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PubMed2005

Response to selection for photoperiod responsiveness on the density and location of mature GnRH-releasing neurons.

Natural variation in neuroendocrine traits is poorly understood, despite the importance of variation in brain function and evolution. Most rodents in the temperate zones inhibit reproduction and other nonessential functions in short winter photoperiods, but some have little or no reproductive response. We tested whether genetic variability in reproductive seasonality is related to individual differences in the neuronal function of the gonadotropin-releasing hormone network, as assessed by the number and location of mature gonadotropin-releasing hormone-secreting neurons under inhibitory and excitatory photoperiods. The experiments used lines of Peromyscus leucopus previously developed by selection from a wild population. One line contained individuals reproductively inhibited by short photoperiod, and the other line contained individuals nonresponsive to short photoperiod. Expression of mature gonadotropin-releasing hormone (GnRH) immunoreactivity in the brain was detected using SMI-41 antibody in the single-labeled avidin-biotin-peroxidase-complex method. Nonresponsive mice had 50% more immunoreactive GnRH neurons than reproductively inhibited mice in both short- and long-day photoperiods. The greatest differences were in the anterior hypothalamus and preoptic areas. In contrast, we detected no significant within-lines differences in the number or location of immunoreactive GnRH neurons between photoperiod treatments. Our data indicate that high levels of genetic variation in a single wild population for a specific neuronal trait are related to phenotypic variation in a life history trait, i.e., winter reproduction. Variation in GnRH neuronal activity may underlie some of the natural reproductive and life history variation observed in wild populations of P. leucopus. Similar genetic variation in neuronal traits may be present in humans and other species.

Animals↗

PubMed2001

Evolution of cerebral infarct volume assessed by diffusion-weighted magnetic resonance imaging.

BACKGROUND: Knowledge of the natural evolution of ischemic brain lesions may be a crucial aspect in the assessment of future stroke therapies. OBJECTIVE: To establish daily changes of ischemic cerebral lesion volume using diffusion-weighted magnetic resonance imaging. DESIGN: Prospective cohort study. SETTING: Referral center. PATIENTS AND METHODS: Serial magnetic resonance imaging scans were performed in consecutive untreated stroke patients. The baseline scan was obtained within 48 hours after symptom onset; subsequent scans, 12 to 48 hours, 3 to 4 days, 5 to 7 days, and 30 days after baseline. Lesion volumes were measured on each scan by 2 independent observers. MAIN OUTCOME MEASURE: Daily change in lesion volume. RESULTS: A total of 112 magnetic resonance imaging scans were obtained in 24 patients. An early increase in lesion volume was seen in all patients. Maximum lesion volume was reached at a mean of 74 hours. Lesion volumes increased by a mean (+/- SEM) of 21% +/- 12% during day 2 and 10% +/- 12% during day 3. No significant change occurred during day 4. During days 5, 6, and 7, statistically significant mean (+/- SEM) decreases of 6% +/- 8%, 3% +/- 4%, and 4% +/- 5%, respectively, were observed. CONCLUSIONS: Ischemic lesions follow a relatively consistent pattern of growth during the first 3 days and subsequent decrease in size. These data in conjunction with data regarding the evolution of lesion volume during the first 24 hours after symptom onset may be useful in the design of pilot studies of therapies for acute stroke.

Brain↗

PubMed1996

Protein serine/threonine kinases (PKA, PKC and CaMKII) involved in ischemic brain pathology.

The protein serine/threonine kinases which are highly expressed in the central nervous system (CNS) are severely affected by brain ischemia. Irrespective of substantial differences among the particular members of this group of kinases, their responses to ischemic stress show a lot of similarities. Initially they are switched on by facilitated interaction with their specific activators/second messengers like cyclic AMP, 1,2-sn-diacylglicerol and particularly Ca2+, then they are translocated to highly specific regions of plasma membranes. After phosphorylation of target proteins, the kinases are deactivated by means of different routes. Activity of PKA is regulated by its direct access to cAMP. In the case of CaMKII, it is probably achieved by its extensive, inhibitory autophosphorylations, while PKC seems to be proteolytically degraded. These biphasic changes in serine/threonine kinases activity may play a critical role in the evolution of postischemic brain injury and provide a mechanism for a variety of short- and long-term signalling events.

