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PubMed2000

Total mercury in human renal cortex, liver, cerebellum and hair.

The aim of this study was: (a) to estimate the concentration of total mercury in the renal cortex, liver, cerebellum and hair of 46 persons who died suddenly in the Gdańsk region, northern Poland, between the ages of 17 and 90; and (b) to assess whether a correlation occurs between mercury content in the investigated biological media. The mean concentrations of mercury in the human hair, renal cortex, liver and cerebellum were: 378 +/- 315.4 ng/g; 68.6 +/- 92.3 ng/g; 29.9 +/- 22 ng/g and 5.3 +/- 6.9 ng/g respectively. Positive correlations were found between mercury levels in: cerebellum and liver (r = 0.873), cerebellum and hair (r = 0.853), cerebellum and renal cortex (r = 0.578), hair and liver (r = 0.771), hair and renal cortex (r = 0.478) liver and renal cortex (r = 0.66). The geometric mean levels of mercury in the renal cortex, liver, cerebellum and hair in the residents of the Gdańsk region are 15-19 times lower than in the population of Tokyo and its environs [Suzuki T, Hongo T, Yoshinaga J et al. The hair-organ relationship in mercury concentration in contemporary Japanese. Arch Environ Health 1993;44:361-365].

Adolescent↗

PubMed1998

Ceruletide inhibits phencyclidine-induced dopamine and serotonin release in rat prefrontal cortex.

Phencyclidine (PCP; 5.0 mg/kg, i.p.) produced a greater increase in extracellular dopamine (DA) levels in the prefrontal cortex than in the striatum, while PCP increased the extracellular 5-hydroxytryptamine (serotonin; 5-HT) levels in the prefrontal cortex but not the striatum, as determined by in vivo microdialysis in awake, freely moving rats. The cholecystokinin (CCK)-related decapeptide ceruletide (120 and 400 microg/kg, i.p.), administered 60 min prior to PCP, significantly attenuated the PCP-induced increase in the extracellular levels of DA and 5-HT in the prefrontal cortex, but not in the striatum. These effects were reversed by PD 135,158, a selective CCK-B receptor antagonist (0.1 mg/kg, s.c.), administered 5 min prior to ceruletide. When administered alone, ceruletide (400 microg/kg, i.p.) significantly increased basal extracellular DA levels only in the prefrontal cortex. The selective N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (0.5 mg/kg, i.p.) also increased extracellular DA levels in the prefrontal cortex, but this effect was unaffected by ceruletide pretreatment. These results suggest that ceruletide may differentially modulate basal and PCP-induced release of DA and 5-HT in the prefrontal cortex.

Animals↗

PubMed2000

Coherence between low-frequency activation of the motor cortex and tremor in patients with essential tremor.

BACKGROUND: In healthy people, rhythmic activation of the motor cortex in the 15-30 Hz frequency range accompanies and contributes to voluntarily-generated postural contractions of contralateral muscle. In patients with Parkinson's disease, an abnormal low-frequency activation of the motor areas of the cortex occurs and has been directly linked to the characteristic 3-6 Hz rest tremor of this disease. We therefore investigated whether the motor cortex is involved in the transmission of the rhythmic motor drive responsible for generating essential tremor. METHODS: Non-invasive recordings of activity from the hand area of the motor cortex were made from six patients with essential tremor by magnetoencephalography. The recordings were made simultaneously with the electromyogram recorded from contralateral finger muscles during periods of postural tremor. A statistical spectral analysis was done to determine at which frequencies the two signals were correlated. FINDINGS: Spectral analysis of the electromyogram signals showed a significant low-frequency component at the frequency of the tremor bursts. However, there was no coherence between magnetoencephalogram and electromyogram recordings at the tremor frequency, indicating that no correlation existed between the tremor signal and low-frequency activity recorded from the primary motor cortex in individuals with essential tremor. Coherence at frequencies higher than the tremor frequency was similar to that in healthy individuals performing voluntary postural contractions. INTERPRETATION: The absence of significant coherence between the magnetoencephalogram and electromyogram at tremor frequencies suggests that in essential tremor the tremor is imposed on the active muscle through descending pathways other than those originating in the primary motor cortex. These findings challenge the model widely used to explain the efficacy of neurosurgical treatment of essential tremor, are in contrast to those of previous studies of parkinsonian rest tremor, and highlight an important difference in the pathophysiology of essential and parkinsonian tremor.

