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PubMed2006

The neural response to transcranial magnetic stimulation of the human motor cortex. I. Intracortical and cortico-cortical contributions.

We investigated the properties of the neural response to transcranial magnetic stimulation (TMS) applied over the human primary motor cortex. Consistent with our previous findings, single pulses of TMS induce a characteristic negative deflection at 45 ms (N45) and a transient oscillation in the beta frequency-range (15-30 Hz), as measured using electroencephalograpy (EEG). Here we show the relative specificity of the beta oscillation and the N45; both are stronger when elicited by stimulation applied over the primary motor cortex, as compared with stimulation over the dorsal premotor cortex. We also provide a quantitative analysis of the beta responses to single pulses of TMS and show that the responses are highly phaselocked to the TMS pulses within single subjects; this phaselocking is similar from subject to subject. A single pulse of TMS applied over the primary motor cortex thus appears to reset the ongoing oscillations of the neurons, bringing them transiently into synchrony. Finally, we examine the effect of local or distal modulation of the excitability of the primary motor cortex on the beta oscillation and the N45 in response to single-pulse TMS. We applied low-frequency subthreshold repetitive TMS either over the primary motor cortex (local modulation) or, on a separate day, over the dorsal premotor cortex (distal modulation). The modulation was evaluated with single suprathreshold test pulses of TMS applied over the primary motor cortex before and after the subthreshold low-frequency rTMS. We recorded the EEG response throughout the testing session, i.e. to both the subthreshold and the suprathreshold pulses. After repetitive TMS applied over the primary motor cortex, but not the dorsal premotor cortex, the amplitude of the N45 in response to suprathreshold pulses tended to decrease (not significant), and subsequently increased (significant); neither type of repetitive TMS affected the amplitude of the beta oscillation. We conclude that (1) the N45 depends on circuits intrinsic to the primary motor cortex; (2) the beta oscillation is specific to stimulation of the primary motor cortex, but is not affected by modulation of either cortical area and; (3) the beta oscillatory response to pulses of TMS arises from resetting of ongoing oscillations rather than their induction.

Adult↗

PubMed1983

Evidence for a direct projection from the superior temporal gyrus to the entorhinal cortex in the monkey.

During the course of a larger study of the afferent and efferent connections of the entorhinal cortex in the macaque monkey we have found evidence for a hitherto undescribed projection to the entorhinal cortex from the superior temporal gyrus. The evidence is derived principally from experiments in which small volumes of wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) were injected into different parts of the entorhinal cortex, but has been confirmed by 3H-amino acid autoradiography. After WGA-HRP injections into the entorhinal cortex, retrogradely labeled neurons have been seen mainly in layer III, but also to some extent in layer VI, throughout much of the superior temporal gyrus. The projection appears to be topographically organized in the sense that the ventral insular cortex and the adjoining temporal operculum have been found to project to the periamygdaloid cortex and the lateral division of the entorhinal cortex; the convexity of the superior temporal gyrus and the cortex along the dorsal bank of the superior temporal gyrus project further caudally to the medial division of the entorhinal cortex; and the cortex surrounding the fundus of the superior temporal sulcus projects to the perirhinal cortex. Following an injection of 3H-amino acids into the convexity of the superior temporal gyrus, terminal labeling has been seen over layers I and II of the entorhinal cortex and over layer I in the most lateral portion of the presubiculum. While the distribution of retrogradely labeled cells in our WGA-HRP experiments encompasses several cytoarchitectonically distinguishable areas in the superior temporal gyrus, the most heavily labeled field appears to coincide with what Gross and his colleagues have termed the 'superior temporal polysensory area' on the dorsal bank of the superior temporal sulcus.

Afferent Pathways↗

PubMed1990

Neural systems contributing to acetylcholinesterase histochemical staining in primary visual cortex of the adult rat.