Animals↗

PubMed1992

Autoradiographic analysis of dopamine D1 receptors in the gerbil brain following transient cerebral ischemia.

1. We studied the postischemic time-course of dopamine D1 receptors in selectively vulnerable areas in the gerbil using receptor autoradiography. 2. [3H]SCH 23390 was used to label dopamine D1 receptors and transient cerebral ischemia was induced for 10 min. 3. [3H]SCH 23390 binding showed no significant alteration in selectively vulnerable areas at an early stage (1-24 hr) of recirculation. Thereafter, [3H]SCH 23390 binding showed a significant reduction in most selectively vulnerable areas 48 hr or 7 days of recirculation. The ventromedial striatum and dentate gyrus which were resistant to ischemia also exhibited a significant reduction in [3H]SCH 23390 binding. 4. Especially, marked reduction was noted in the dorsolateral striatum. However, this reduction in the dorsolateral striatum was not seen early in the recirculation prior to morphological neuronal damage. 5. The result suggests that transient cerebral ischemia can cause a severe reduction in dopamine D1 receptors in most selectively vulnerable areas. Furthermore, they suggest that dopamine D1 transmission is not always responsible for the evolution of ischemic brain damage. 6. These findings are discussed in relation to the mechanism of ischemic brain damage.

Animals↗

PubMed2005

The inflammatory reaction in human traumatic oedematous cerebral cortex.

The inflammatory reaction surrounding hemorrhagic and perihematomal brain parenchyma has been studied by means of light and transmission electron microscopy in 12 patients with severe traumatic head injuries complicated with subdural or extradural hematoma or hygroma. Perivascular cells, ameboid phagocytic microglial cells, and infiltrated macrophage/monocyte system were observed surrounding perivascular and intraparenchymal hemorrhagic foci. They showed phagocytic activity of degenerated nerve cell processes, and organized proteinaceous edema fluid present in the enlarged extracellular space. Endocytosis by means of clathrin coated vesicles also was observed. Facultative and professional phagocytes exhibited a full repertoire of lysosomes, phagosomes containing nerve cell debris, lipid droplets, and lipofucsin granules. Phagocytic pericytes remaining within the capillary basement membrane were also observed around perivascular hemorrhages. The inflammatory reaction was examined in young and old patients with an evolution time of brain injury ranging from 1 day to 2 years. The inflammatory process developed according to the intensity of traumatic insult, patient age, associated hematoma or hygroma, severity of vasogenic and cytotoxic oedema, and anoxic-ischemic conditions of brain parenchyma.

Adolescent↗

PubMed2003

Antisense in vivo knockdown of synaptotagmin I and synapsin I by HVJ-liposome mediated gene transfer modulates ischemic injury of hippocampus in opposing ways.

Neurotransmitter release during and after ischemic event is thought to be involved in excitotoxicity as a pathogenesis for the ischemic brain damage, which is mediated by excessive activation of glutamate receptors and attendant calcium overload. To ascertain the role of transmitter release from nerve terminals in promoting the ischemic neurodegeneration, we delivered antisense oligodeoxynucleotides (ODNs) to synaptotagmin I or synapsin I into the rat brain by using HVJ-liposome gene transfer technique. The antisense ODNs were injected into the lateralventricle in rats 4 days prior to transient forebrain ischemia of 20 min. With a single antisense treatment, long-lasting downregulation of the transmitter release relating protein levels at overall synaptic terminals was achieved. The antisense in vivo knockdown of synaptotagmin I prevented almost completely the ischemic damage of hippocampal CA1 neurons, while the in vivo knockdown of synapsin I markedly promoted the ischemic damage of CA1 pyramidal neurons and extended the injury to relatively resistant CA2/CA3 region. The modulation of ischemic hippocampal damage by the in vivo knockdown of synaptotagmin I or synapsin I suggests that transmitter release from terminals plays an important role in the evolution of ischemic brain damage and therefore the transmitter release strategy by the use of antisense ODNs-HVJ-liposome complex is reliable for neuroprotective therapies.

Animals↗

PubMed1995

A YAC contig containing the reeler locus with preliminary characterization of candidate gene fragments.