Adolescent↗

PubMed1999

Miniature carrier with six independently moveable electrodes for recording of multiple single-units in the cerebellar cortex of awake rats.

Ensemble recording in cerebellar cortex of awake rats presents unique methodological challenges not encountered when recording from the cerebral cortex or from deep brain structures with more homogeneous cell populations. Compared to the cerebral cortex, removal of dura over the cerebellum evokes pronounced swelling, and insertion of multiple closely spaced electrodes in the cerebellar cortex causes considerable dimpling (Welsh JP, Schwartz C. Multielectrode recording from the cerebellum. In: Nicolelis MAL, editor. Methods for Neural Ensemble Recordings, CRC Methods in Neuroscience Series. Boca Raton, FL: CRC Press LLC, 1999, pp. 79-100). Also, a repetitious and well-defined neural circuit characterizes the cerebellar cortex across its entire surface. With conventional multi-electrode methods, such as chronically implanted bundles or arrays of microwires, the risk of disrupting the cerebellar cytoarchitecture is high. In most conventional multi-electrode systems, electrodes have rather low impedance and cannot be moved independently after implantation. These limitations make proper unit isolation, necessary to identify each of the recorded cerebellar units, very difficult. We designed a lightweight (14 g), miniature (base plate: 19 x 23 mm; total height: 16 mm) multi-electrode system to allow for the chronic implantation of six independently moveable sharp electrodes with high impedance, in the cerebellar cortex. The six electrodes are arranged in a 2 x 3 matrix (inter-electrode distance: 0.6 mm). At any time after the implantation the vertical position of each individual electrode can be adjusted by screwing spring-loaded electrode heads up or down. The system preserves the integrity of the cerebellar cytoarchitecture, and enables easy isolation and identification of individual cerebellar units in awake, freely moving rats.

Animals↗

PubMed1998

Calbindin-D28k- and astroglial protein-immunoreactivities, and ultrastructural differentiation in the prenatal rat cerebral cortex and hippocampus are affected by maternal adrenalectomy.

Maternal adrenal steroid hormones have been proven to be crucial for lung and adrenal prenatal maturation. These hormones mediate the effects of prenatal stress crossing the placenta and influencing the development of the hypothalamus-pituitary-adrenal axis of fetuses. In the present study, we have compared the prenatal development of fetuses from adrenalectomized mothers (ADX group) and from sham-operated mothers. We have used immunohistochemistry for calcium binding-protein Calbindin-D28k, astroglial proteins vimentin and glial fibrillary acidic protein (GFAP), and the ultrastructural differentiation of the cerebral cortex and hippocampus to measure putative differences. The ontogeny of the Calbindin-D28k immunoreactivity was delayed, as transient Calbindin-positive neuronal populations in the ADX group disappeared later during development as compared to that of control animals both in cerebral cortex and hippocampus; cell counts revealed that ADX animals had a significantly higher number of Calbindin-positive cells than controls in the cerebral cortex, while that number was lower in ADX fetuses' hippocampus. Cerebral cortex of ADX animals also had a scattered distribution of stained cells compared with controls, while the hippocampi of the ADX animals had an impaired migration of marginal zone interneurons. No GFAP immunoreactivity was found in the studied prenatal stages. Instead, vimentin-immunoreactivity appeared more profusely distributed throughout the cerebral cortex, in the ADX group than in control animals. At the ultrastructural level, no remarkable differences were found before E20, when a higher undifferentiation in the ADX group, in both cerebral cortex and hippocampus, was evident. The results show for the first time the vulnerability of the prenatal rat brain to maternal adrenalectomy and the necessity of maternal glucocorticoids for encephalic development.

Adrenalectomy↗

PubMed2002

Spatial and nonspatial Morris maze learning: impaired behavioral flexibility in mice with ectopias located in the prefrontal cortex.

About half of BXSB/MpJ-Yaa (BXSB) mice have neocortical ectopias (misplaced clusters of neurons located in layer I of cortex). Previous behavioral studies have suggested that ectopic mice have superior spatial, but equivalent nonspatial, reference memory learning. However, since spatial and nonspatial learning were not assessed in the same apparatus and with the same testing procedure, it is unclear if this conclusion is accurate. We have created a new nonspatial Morris maze for mice that differs from the spatial task only in the type of cues that must be utilized to efficiently locate the platform (intra-maze black/white patterns vs. extra-maze room cues) and does not differ in the level of task complexity or the presence of objects within the maze. Ectopic mice were very good in utilizing extra-maze cues when learning the spatial version and in utilizing intra-maze cues when learning the nonspatial version of the Morris maze, while non-ectopics were not, suggesting that ectopics have superior spatial and nonspatial reference memory. Ectopias in BXSB mice are usually located in prefrontal and/or motor cortex. The prefrontal cortex is involved in behavioral flexibility (e.g. being able to easily switch from using spatial to nonspatial cues). Only ectopic mice with ectopias specifically located in the prefrontal region of cortex demonstrated difficulty switching from using extra-maze to intra-maze cues and vice versa. Thus, the presence of one or more ectopias in the prefrontal region of cortex disrupted one of the normal functions of the prefrontal cortex.