Histochemical studies demonstrate that cortical area 17 (primary visual cortex) of the adult rat displays a characteristic laminar pattern of acetylcholinesterase (AChE) activity. While AChE-positive axons are found throughout the cortical layers, most intense staining occurs in a band that corresponds to layer V and the deep portion of layer IV. The present studies were directed toward determining the neural systems containing this AChE activity. Unilateral electrolytic or excitatory amino acid induced lesions of the basal forebrain result in reductions of AChE staining in ipsilateral visual cortex, particularly in layers IV and V. Electrolytic or scalpel lesions, placed in white matter underlying dorsal and lateral neocortex to interrupt basal forebrain projections to visual cortex, also reduce AChE staining in visual cortex. Lesions in the cingulate bundle and supracallosal stria reduced AChE staining retrosplenial cortex but did not affect staining visual cortex. Placement of electrolytic lesions in the hypothalamus produced no detectable change in the pattern of AChE in visual cortex. Electrolytic lesions in the midbrain tegmentum, placed to interrupt ascending axons from brainstem monoamine neurons, produced no detectable change in the pattern of AChE in visual cortex. Placement of lesions in the dorsal thalamus that include all of the dorsal lateral geniculate nucleus did not alter AChE staining in visual cortex. The results indicate that AChE activity in adult visual cortex is found primarily within afferent axons from the basal forebrain system. These data demonstrate further that the AChE staining characteristic of adult visual cortex is associated with neural systems that are distinctly different from those associated with AChE staining in visual cortex of the infant rat.

Acetylcholinesterase↗

PubMed2001

Behavioral cartography of visual functions in cat parietal cortex: areal and laminar dissociations.

The purpose of this review is to: (1) compare and contrast the relative contributions that the four principle regions in cat extrastriate parietal cortex make to a battery of visual tasks which require motion, spatial, or attentional processing; and (2) examine the laminar parcellation of visual behaviors within one of these parietal regions which mediates multiple visual behaviors. We examined a battery of visual tasks presumed to be mediated by parietal cortex, including direction of motion, differential motion, and landmark discriminations, and visual orienting to moving stimuli. As a control, we also examined performance on form (pattern and object) recognition tasks mediated by the temporal processing stream. The four regions of parietal cortex we examined included the: middle suprasylvian (MS) gyrus (area 7), anterior middle suprasylvian (aMS) sulcus (AMLS, ALLS), posterior middle suprasylvian (pMS) sulcus (PMLS, PLLS), and the dorsal posterior suprasylvian (dPS) gyrus (area 21a). The contributions made to each of the six different behavioral tasks was examined before, during, and after reversible cooling deactivation of each cortical area. Deactivation of pMS sulcal cortex resulted in deficits on all four tasks that required motion, spatial or attentional processing. Deactivation of aMS sulcal cortex resulted in deficits on only tasks that required motion processing. Deactivation of neither aMS nor pMS sulcal cortex yielded any deficits on the form recognition tasks. In contrast, deactivation of dPS cortex only produced deficits on the form recognition tasks. This finding confirmed our early hypothesis that dPS cortex is a key component of the temporal, and not the parietal, processing stream. Regardless of the task, no deficits were identified on any of the six tasks during deactivation of the MS gyrus. We then more closely examined pMS sulcal cortex to determine if its multiple functions could be dissociated on a laminar level. We found that cooling deactivation of the superficial layers (I-III) of pMS sulcal cortex selectively and completely impaired performance on the direction of motion discrimination task, while leaving visual attention unimpaired. Additional deactivation of the deeper layers (IV-VI) resulted in impaired visual attention as assessed with visual orienting. These results show a functional bipartite division of labor between upper and lower cortical layers of pMS sulcal cortex. Therefore, spatial, motion and attentional functions can be localized within visuoparietal cortex on both an areal and laminar level.

Animals↗

PubMed2003

Activity-dependent change in the protein level of brain-derived neurotrophic factor but no change in other neurotrophins in the visual cortex of young and adult ferrets.