The reeler mutation in the mouse maps to proximal chromosome 5 and defines a key gene involved in brain development and evolution. No gene product is known, and the locus is currently being characterized by positional cloning. YAC clones corresponding to the closest markers D5Mit61 and D5Mit72 have been isolated. Cloned extremities of the YAC inserts were used to construct a 1.1-Mb contig, a 700-kb fragment of which was shown to contain the reeler locus. The integrity of the contig was verified by physical mapping on genomic DNA. The classical allele of the reeler mutation was associated with a 150-kb deletion between D5Mit61 and D5Mit72, while no gross chromosomal anomaly was found in the Orleans allele. Candidate coding sequences were isolated to construct a preliminary transcriptional map of the reeler region. Cosmid clones mapping within the rl deletion revealed a large transcript of more than 11 kb, which was present in normal embryonic brain but barely detectable in homozygous rlOrl/rlOrl embryonic brain, suggesting strongly that it corresponds to the reeler transcript.

Animals↗

PubMed2007

In vivo analysis of the post-natal development of normal mouse brain by DTI.

The water diffusion characteristics of wild-type mouse brains have been studied in vivo by DTI to follow developmental changes. Here, axial (lambda(//)) and radial (lambda(perpendicular)) diffusivities and fractional anisotropy were measured from the fifth day of life (P5) and at three other post-natal ages (P12, P19 and P54). Magnetic resonance images were collected from a single sagittal slice in the middle of the two hemispheres; ROI were chosen in nine different structures of both grey and white matter. Fractional anisotropy (FA) from P5 onwards distinguished structures of both white and grey matter, even though myelination had yet to occur. Between P5 and P54, a significant increase in FA was observed in the genu of the corpus callosum due to a significant decrease in lambda(perpendicular) whereas lambda(//) remained stable. Many other significant variations of lambda(//) and lambda(perpendicular) were measured in different structures. They were substantially correlated with axon and myelin maturation which are responsible for the main evolutions of the brain during its post-natal development. These quantitative data show that in vivo characterization of the anatomy and microstructure of the normal mouse brain during development is possible. The normative data will greatly improve the characterization of abnormal development in the transgenic mouse brain.

Aging↗

PubMed2006

Astrocytic-inducible nitric oxide synthase in the ischemic developing human brain.

Variability in the expression of apoptotic and inflammatory mediators with time after an ischemic insult and their role in the expansion of cerebral infarcts are still controversial. This study examines DNA degradation and the expression of activated caspase-3 and iNOS, inducible nitric oxide (iNOS) in the human developing brain. Autopsy specimens from children with a neuropathologic diagnosis of focal ischemic infarct were included in the study. The specimens were classified based on the clinical history as acute (< 24 h, n = 5), subacute (24-72 h, n = 8), or old (> 72 h, n = 6) infarcts. Immunohistochemical staining for caspase-3, iNOS and TUNEL were then performed on all infarcts alongside age-matched controls. TUNEL staining was detected in regions of all infarcts. Expression of iNOS was significantly higher than that of caspase-3 in the penumbra of subacute infarcts (p = 0.02). Glial fibrillary acidic protein and iNOS staining co-localized in the penumbra of acute and subacute infarcts. These results suggest that cell death continues to occur for more than 3 d post ischemic insult. Cell death in the penumbra of subacute infarcts is partially caspase-3 independent and may be attributed to nitric oxide. Astrocytes are a source of iNOS and may play a role in the evolution of pediatric brain injury days after the initial insult.

Adolescent↗

PubMed2006

Genetic, physiologic and ecogeographic factors contributing to variation in Homo sapiens: Homo floresiensis reconsidered.

A new species, Homo floresiensis, was recently named for Pleistocene hominid remains on Flores, Indonesia. Significant controversy has arisen regarding this species. To address controversial issues and refocus investigations, I examine the affinities of these remains with Homo sapiens. Clarification of problematic issues is sought through an integration of genetic and physiological data on brain ontogeny and evolution. Clarification of the taxonomic value of various 'primitive' traits is possible given these data. Based on this evidence and using a H. sapiens morphological template, models are developed to account for the combination of features displayed in the Flores fossils. Given this overview, I find substantial support for the hypothesis that the remains represent a variant of H. sapiens possessing a combined growth hormone-insulin-like growth factor I axis modification and mutation of the MCPH gene family. Further work will be required to determine the extent to which this variant characterized the population.