Animals↗

PubMed1992

Medial frontal cortex lesions impair the aiming component of rat reaching.

This study examined the contribution of medial frontal cortex (the medial portion of supplementary motor cortex, or Fr1) to the performance of rats on trained, or 'skilled', reaching tasks. Unilateral medial frontal cortex lesions moderately impaired reaching success on a task that demanded accuracy but they did not impair performance on a less demanding reaching task nor did they affect limb preference. Kinematic analyses indicated that the aiming component, in which the forearm of the limb is aligned along the midline of the body by adduction of the elbow, was chronically impaired. Rather than adducting the elbow to aim, the rats used a number of limb and whole body postural adjustments to compensate for incomplete or absent aiming. That medial frontal cortex is involved in the execution of at least one component of skilled reaching implies that a larger area of frontal cortex is involved in skilled limb movement than has been suggested by previous studies. The results also suggest that the different regions of frontal cortex may each have a relatively selective involvement in the execution of only a subset of the movements comprising a reach.

Animals↗

PubMed1997

Force and the motor cortex.

The relation between the activity of cells in the motor cortex and static force has been studied extensively. Most studies have concentrated on the relation to the magnitude of force; this relation is more or less monotonic. The slope of the relation, however, shows considerable variation among different studies and seems to be inversely associated with the range of forces over which the cell activity has been studied. Cells in the motor cortex also show variation in activity with the direction of static force. When both the direction and the magnitude of static force are allowed to vary, a majority of cells show significant changes in activity with direction of force alone, an intermediate number relate to both direction and magnitude, while a small number relate purely to the magnitude. This suggests that the direction of static force can be controlled independently of its magnitude and that this directional signal is especially prominent in the motor cortex. In general, it has been more difficult to study the relations to dynamic force. There is a correlation between motor cortex cell activity and the rate of change of force. The direction of dynamic force is also an important determinant of cell activity. When both static and dynamic force output are required (for example, with arm movement in the presence of gravity) it is the dynamic signal that is most clearly reflected in motor cortex activity. The relations between motor cortex activity and static or dynamic force are not invariant, but may be modified by the behavioral context of the motor output.

Animals↗

PubMed1998

Spatial memory, habituation, and reactions to spatial and nonspatial changes in rats with selective lesions of the hippocampus, the entorhinal cortex or the subiculum.

Various spatial memory deficits have been described in rats with damage to the hippocampal formation (including the subiculum and the entorhinal cortex) and particularly in rats with selective lesions of the hippocampus proper. So far, the involvement of the entorhinal cortex in spatial memory is still controversial and the role of the subiculum is poorly documented. The aim of the present study was to compare the behavioural effects of selective lesions of the hippocampus, the entorhinal cortex or the subiculum in (a) a water-maze task using testing procedures sensitive to the disruption of reference or working memory and (b) in an object exploration task designed to evaluate habituation and subsequently reactions to changes of the spatial layout of objects (spatial change) or to the substitution of a familiar object by a new one (nonspatial change). Our results showed several similarities between the behavioural consequences of damage to each of the three structures. A few differences were also noted. Hippocampal rats were impaired in all spatial tasks, but they reacted like controls to a nonspatial change. The rats sustaining lesions of the entorhinal cortex or the subiculum were not impaired in the reference-memory procedure of the water-maze task and showed a deficit in reacting to a nonspatial change. Overall, our results confirm the central role of the hippocampus in spatial memory and also suggest a role for the entorhinal cortex and the subiculum in processing spatial informations. In addition, they indicate that the entorhinal cortex and the subiculum may have a hippocampal-independent role in memory.

Animals↗

PubMed1997

Force and the motor cortex.

Animals↗

PubMed2003

Cortical spreading depression affects Fos expression in the hypothalamic paraventricular nucleus and the cerebral cortex of both hemispheres.