Neurotrophins are suggested to play a role in activity-dependent plasticity of visual cortex during the critical period of postnatal development. Thus, the concentration of neurotrophins in the cortex is expected to change with development and/or with alteration in neuronal activities. To test this, we measured protein levels of nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4/5 in visual cortex of young (postnatal day 38-46, at the peak of the critical period) and adult ferrets with two-site enzyme-immunoassay systems. Measurements were carried out also in somatosensory cortex, hippocampus and cerebellum as control. With development the level of brain-derived neurotrophic factor did not significantly change, while those of the other neurotrophins changed in the visual cortex. A blockade of visual inputs for 24 h by an injection of tetrodotoxin into both eyes significantly decreased brain-derived neurotrophic factor protein level in the visual cortex, but not in the other regions in both young and adult ferrets. On the other hand, no significant decrease was seen in the protein level of the other neurotrophins in the visual cortex of young and adult ferrets. A monocular injection of tetrodotoxin in young ferrets resulted in the reduction of brain-derived neurotrophic factor by approximately half that by binocular injection. The degree of the decrease in the contralateral cortex to the injected eye was significantly larger than that in the ipsilateral cortex, reflecting that the contralateral eye is dominantly represented in the cortex in ferrets. Blockade of cortical neuronal activities by a GABA(A) receptor agonist led to a remarkable reduction of brain-derived neurotrophic factor protein in the visual cortex. These results suggest that the level of brain-derived neurotrophic factor protein in visual cortex is regulated by activities of cortical neurons.

Aging↗

PubMed2004

p-Nonylphenol, 4-tert-octylphenol and bisphenol A increase the expression of progesterone receptor mRNA in the frontal cortex of adult ovariectomized rats.

Alkylphenols, such as p-nonylphenol (NP) and 4-tert-octylphenol (OP) and bisphenol A (BPA) are thought to mimic oestrogens in their action, and are called endocrine disrupters. We examined whether these endocrine disrupters affected progesterone receptor (PR) mRNA expression in the adult female rat neocortex. In one experiment, at 12.00 h, ovariectomized rats were given a subcutaneous injection of 10 mg of NP, 10 mg of OP or 10 mg of BPA, or sesame oil alone as control. Twenty-four hours after injection, the left side of the frontal cortex, parietal cortex and temporal cortex was collected. In a second experiment to study the time-course of the effects of BPA on PR mRNA, the ovariectomized rats were given a subcutaneous injection of 10 mg of BPA and killed 0, 6, 12 and 24 h after injection. In addition to the frontal cortex and temporal cortex, the occipital cortex was also collected. Northern blotting revealed that, in the first experiment, injection of NP, OP or BPA significantly increased PR mRNA expression in the frontal cortex but not in the parietal cortex. In the temporal cortex, BPA significantly decreased PR mRNA, but NP and OP produced no significant changes. The second experiment revealed that, in the frontal cortex, BPA induced a significant increase in PR mRNA expression at 6 h after injection, which lasted until 24 h after injection. In the temporal cortex, PR mRNA expression was significantly decreased 6 h after injection of BPA and was still significantly low 24 h after injection. No significant change was observed in the occipital cortex. These results suggest that, even in adult rats, endocrine disrupters alter the neocortical function by affecting the PR system, although the physiological significance of PR in the affected area is unknown.

Animals↗

PubMed1993

Postnatal changes in N-methyl-D-aspartate receptor binding and stimulation by glutamate and glycine of [3H]-MK-801 binding in human temporal cortex.

1. Homogenates of human infant and adult temporal cortex were used to measure [3H]-TCP and [3H]-MK-801 binding to the N-methyl-D-aspartate (NMDA)-coupled ion channel phencyclidine site. 2. Both [3H]-TCP and [3H]-MK-801 binding increased in infant cortex by > 100% between term and 26 weeks suggesting that the numbers of NMDA receptors increase during postnatal brain development. 3. [3H]-MK-801 binding was measured under non-equilibrium conditions in temporal cortex homogenates with the addition of 100 microM of L-glutamate plus a range of concentrations (0.05 microM-100 microM) of glycine. Glutamate and glycine increased [3H]-MK-801 binding by stimulating NMDA receptors and improving [3H]-MK-801 access to ion channel binding sites; maximum stimulation in adult and infant temporal cortex was achieved with 100 microM glutamate plus 5 microM glycine; a higher concentration of glycine (50 microM) reduced [3H]-MK-801 binding to below maximum. 4. The stimulation by 100 microM glutamate plus 5 microM glycine of [3H]-MK-801 binding in infant temporal cortex was affected by postnatal age. For example, although the stimulation of [3H]-MK-801 binding in 5-6 week infant cortex (236% of basal) was similar to adult cortex (230% of basal), in samples taken from infants aged 5-6 months glycine (plus glutamate) stimulation of [3H]-MK-801 binding (392% of basal) was substantially greater than that measured in adult temporal cortex. 5. The binding of [3H]-glycine to the glycine modulatory site associated with the NMDA receptor in infant cortex also increased with postnatal age by > 100% between term and 26 weeks. 6. It is concluded that NMDA receptors in infant cortex increase to levels greater than those in adult cortex during postnatal development. The results do not exclude the possibility that the transiently increased NMDA receptor-ion channel complex in infant cortex shows enhanced responses to agonists and modulators.