Animals↗

PubMed1996

The possible role of long-chain, omega-3 fatty acids in human brain phylogeny.

I propose that one of the key factors in human encephalization was increased HUFA intake, especially long-chain, omega-3 fatty acids from aquatic and terrestial meat source. This provided the needed neural membrane fluidity and transmitter/receptor functions for rapid acquisition of more advanced human traits and allowed the expansion of H. erectus into more northern climates. The human brain initially could build ecophenotypically, or adaptive/directed mutationally upon previously evolved mammalian sensor/motor structures, and could rapidly expand cognitive functions within a few million years; as more niches were invaded, more brain diversity was needed to guarantee reproductive success. The metabolically expensive and expanding brain was nutritionally and biochemically set, as it were, for rapid accommodation to tool making, rock throwing, culture language, electronics, and the eventual endless discussion and writings about the brain itself, the evolution of consciousness, and the mid-bran problem [107]. All of this fits, no matter which theory of human evolution one adheres to--i.e., out of Africa, multiregional, etc.--or even the precis fossil chronology [108]. This proposal, based as it is on known facts and certain assumptions appears logical, simple, and satisfying, but it may be wrong. Yet Charles Darwin himself would have approved, because as he so aptly said: false facts are highly injurious to the progress of science, for they often endure long; but false views, if supported by some evidence do little harm for everyone takes a salutory pleasure in providing their falseness; and when this is done our path toward error is closed and the road to truth is often opened. [109].

Animals↗

PubMedDate not supplied

[Cognition disorders in HIV infection. Validation of a brief neuropsychological evaluation battery].

UNLABELLED: The objective of our study was the elaboration and the validation of a brief neuropsychological battery sensitive to the main cognitive and psychomotor deficits in HIV+ patients with HIV encephalopathy and cognitive impairment associated with seropositivity. We evaluated the sensitivity of this brief battery with respect to a large neuropsychological battery of standardized tests. METHODOLOGY: A brief battery (BB) (30 mn, with simple and portable material) of 5 standardized subtests and 7 new elaborated tests and a large battery (LB) (2 h to 2 h 30) of 16 standardized subtests, were constituted. Both screened 6 major cognitive areas (attention, memory, visuospatial function, psychomotor speed, motor dexterity, language). On the LB, subjects' age and educational level were considered while appraising performances to determine whether subjects had normal cognitive status (less than 4 abnormal test scores), borderline cognitive impairment (4 or 5 abnormal test scores); on the BB norms for the new tests were generated from the results of 24 HIV+ subjects with normal cognitive status on the LB and 15 HIV- subjects of a control group; performance on the BB was considered normal if less than 3 test scores were abnormal, or impaired if more than 3 test scores were abnormal. Conclusions deduced from the assessments with BB were compared to those obtained from LB. For all subjects, a possible anxio-depressive component was evaluated on the basis of DSM III-R criteria and clinical scales (MADRS and STAXI). Subjects were included in the study notwithstanding mode of contamination and stage of illness and anxiodepressive antecedents; patients with identified brain disease or evolutive non neurological pathology were not included. 102 evaluations were performed on a population of HIV+ patients comprising 89 men and 13 women: 19 CDC II, 35 CDC III or IV C 2 and 48 CDC IV; 76 homosexuals, 8 heterosexuals, 16 drug users and 2 transfused. RESULTS: the BB led to the same conclusions for 90.6% of the 53 impaired cases (on LB) and for 96% of the 24 normal cases. The reliability of the BB is therefore of 92%; there was only 1 false positive (less than 2%) and less than 6.5% false negatives. Among the 25 subjects with borderline cognitive impairment, half were impaired and half were normal on the BB; most (84%) presented with anxio-depressive symptoms. COMMENTS AND CONCLUSION: The brief battery (BB) testing 6 cognitive functions could be considered as a sensitive, practical instrument for rapid detection of cognitive impairment in HIV+ patients, with a few rate of false positive or negative diagnosis. However, it is not adequate for determining whether psychiatric or/and organic brain pathology is at the origin of the deficit. Evaluation and follow-up of a possible anxio-depressive component has to be considered together before concluding.