The present experiments were performed to clarify the brain sites whose activity is affected exclusively by cortical spreading depression (CoSD). For this purpose, Fos protein, a product of an immediate early gene, was used as a marker of neuronal activation. Because Fos can be induced by many manipulations such as stress stimuli, we verified CoSD-induced Fos expression by excluding the influence of other factors such as anaesthesia and surgical manipulation. CoSD was induced by applying a KCl solution directly to the dura mater over the cerebral cortex, and Fos expression in the brain was assessed by immunohistochemistry using antibodies against Fos protein. We found that during CoSD, Fos expression was increased specifically in the magnocellular region of the hypothalamic paraventricular nucleus (PVN), as well as in the ipsilateral cortex, whereas reduced Fos expression was observed in both the parvocellular region of the PVN and the whole cortex contralateral to the CoSD site. Consistent with the reduced Fos expression, approximately 40% of neurons in the contralateral cortex revealed a suppression of electrical activity during CoSD. These results suggest that in addition to the ipsilateral cortex, CoSD affects Fos expression exclusively in the PVN and the contralateral cortex.

Animals↗

PubMed2004

The roles of orbital frontal cortex in the modulation of antisocial behavior.

This article considers potential roles of orbital frontal cortex in the modulation of antisocial behavior. Two forms of aggression are distinguished: reactive aggression elicited in response to frustration/threat and goal directed, instrumental aggression. It is suggested that orbital frontal cortex is directly involved in the modulation of reactive aggression. It is argued that orbital frontal cortex does not "inhibit" reactive aggression but rather may both increase or decrease its probability as a function of social cues present in the environment. Early dysfunction in this function of orbital frontal cortex may be linked to the development of Borderline Personality Disorder. Instrumental aggression is linked to a fundamental failure in moral socialization. However, the available data suggest that the amygdala, but not orbital frontal cortex, is required for functions such as aversive conditioning and passive avoidance learning that are necessary for moral socialization. Psychopathic individuals who present with significant instrumental aggression, are impaired in aversive conditioning and passive avoidance learning and show evidence of amygdala dysfunction. Orbital frontal cortex and the amygdala are involved in response reversal where instrumental responses must be reversed following contingency change. Impairments in response reversal are also seen in psychopathic individuals. However, it remains unclear whether impairment in response reversal per se is associated with antisocial behavior.

Adult↗

PubMed1998

Adenosinergic modulation of ethanol-induced motor incoordination in the rat motor cortex.

1. On going work in our laboratory has shown that adenosine modulates ethanol-induced motor incoordination (EIMI) when given systemically as well as directly into the cerebral ventricles, cerebellum and corpus striatum of the rat and/or mouse. 2. The objective of this study was to determine what effect adenosine agonists and antagonists would have within the rat motor cortex on EIMI. 3. The participation of the motor cortex in EIMI was suggested when microinfusion of the anti-ethanol compound, Ro15-4513, an inverse agonist of the benzodiazepine binding site, directly into the motor cortex significantly attenuated EIMI. Further, the adenosine agonists N6-cyclohexyladenosine (CHA) and 2-p-(2-carboxyethyl)-phenethylamino-5'-N-carboxaminoadenosine++ + hydrochloride (CGS-21680) significantly accentuated EIMI in a dose-related manner. The adenosine A1 receptor-selective agonist, CHA, appeared most potent in this modulatory effect when compared to the A2-selective agonist, CGS-21680. 4. The extent of diffusion of the adenosine drugs within the cortical tissue after their microinfusion was also checked by measuring the dispersion of microinfused [3H]CHA. The [3H]CHA dispersion study indirectly confirmed that the results of the present investigation were based on the effect of adenosine drugs within the motor cortex only. 5. Accentuation by the A1- and A2-selective adenosine agonists was significantly attenuated by the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) but not by the A2 receptor-selective antagonist 8-(3-chlorostyryl)caffeine (CSC) further suggesting modulation mainly by the A1-subtype. 6. Pretreatment of the motor cortex with pertussis toxin (PT) significantly reduced the capacity of both A1- and A2-selective adenosine agonists to accentuate EIMI suggesting the involvement of a PT-sensitive Gi/Go protein. 7. These data support earlier work which showed that adenosine modulates EIMI within the central nervous system (CNS), most likely via the A1 receptor, and moreover, extend that work by including the motor cortex as a brain area participating in the adenosinergic modulation of ethanol-induced motor impairment.