Adult↗

PubMed1987

Effects of cholinergic depletion on neuron activities in the cat visual cortex.

1. Unilateral lesions of the nucleus basalis magnocellularis (nBM), a source of cholinergic projection to the cerebral cortex, were produced by injection of kainic acid in the cat. The lesions caused a significant reduction in density of choline acetyltransferase-immunoreactive terminals in the visual cortex ipsilateral to the lesions. 2. In the primary visual cortex ipsilateral to the lesions [acetylcholine (ACh)-depleted cortex], about half of the cells had weak or undetectable visual responses, whereas in the contralateral visual cortex almost all the cells had normal responsivity. The response selectivity, such as orientation and direction selectivities, of cortical cells was not affected by the depletion of ACh. 3. The microionophoretic application of ACh to cells under observation facilitated visual responses in 83% of the cells recorded from the ACh-depleted cortex, whereas it suppressed the responses in only 9%. The application of a muscarinic antagonist, atropine, to cells in the ACh-depleted cortex was ineffective, suggesting no residual ACh activity. 4. The mean current required to induce facilitation in the cortex ipsilateral to the lesion was significantly smaller than that required in the contralateral cortex and the visual cortex of the normal cat, suggesting a supersensitivity of receptors mediating the effect or a reduction in catabolism of exogenous ACh in the ACh-depleted cortex. 5. More than half of the cells that had been unresponsive to visual stimuli became clearly responsive during the ACh application. The response magnitude of cortical cells, as a whole, increased to the same degree as that observed during the ACh application in the normal cat. 6. In addition to the decrease in the average response magnitude, there was a remarkable variability in responses of cells to motion of the slit from sweep to sweep in the ACh-depleted cortex. The application of ACh to cortical cells decreased the variability of responses and consequently made the responses much more consistent. 7. These results suggest that without ACh supplied from the nBM, most of the cortical neurons could not respond briskly and consistently to excitatory inputs and that exogenously applied ACh could reverse such an impairment of cortical neurons through intact or even supersensitive postsynaptic receptors.

Acetylcholine↗

PubMed1993

Anatomic organization of evoked potentials in rat parietotemporal cortex: somatosensory and auditory responses.

1. Two 8 x 8-channel microelectrode arrays were used to map epicortical field potentials from a 3.5 x 3.5-mm2 area in homologous regions of right and left parietotemporal cortex of four rats. Potentials were evoked with bilaterally presented click stimuli and with bilateral tactile stimulation of the 25 major vibrissae. The spatial distribution of temporal components of the somatosensory evoked potential (SEP) and auditory evoked potential (AEP) complex were compared directly with cytochrome oxidase-stained sections of the recorded region. 2. Epicortical responses in both hemispheres to bilateral vibrissal stimuli consisted of a biphasic sharp wave (P1a-N1) constrained to the vibrissa/barrel granular region of primary somatosensory cortex (SmI). A slightly later sharp positive wave (P1b) was localized to secondary somatosensory cortex (SmII) and to perigranular cortex medial to the vibrissa/barrel field. The SEP complex ended with a biphasic slow wave (P2-N2). The P2 was centered on SmI and spread to dysgranular lateral cortex, caudal to but excluding SmII. The N2 was centered on SmII and spread to dysgranular cortex caudal to but excluding SmI. 3. The anatomic organization of the AEP in many ways approximated that of the SEP in the same animals. The timing and morphology of the AEP were nearly identical to the SEP. The AEP consisted of a P1a-N1 sharp wave constrained to the estimated region of primary auditory cortex (AI) in the lateral parietotemporal region, a later P1b localized to secondary auditory cortex (AII), and subsequent slow waves (P2 and N2) that were centered on AI and AII, respectively, and spread to dysgranular regions overlapping the distributions of the P2 and N2 of the SEP complex. 4. These data suggest that the basic neural generators for the SEP and AEP in parietotemporal cortex are quite similar, and provide evidence for the functional anatomy of each temporal component of the sensory evoked potential complex. It is concluded that the early fast waves of the SEP and AEP are modality specific and may represent the parallel activation of primary and secondary sensory cortex through established parallel afferent projections from lateral and medial thalamic nuclei. The later slow waves of the SEP and AEP appear to selectively involve primary and secondary sensory cortex but are more widely distributed, possibly reflecting a less modality-specific level of information processing in dysgranular cortex.