AIDS Dementia Complex↗

PubMed1998

Is posttraumatic stress disorder an overlearned survival response? An evolutionary-learning hypothesis.

Contemporary learning theories of posttraumatic stress disorder (PTSD) provide an explanation for the phobic avoidant features but do not account fully for the intrusive phenomena that are so characteristic of the disorder. This article hypothesizes that a primitive learning center in the limbic system rehearses traumatic memories immediately following exposure to trauma, thus inducing durable memories of the sources of novel threat. It is postulated that the mechanism developed during early evolution when, in the absence of cognitive mechanisms, automatic learning following single exposure to novel threat would have conferred survival value on the species. With evolution of the brain, a second cortical pathway developed for the cognitive processing of trauma memories. It is possible that synchrony between the two phylogentically distinct pathways may be lost in vulnerable individuals under conditions of extreme stress resulting in failure of cortical inhibition of limbic trauma rehearsal mechanisms. A mismatch between archaic biological mechanisms and novel cues in the modern environment also may play a role in triggering traumatic memories and associated fight and flight reactions. The intrusive phenomena of PTSD thus may reflect an "overlearned survival response" in those in whom the putative limbic rehearsal mechanism evades cortical control. The heuristic value and limitations of such an evolutionary-learning theory are discussed.

Animals↗

PubMed2003

Why do seizures cause loss of consciousness?

Model systems are needed for the scientific investigation of consciousness. A good model system should include variable states of consciousness, allowing the relationship between brain activity and consciousness to be investigated. Examples include sleep, anesthesia, focal brain lesions, development, evolution, and epilepsy. One advantage of epilepsy is that changes are dynamic and rapidly reversible. The authors review previous investigations of impaired consciousness in epilepsy and describe new findings that may shed light on both normal and abnormal mechanisms of consciousness. Abnormal increased activity in fronto-parietal association cortex and related subcortical structures is associated with loss of consciousness in generalized seizures. Abnormal decreased activity in these same networks may cause loss of consciousness in complex partial seizures. Thus, abnormally increased or decreased activity in the same networks can cause loss of consciousness. Information flow during normal conscious processing may require a dynamic balance between these two extremes of excitation and inhibition.

Animals↗

PubMed1992

Brain-derived neurotrophic factor is more highly conserved in structure and function than nerve growth factor during vertebrate evolution.

Mammalian nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are members of a protein family with perfectly conserved domains arranged around the cysteine residues thought to stabilize an invariant three-dimensional scaffold in addition to distinct sequence motifs that convey different neuronal functions. To study their structural and functional conservation during evolution, we have compared NGF and BDNF from a lower vertebrate, the teleost fish Xiphophorus, with the mammalian homologues. Genomic clones encoding fish NGF and BDNF were isolated by cross-hybridization using probes from the cloned mammalian factors. Fish NGF and BDNF were expressed by means of recombinant vaccinia viruses, purified, and their neuronal survival specificities for different classes of neurons were found to mirror those of the mammalian factors. The half-maximal survival concentration for chick sensory neurons was 60 pg/ml for both fish and mammalian purified recombinant BDNF. However, the activity of recombinant fish NGF on both chick sensory and sympathetic neurons was 6 ng/ml, 75-fold lower than that of mouse NGF. The different functional conservation of NGF and BDNF is also reflected in their structures. The DNA-deduced amino acid sequences of processed mature fish NGF and BDNF showed, compared to mouse, 63% and 90% identity, respectively, indicating that NGF had reached an optimized structure later than BDNF. The retrograde extrapolation of these data indicates that NGF and BDNF evolved at strikingly different rates from a common ancestral gene about 600 million years ago. By RNA gel blot analysis NGF mRNA was detected during late embryonic development; BDNF was present in adult brain.

Amino Acid Sequence↗

PubMed2005

The plastic human brain cortex.

Plasticity is an intrinsic property of the human brain and represents evolution's invention to enable the nervous system to escape the restrictions of its own genome and thus adapt to environmental pressures, physiologic changes, and experiences. Dynamic shifts in the strength of preexisting connections across distributed neural networks, changes in task-related cortico-cortical and cortico-subcortical coherence and modifications of the mapping between behavior and neural activity take place in response to changes in afferent input or efferent demand. Such rapid, ongoing changes may be followed by the establishment of new connections through dendritic growth and arborization. However, they harbor the danger that the evolving pattern of neural activation may in itself lead to abnormal behavior. Plasticity is the mechanism for development and learning, as much as a cause of pathology. The challenge we face is to learn enough about the mechanisms of plasticity to modulate them to achieve the best behavioral outcome for a given subject.

