations on swallowing after stroke and explain why recovery is common in the long term. In addition, we examine approaches that may be useful in speeding up recovery of swallowing. Swallowing may be a useful model in which to study central nervous reorganization after injury.
Chronic Restraint Stress Induces an Isoform‐Specific Regulationon the Neural Cell Adhesion Molecule in the Hippocampus
Authors: Touyarot K. , Sandi C.
Published: March 2007

Existing evidence indicates that 21‐days
exposure of rats to restraint stress induces
dendritic atrophy in pyramidal cells of the
hippocampus. This phenomenon has been
related to altered performance in hippocampal‐dependent
learning tasks. Prior studies have
shown that hippocampal expression of cell
adhesion molecules is modified by such stress
treatment, with the neural cell adhesion molecule
(NCAM) decreasing and L1 increasing, their
expression, at both the mRNA and protein
levels. Given that NCAM comprises several
isoforms, we investigated here whether chronic
stress might differentially affect the expression
of the three major isoforms (NCAM‐120,
NCAM‐140, NCAM‐180) in the hippocampus.
In addition, as glucocorticoids have been
implicated in the deleterious effects induced by
chronic stress, we also evaluated plasma
corticosterone levels and the hippocampal
expression of the corticosteroid mineralocorticoid
receptor (MR) and glucocorticoid
receptor (GR). The results showed that the
protein concentration of the NCAM‐140
isoform decreased in the hippoampus of
stressed rats. This effect was isoform‐specific,
because NCAM‐120 and NCAM‐180 levels were
not significantly modified. In addition, whereas
basal levels of plasma corticosterone tended to
be increased, MR and GR concentrations were
not significantly altered. Although possible
changes in NCAM‐120, NCAM‐180 and
corticosteroid receptors at earlier time points of
the stress period cannot be ignored; this study
suggests that a down‐regulation of NCAM‐140
might be implicated in the structural
alterations consistently shown to be induced in
the hippocampus by chronic stress exposure. As
NCAM‐140 is involved in cell‐cell adhesion and
neurite outgrowth, these findings suggest that
this molecule might be one of the molecular
mechanisms involved in the complex interactions
among neurodegeneration‐related events.
Long‐Term Recording of LTP in Cultured Hippocampal Slices
Authors: Shimono Ken , Baudry Michel , Ho Lam , Taketani Makoto , Lynch Gary
Published: March 2007

Long‐term potentiation (LTP) was elicited
by high frequency stimulation in hippocampal
slices cultured on multi‐electrode arrays. LTP
lasting more than 1 h was recorded in 75% of
slices, and a significant number of slices
exhibited a non‐decaying LTP that lasted more
than 48 h. LTP induction was completely and
reversibly blocked by an antagonist of the
NMDA receptor, APV. Our results suggest the
possibility of using chronic recording in
hippocampal slices cultured on multi‐electrode
arrays to study the mechanisms underlying
LTP maintenance and stabilization.
Spontaneous Object Recognition in the Göttingen Minipig
Authors: Moustgaard Anette , Lind Nanna Marie , Hemmingsen Ralf , Hansen Axel Kornerup
Published: March 2007

Göttingen minipigs were tested in an object
recognition procedure based on spontaneous
exploration. Eight pigs were exposed to two
similar objects in a sample trial and after a one‐hour
delay exposed to two objects, one familiar
and one novel, in a test trial. The pigs explored
the novel object significantly more than the
familiar object in the test trial (p < 0.05), thereby
showing recognition of the familiar object.
Furthermore, habituation of exploration of the
familiar object between the sample trial and the
test trial was found (p < 0.05). The procedure can be useful for testing of spontaneous trial‐unique
memory in pigs.
Perirhinal Cortex Neuronal Activity is Actively Related toWorking Memory in the Macaque
Authors: Hölscher Christian , Rolls Edmund T.
Published: March 2007

Lesion studies suggest that the perirhinai
cortex plays a role in object recognition memory.
To analyze its role, we recorded the activity of
single neurons in the perirhinal cortex in a
rhesus monkey (Macaca mulatta) performing a
delayed matching‐to‐sample task with up to four
intervening stimuli. Certain neurons (40 of 90
analyzed) showed a smaller response to an image
when it was shown the second time within a trial
(as a match image) than when it had been shown
(as a sample image) the first time. A new finding
was that the perirhinal cortex neurons were
actively reset between trials: when a particular
image was shown as a sample on a succeeding
trial, the response was much larger than when it
had been shown as a match image a short time
previously on the previous trial. This resetting
between trials appears to reflect the operation of
an active working memory process rather than a
passive temporal decay in a neuronal response.
The results thus provide evidence that the
perirhinal cortex plays an active role in visual
working memory, perhaps in association with
other brain areas such as the prefrontal cortex.
Toward An Understanding of Developmental Coordination Disorder:Terminological and Diagnostic Issues
Authors: Henderson Sheila E. , Henderson Leslie
Published: March 2007

Awareness of children who experience
unexpected difficulty in the acquisition of
motor skills has increased dramatically over the
last twenty years. Although the positing of a
distinct syndrome has proven seminal in
provoking further questions, several basic
terminological problems remain unresolved. In
this paper, we conduct a component analysis of
the three, principal competing labels for this
disorder, two of them being elements derived
from systematic diagnostic frameworks. Our
preference for the DSM IV term Developmental
Coordination Disorder (DCD) is stated find
justified. Problems in diagnosis are discussed,
especially in relation to the etiology‐dominated
medical model. We argue that an attempt should
be made to identify (pathological) positive signs
that can reliably be detected rather than relying
entirely on normative evidence of a lack of
skills exhibited by other children of the same
age. The high degree of overlap between DCD
and other developmental disorders suggests
that DCD might not constitute a distinct
syndrome. In this context, we emphasize the
need to determine whether incoordination takes
a different form when it occurs alone or
whether it is combined with general
developmental delay or with other specific
disorders in children of normal intelligence.
The Basal Ganglia and Motor Control
Authors: Groenewegen Henk J.
Published: March 2007

This paper briefly reviews the functional
anatomy of the basal ganglia and their
relationships with the thalamocortical system.
The basal ganglia, including the striatum,
pallidum, subthalamic nucleus, and substantia
nigra, are involved in a number of parallel,
functionally segregated cortical‐subcortical
circuits. These circuits support a wide range of
sensorimotor, cognitive and emotional‐motivational brain functions. A main role of the
basal ganglia is the learning and selection of the
most appropriate motor or behavioral
programs. The internal functional organization
of the basal ganglia is very well suited for such
selection mechanisms, both in development and
in adulthood. The question of whether
clumsiness may be, at least in part, attributed
to dysfunction of the basal ganglia is discussed
in the context of the differential, complementary,
or interactive roles of the basal
ganglia and the cerebellum in the development
of motor control.
Reward Processing in the Brain: A Prerequisite for Movement Preparation?
Authors: Keitz M. , Martin-Soelch C. , Leenders K. L.
Published: March 2007

In the last decade, expanding animal studies
on the cerebral organization of reward processing
toward human in vivo situations has become
possible. In this review, we define some of the
concepts associated with reward, summarize the
crucial importance of the dopaminergic system,
and discuss the currently available neuroimaging
studies in man. We will show that
abstract concepts of human behavior like
emotions, drive, arousal, and reinforcement are
now open for further exploration in man at the
level of neuronal circuit organization. The
cerebral dopaminergic neurotransmitter circuitry
does play an important role in the organization
of both the motor and motivational system.