Acoustic Stimulation↗

PubMed1996

Effects of rhinal cortex lesions combined with hippocampectomy on visual recognition memory in rhesus monkeys.

1. We assessed the visual recognition abilities, as measured by delayed nonmatching-to-sample with trial-unique objects, of rhesus monkeys with hippocampectomy (i.e., removal of the hippocampal formation plus parahippocampal gyrus) combined with ablations of the rhinal cortex (i.e., entorhinal cortex plus perirhinal cortex). 2. Relative to unoperated controls, monkeys with combined hippocampectomy and rhinal cortex ablation (H+Rh) were significantly impaired in visual recognition. 3. Comparison of the scores of the monkeys in the present H+Rh group, which sustained near-complete rhinal cortex damage, with the scores of monkeys in an earlier H+Rh group in which the rostral part of the rhinal cortex had been spared indicates that the magnitude of the impairment is greater in the group with the more complete rhinal cortex damage. This finding is consistent with the idea that the rhinal cortex is critical for visual recognition. 4. Comparison of the present results with those from an earlier study on visual recognition that employed lesions limited to the rhinal cortex (Rh group) shows, paradoxically, that adding removal of the hippocampal formation and parahippocampal gyrus to a rhinal cortex lesion significantly reduces the recognition impairment produced by rhinal cortex lesions alone. 5. Our findings do not fit the view that the hippocampal formation, parahippocampal gyrus, and rhinal cortex constitute parts of a single functional system, such that the greater the damage to the entire system, the more severe the impairment. Instead, the results are consistent with the view that there are multiple functional subdivisions within the medial temporal lobe.

Animals↗

PubMed1978

Evidence that the severity of depletion of inorganic phosphate determines the severity of the disturbance of adenine nucleotide metabolism in the liver and renal cortex of the fructose-loaded rat.

To test the hypothesis that in both the liver and renal cortex of the fructose-loaded rat, severity of depletion of inorganic phosphate (P(i)), and not the magnitude of accumulation of fructose-1-phosphate (F-1-P), determines the severity of the dose-dependent reduction of ATP, we intraperitoneally injected fed rats with fructose, 20 and 40 mumol/g, alone, and at the higher load, in combination with (a) sodium phosphate, 20 mumol/g, administered shortly beforehand or subsequently or, (b) adenosine, 2 mumol/g, administered beforehand. The following observations were made: (a) With fructose loading alone, at the higher load, both P(i) and total adenine nucleotides (TAN) were reduced by one third in the renal cortex and (as previously observed) by two thirds in the liver; and at either load, the reduction of ATP (and TAN) and the accumulation of F-1-P were less severe in the renal cortex than in the liver. (b) Prior phosphate loading largely prevented the reductions of ATP and TAN in the renal cortex and significantly attenuated them in the liver, yet doubled the renal cortical accumulation of F-1-P. (c) Adenosine loading substantially attenuated the reductions of ATP, TAN, and P(i) only in the renal cortex. (d) ATP varied directly with P(i) (P < 0.001, r = 0.98) in the domain of control and reduced values of P(i) taken from both liver and renal cortex. (e) As judged from tissue and plasma concentrations of fructose and glucose, and tissue concentrations of fructose-6-phosphate and glucose-6-phosphate, the rate at which the renal cortex and liver converted fructose to glucose was much lower at the higher fructose load. (f) Prior phosphate loading prevented this decrease in rate in the renal cortex and attenuated it in the liver; adenosine loading attenuated it only in the renal cortex. We conclude that in both the renal cortex of the fructose-loaded rat: (a) Depletion of P(i) is critical to the causation of the reductions in both ATP and TAN and, at the higher fructose load, of a decrease in the rate at which ATP is regenerated. (b) The severity of depletion of P(i) determines the severity of these disturbances. (c) By differentially mitigating the depletion of P(i), prior phosphate loading largely prevents these disturbances in the renal cortex, and attenuates them in the liver; and adenosine loading attenuates them only in the renal cortex. The findings provide some basis for the observation that in patients with hereditary fructose intolerance experimentally exposed to fructose, prior loading with sodium phosphate substantially attenuates the renal but not hepatic dysfunction.