Blindness↗

PubMed2004

Effects of reperfusion on ADC and CBF pixel-by-pixel dynamics in stroke: characterizing tissue fates using quantitative diffusion and perfusion imaging.

The effects of reperfusion on the spatiotemporal dynamics of transient (60 minutes) focal ischemic brain injury in rats were evaluated on a pixel-by-pixel basis using quantitative cerebral blood flow (CBF) and apparent diffusion coefficient (ADC) measurements every 30 minutes for 3 hours and compared to post-mortem histology at 24 hours. Four biologically relevant clusters were classified based on ADC (0.53 +/- 0.02 x 10mm/s, SD) and CBF (0.30 +/- 0.09 ml/g/min) viability thresholds, namely: (1) the "normal" cluster with ADC and CBF > thresholds; (2) the "mismatch" cluster with ADC > threshold but CBF < threshold; (3) the "core" cluster with ADC and CBF < thresholds; and (4) "non-nourishing reperfusion zone" where ADC < threshold but CBF > threshold. The spatio-temporal progression of tissue volumes, ADC and CBF of each cluster were evaluated. Pixels of each cluster on the CBF-ADC space were mapped onto the image space. Following reperfusion, 28% of the "core" pixels and 90% of the "mismatch" (defined at 60 minutes) pixels were salvaged at 180 minutes, which correlated with histology. The ADC and CBF of subsequently salvaged tissues were significantly higher than those became infarcted. Salvaging "core" pixels indicated that reduced ADC was not synonymous with irreversible injury; duration of exposure and severity of reduced ADC and CBF were likely critical. Projection profiles showed a bimodal ADC, but uni-modal CBF, distributions. The ADC bimodal minima, obtained without histological correlation, were similar to the histology-derived ADC and CBF viability thresholds, and could have potential clinical applications. This study demonstrated a simple but powerful approach to evaluate, on a pixel-by-pixel basis, the spatio-temporal evolution of ischemic brain injury, and a potential for statistical prediction of tissue fate.

Animals↗

PubMed1999

The evolution of cerebral blood flow in the developing brain: evaluation with iodine-123 iodoamphetamine SPECT and correlation with MR imaging.

BACKGROUND AND PURPOSE: Although it is well established that brain maturation correlates temporally with the functions the newborn or infant performs at various stages of development, the precise relationship between function and anatomic brain maturation remains unclear. The purpose of this study was to investigate the developmental changes of regional cerebral blood flow (rCBF) in infants and children using iodine-123 iodoamphetamine (123I-IMP) and single-photon emission computed tomography (SPECT). These findings were correlated with the MR imaging appearance of the brain and with known developmental changes. METHODS: Twenty-one 123I-IMP SPECT examinations of 17 patients, ranging in age from neonates to 2 years, were reviewed retrospectively. All children had had transient neurologic events in the neonatal period that did not significantly affect subsequent neuropsychological development. MR studies were performed in 12 of these patients and the MR findings were correlated with the SPECT results. RESULTS: SPECT studies showed a consistent pattern of evolving changes in 123I-IMP uptake, most likely reflecting evolution of rCBF. From the 34th postconceptional week until the end of the second month after term delivery, there was predominant uptake in the thalami, brain stem, and paleocerebellum, with relatively less cortical activity. Radionuclide uptake in both the perirolandic and occipital cortices was well seen around the 40th postconceptional week and increased rapidly thereafter, with a predominance of parietal activity. By 3 months, radionuclide uptake in the cerebellar hemispheres and parietofrontal cortices increased. Frontal and temporal activity increased by age 6 to 8 months. Uptake in the basal ganglia increased by 8 months. By the beginning of the second year, rCBF showed a similar topographic pattern to that in adults. CONCLUSION: The time course of the changes in 123I-IMP uptake in the developing brain as detected by SPECT is similar to that of myelination and most likely reflects an overall topologic maturational pattern of the brain.

Amphetamines↗