Adenosine↗

PubMed1997

Primary motor cortex influences on the descending and ascending systems.

The motor cortex plays a crucial role in the co-ordination of movement and posture. This is possible because the pyramidal tract fibres have access both directly and through collateral branches to structures governing eye, head, neck trunk and limb musculature. Pyramidal tract axons also directly reach the dorsal laminae of the spinal cord and the dorsal column nuclei, thus aiding in the selection of the sensory ascendant transmission. No other neurones in the brain besides pyramidal tract cells have such a wide access to different structures within the central nervous system. The majority of the pyramidal tract fibres that originate in the motor cortex and that send collateral branches to multiple supraspinal structures do not reach the spinal cord. Also, the great majority of the corticospinal neurones that emit multiple intracraneal collateral branches terminate at the cervical spinal cord level. The pyramidal tract fibres directed to the dorsal column nuclei that send collateral branches to supraspinal structures also show a clear tendency to terminate at supraspinal and cervical cord levels. These facts suggest that a substantial co-ordination between descending and ascending pathways might be produced by the same motor cortex axons at both supraspinal and cervical spinal cord sites. This may imply that the motor cortex co-ordination will be mostly directed to motor responses involving eye-neck-forelimb muscle synergies. The review makes special emphasis in the available evidence pointing to the role of the motor cortex in co-ordinating the activities of both descending and ascending pathways related to somatomotor integration and control. The motor cortex may function to co-operatively select a unique motor command by selectively filter sensory information and by co-ordinating the activities of the descending systems related to the control of distal and proximal muscles.

Afferent Pathways↗

PubMed2000

Neuronal and behavioral correlations in the medial prefrontal cortex and nucleus accumbens during cocaine self-administration by rats.

Up to 31 neurons per animal were simultaneously recorded from the medial prefrontal cortex and nucleus accumbens in 15 rats during i.v. cocaine self-administration sessions, using a multi-channel, single-unit recording technique. Alterations of neuronal activity (both excitatory and inhibitory) were found a few seconds before each lever press for cocaine infusion; we have called these pre-lever press neuronal activations "anticipatory responses". A detailed video analysis revealed that these neuronal firing alterations were associated with specific portions of the behavioral sequence performed before each lever press in both recording areas. Some of the simultaneously recorded neurons displayed similar firing patterns in relation to a given behavioral episode within the behavioral sequence (turning, raising head, etc.), while others fired at different times relative to each behavioral event. Cross-correlational analyses revealed inter-regional and intra-regional correlated firing patterns between pairs of simultaneously recorded medial prefrontal cortex and nucleus accumbens neurons. This correlated firing occurred in the neurons with and without anticipatory responses, although the incidence of correlations between anticipatory neuron pairs was much higher than that between non-anticipatory neuron pairs (18.4% vs 3.6%). Many correlated neuron pairs displayed a time lag in the peak of correlational activity that indicated a temporal sequence in correlated activity. In contradiction to our hypothesis, the temporal pattern of correlation reveals that there are more cases in which nucleus accumbens neurons fired ahead of medial prefrontal cortex neurons. The results suggest that multiple mesocorticolimbic neuronal circuits may code sequential steps during the behavioral sequence performed to obtain an infusion of cocaine. The observed correlated firing between the medial prefrontal cortex and the nucleus accumbens indicates that dynamic, coherent activity occurs within the mesocorticolimbic circuit. Because this circuit is hypothesized to drive drug-seeking behavior, we suggest that this correlated firing between the nucleus accumbens and the medial prefrontal cortex may participate in the control of cocaine self-administration. In addition, the finding that correlated activity within the nucleus accumbens more often precedes that of the medial prefrontal cortex suggests that the nucleus accumbens may play a prime role in the initiation of cocaine self-administration.

Animals↗

PubMed2000

Modelling cognitive dysfunctions with bilateral injections of ibotenic acid into the rat entorhinal cortex.