Adenine Nucleotides↗

PubMed2004

Impairment of social perception associated with lesions of the prefrontal cortex.

OBJECTIVE: Behavioral and social impairments have been frequently reported after damage to the prefrontal cortex in humans. This study evaluated social perception in patients with prefrontal cortex lesions and compared their performance on a social perception task with that of healthy volunteers. METHOD: Thirty-three patients with prefrontal cortex lesions and 31 healthy volunteers were tested with the Interpersonal Perception Task. In this task, subjects viewed videotaped social interactions and relied primarily on nonverbal cues to make interpersonal judgments, such as determining the degree of intimacy between two persons depicted in the videotaped scene. Patients with prefrontal cortex lesions were classified according to lesion involvement of specific regions, including the orbitofrontal cortex, dorsolateral prefrontal cortex, and anterior cingulate cortex. RESULTS: Relative to the comparison subjects, patients whose lesions involved the orbitofrontal cortex demonstrated impaired social perception. Contrary to predictions, patients with lesions in the dorsolateral prefrontal cortex also showed deficits in using social cues to make interpersonal judgments. All patients, particularly those with lesions in the dorsolateral prefrontal cortex, showed poorer insight into their deficits, relative to healthy volunteers. CONCLUSIONS: These findings of deficits in social perception after damage to the orbitofrontal cortex extend previous clinical and experimental evidence of damage-related impairment in other aspects of social cognition, such as the ability to accurately evaluate emotional facial expressions. In addition, the results suggest that the dorsolateral prefrontal cortex is recruited when inferences about social interactions are made on the basis of nonverbal information.

Brain Injuries↗

PubMed2004

The entorhinal cortex in first-episode psychotic disorders: a structural magnetic resonance imaging study.

OBJECTIVE: Neuropathological findings regarding the entorhinal cortex in schizophrenia are conflicting. The authors used structural magnetic resonance imaging to examine the entorhinal cortex volumes of healthy subjects and medication-naive patients experiencing their first episode of psychotic illness. METHOD: The study included 33 patients with schizophrenia and related disorders, 11 patients with nonschizophrenic disorders, and 43 matched healthy subjects. All subjects were rated on the Scale for the Assessment of Positive Symptoms and the Scale for the Assessment of Negative Symptoms, and volumetric measurements of the entorhinal cortex were obtained for all subjects. The authors examined differences across the groups as well as clinical correlations of entorhinal cortex volumes adjusted for intracranial volume. RESULTS: A significant diagnosis effect was seen in the left entorhinal cortex: patients with schizophrenia and related disorders and patients with nonschizophrenic psychotic disorders had smaller left entorhinal cortex volumes than healthy subjects. The mean entorhinal cortex volume of patients with schizophrenic disorders did not differ from that of patients with nonschizophrenic psychotic disorders. In patients with schizophrenic disorders, the entorhinal cortex volume positively correlated with severity of delusions. The mean entorhinal cortex volume of patients with nondelusional psychotic disorders was significantly smaller than that of patients with delusional psychotic disorders and healthy subjects. CONCLUSIONS: Smaller entorhinal cortex volume in first-episode, neuroleptic-naive psychotic disorders may not be a confound of the effects of illness chronicity or antipsychotic treatment. Entorhinal cortex pathology appears to have a significant association with positive symptoms, specifically delusions. The impairment of functions in which the entorhinal cortex participates-such as novelty detection, associative learning, and processing episodic, recognition, and autobiographical memory-could be responsible for its association with psychotic disorders and delusions.

Adult↗

PubMed2005

Borderline personality disorder, impulsivity, and the orbitofrontal cortex.

OBJECTIVE: Orbitofrontal cortex lesions produce disinhibited or socially inappropriate behavior and emotional irregularities. Characteristics of borderline personality disorder include impulsivity and affective instability. The authors investigated whether aspects of borderline personality disorder, in particular impulsivity, are associated with orbitofrontal cortex dysfunction. METHOD: Measures of personality, emotion, impulsivity, time perception, sensitivity to reinforcers, and spatial working memory were administered to patients with borderline personality disorder (N=19), patients with orbitofrontal cortex lesions (N=23), patients with lesions in the prefrontal cortex but not in the orbitofrontal cortex (N=20), and healthy comparison subjects (N=39). RESULTS: The patients with orbitofrontal cortex lesions and the patients with borderline personality disorder performed similarly on several measures. Both groups were more impulsive and reported more inappropriate behaviors, borderline personality disorder characteristics, and anger and less happiness than the two comparison groups, and both groups were less open to experience and had a faster perception of time (underproduced time) than the healthy comparison subjects. The patients with orbitofrontal cortex lesions and the borderline personality disorder patients performed differently on other measures. The borderline personality disorder patients were less extraverted and conscientious and more neurotic and emotional than all other groups. Patients with orbitofrontal cortex lesions had deficits in reversing stimulus-reinforcer associations and a faster perception of time (overestimated time) than the healthy comparison subjects. CONCLUSIONS: Orbitofrontal cortex dysfunction may contribute to some core characteristics of borderline personality disorder, in particular impulsivity. Other characteristics of borderline personality disorder, such as high levels of emotionality and personality irregularities, do not appear to be related to the type of dysfunction produced by orbitofrontal cortex damage. The similarities and differences found between the borderline personality disorder patients and the patients with orbitofrontal cortex lesions may lead to a better understanding of the etiology of borderline personality disorder and the functions of the orbitofrontal cortex.

Adolescent↗

PubMed1998

Decreased N-acetylaspartate in motor cortex and corticospinal tract in ALS.

The primary objectives of this study were to test whether 1) N-acetylaspartate (NAA), a neuronal marker, is reduced in motor cortex and corticospinal-tract (CST) brain regions of ALS patients; and 2) motor cortex NAA correlates to a clinical measurement of upper motor neuron function in ALS patients. Ten probable or definite ALS patients and nine neurologically normal control subjects were studied. Three axial planes of two-dimensional 1H MRSI data were collected, using a single spin-echo multislice sequence (TE140/TR2000). Two of the 1H MRSI planes were positioned superior to the lateral ventricles, and one plane was positioned at the level of the internal capsule. Spectroscopy voxels were selected from motor cortex, frontal cortex, parietal cortex, medial gray matter, centrum semiovale white matter, anterior internal capsule, and posterior internal capsule. Peak integrals were obtained for the three major 1H MRSI singlet resonances, NAA, creatine and phosphocreatine (Cr), and cholines (Cho). Maximum finger-tap rate was used as a clinical measurement of upper motor neuron function. In ALS, brain NAA/(Cho+Cr) was reduced 19% (p=0.024) in the motor cortex and 16% (p=0.021) in the CST (centrum semiovale and posterior internal capsule) regions. NAA/ (Cho+Cr) was not reduced in frontal cortex, parietal cortex, medial gray matter, or anterior internal capsule. There was a significant relation between ALS motor cortex NAA/(Cho+Cr) and maximum finger-tap rate (r=0.80; p=0.014). NAA/(Cho+Cr) was reduced in motor cortex and CST regions and unchanged in other brain regions of ALS patients when compared with controls. These findings are consistent with the known distribution of neuronal loss in ALS. The positive correlation between motor cortex NAA/(Cho+Cr) and maximum finger-tap rate suggests that reduced NAA/(Cho+Cr) is a surrogate marker of motor cortex neuron loss in ALS. These findings support the study of 1H MRSI NAA measurement as an objective and quantitative measurement of upper motor neuron dysfunction in ALS.

Adult↗

PubMed1975

Effect of diuretics on ion transport of kidney cortex mitochondria. III. Species difference in calcium accumulation and in ethacrynic acid effect.