Neurodegenerative diseases, traumatic brain injury and stroke are likely to result in cognitive dysfunctioning. Animal models are needed in which these deficits and recovery of the affected functions can be investigated. In the present study, the entorhinal area was chosen as the target for lesioning and for assessing the lesion-induced deficits in the Morris water maze. The entorhinal cortex is regarded as an interface between the hippocampus and neocortex. Deafferentiating the hippocampus through entorhinal lesions impairs spatial learning. The effects of lesions, induced by either electrocoagulation (experiment 1) or ibotenate excitotoxicity (experiment 2), on spatial orientation behaviour were investigated. Water maze performance after unilateral or bilateral ibotenate injections into the entorhinal cortex was studied in the third experiment. In an additional study, the replicability of the spatial learning deficit after lesions induced by bilateral injections of ibotenic acid into the entorhinal cortex was assessed by comparing the results of nine experiments. We found that spatial learning was impaired after bilateral lesions aimed at the entorhinal cortex. The electrolytic lesion technique produced a relatively large sham effect, whereas the excitotoxic lesioning method did not. Unilateral injections of ibotenic acid into the entorhinal cortex did not affect spatial navigation. The ibotenate-induced lesions replicably produced deficits in the Morris tasks. The degree of the induced spatial learning impairments and the effects on the rate of acquisition during training, however, differed between experiments. This result suggests that the fundamental biological diversity between shipments of rats can account for variation in the effects of parahippocampal damage on spatial learning even in highly standardized experimental set-ups. Rats lesioned by bilateral injections of ibotenic acid into the entorhinal cortex provide an interesting and reliable model for investigating cognitive dysfunctions in neurodegenerative diseases, stroke or traumatic brain injury.

Brain Injuries↗

PubMed2001

Expression of c-Fos, Fos B, Jun B, and Zif268 transcription factor proteins in rat barrel cortex following apomorphine-evoked whisking behavior.

Apomorphine-evoked expression of transcription factor proteins: c-Fos, Fos B, Jun B, and Zif268 (also named Krox-24, NGFI-A, Egr-1), was investigated in rat somatosensory (barrel) cortex. The effect of the N-methyl-D-aspartate receptor antagonist MK-801 on their expression was also analyzed. Apomorphine is a dopamine receptor agonist, eliciting motor activity, including enhanced whisking leading to the activation of vibrissae representation in the barrel cortex. Rats had their whiskers clipped on one side of the snout. The Zif268 levels were markedly reduced by this procedure alone. In contrast, apomorphine (5.0 mg/kg) evoked marked c-Fos elevation, less pronounced changes in Jun B and Zif268 and no change in Fos B. The greatest apomorphine-evoked c-Fos accumulation was observed in layers IV and V/VI of non-deprived barrel cortex and was not significantly influenced by MK-801 injection at 0.1 mg/kg. A higher dose of MK-801 (1.0 mg/kg) produced abnormalities in locomotor behavior and diminished c-Fos levels on the non-deprived side to the ones observed in the sensory stimulus-deprived cortex. We conclude that the response of the somatosensory cortex is selective with respect to both the gene activated and its cortical layer localization. Furthermore, sensory stimulation provides a major but not the only component to apomorphine-evoked barrel cortex gene activation.

Afferent Pathways↗

PubMed2003

Prolonged exercise induces angiogenesis and increases cerebral blood volume in primary motor cortex of the rat.

Plastic changes in motor cortex capillary structure and function were examined in three separate experiments in adult rats following prolonged exercise. The first two experiments employed T-two-star (T(2)*)-weighted and flow-alternating inversion recovery (FAIR) functional magnetic resonance imaging to assess chronic changes in blood volume and flow as a result of exercise. The third experiment used an antibody against the CD61 integrin expressed on developing capillaries to determine if motor cortex capillaries undergo structural modifications. In experiment 1, T(2)*-weighted images of forelimb regions of motor cortex were obtained following 30 days of either repetitive activity on a running wheel or relative inactivity. The proton signal intensity was markedly reduced in the motor cortex of exercised animals compared with that of controls. This reduction was not attributable to alterations of vascular iron levels. These results are therefore most consistent with increased capillary perfusion or blood volume of forelimb regions of motor cortex. FAIR images acquired during experiment 2 under normocapnic and hypercapnic conditions indicated that resting cerebral blood flow was not altered under normal conditions but was elevated in response to high levels of CO(2), suggesting that prolonged exercise increases the size of a capillary reserve. Finally, the immunohistological data indicated that exercise induces robust growth of capillaries (angiogenesis) within 30 days from the onset of the exercise regimen. Analysis of other regions failed to find any changes in perfusion or capillary structure suggesting that this motor activity-induced plasticity may be specific to motor cortex.These data indicate that capillary growth occurs in motor areas of the cerebral cortex as a robust adaptation to prolonged motor activity. In addition to capillary growth, the vascular system also experiences heightened flow under conditions of activation. These changes are chronic and observable even in the anesthetized animal and are measurable using noninvasive techniques.

Aging↗