Effect of inorganic phosphate (4 X 10(-3) M) on Ca++-accumulation was examined in kidney cortex mitochondria. Ca++-accumulation of rat kidney cortex mitochondria was slightly influenced by inorganic phosphate. On the other hand, dog kidney cortex mitochondria did not accumulate calcium from the incubation medium until the inorganic phosphate had been added. Ca++-accumulation of rabbit kidney cortex mitochondria was markedly stimulated by inorganic phosphate. When ethacrynic acid was added to the reaction medium in the absence of inorganic phosphate, Ca++-accumulation of rat kidney cortex mitochondria was depressed and the decrease in calcium content of rabbit and dog kidney cortex mitochondria was enhanced. In the presence of inorganic phosphate, the inhibition of Ca++-accumulation by ethacrynic acid was observed only on dog kidney cortex mitochondria. Subsequently, the effect of inorganic phosphate (4 X 10(-4) M) and ethacrynic acid (1 X 10(-4) M on Ca++-ATPase was examined in kidney cortex mitochondria. The low concentration of inorganic phosphate (4 X 10(-4) M) activated Ca++-ATPase of kidney cortex mitochondria in all animal species. The greatest activation of Ca++-ATPase occurred in rabbits, but the activity of the enzyme was lower than that in rats and dogs. Inhibition of Ca++-ATPase by ethacrynic acid was depressed by the addition of inorganic phosphate in kidney cortex mitochondria of experimental animals. Ca++-accumulation may be regulated through the stimulating effect of inorganic phosphate and the inhibitory effect of ethacrynic acid on Ca++-ATPase in kidney cortex mitochondria. Species difference in ethacrynic acid effect on Ca++-accumulation in kidney cortex mitochondria of rats, rabbits and dogs is discussed.

Adenosine Triphosphatases↗

PubMed1991

Organization of visual inputs to the inferior temporal and posterior parietal cortex in macaques.

It has been proposed that visual information in the extrastriate cortex is conveyed along 2 major processing pathways, a "dorsal" pathway directed to the posterior parietal cortex, underlying spatial vision, and a "ventral" pathway directed to the inferior temporal cortex, underlying object vision. To determine the relative distributions of cells projecting to the 2 pathways, we injected the posterior parietal and inferior temporal cortex with different fluorescent tracers in 5 rhesus monkeys. The parietal injections included the ventral intraparietal (VIP) and lateral intraparietal (LIP) areas, and the temporal injections included the lateral portions of cytoarchitectonic areas TE and TEO. There was a remarkable segregation of cells projecting to the 2 systems. Inputs to the parietal cortex tended to arise either from areas that have been implicated in spatial or motion analysis or from peripheral field representations in the prestriate cortex. By contrast, inputs to the temporal cortex tended to arise from areas that have been implicated in form and color analysis or from central field representations. Cells projecting to the parietal cortex were found in visual area 2 (V2), but only in the far peripheral representations of both the upper and lower visual field. Likewise, labeled cells found in visual areas 3 (V3) and 4 (V4) were densest in their peripheral representations. Heavy accumulations of labeled cells were found in the dorsal parieto-occipital cortex, including the parieto-occipital (PO) area, part A of V3 (V3A), and the dorsal prelunate area (DP). In the superior temporal sulcus, cells were found within several motion-sensitive areas, including the middle temporal area (MT), the medial superior temporal area (MST), the fundus of the superior temporal area (FST), and the superior temporal polysensory area (STP), as well as within anterior portions of the sulcus whose organization is as yet poorly defined. Cells projecting to areas TE and TEO in the temporal cortex were located within cytoarchitectonic area TG at the temporal pole and cytoarchitectonic areas TF and TH on the parahippocampal gyrus, as well as in noninjected portions of area TE buried within the superior temporal sulcus. In the prestriate cortex, labeled cells were found in V2, V3, and V4, but, in contrast to the loci labeled after parietal injections, those labeled after temporal injections were concentrated in the foveal or central field representations. Although few double-labeled cells were seen, 2 regions containing intermingled parietal- and temporal-projection cells were area V4 and the cortex at the bottom of the anterior superior temporal sulcus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1995

The spatiotemporal organization of auditory, visual, and auditory-visual evoked potentials in rat cortex.

Four placements of an 8 x 8 channel microelectrode array were used to map auditory, visual, and combined auditory-visual evoked potentials (AEP, VEP, AVEP) from a total of 256 electrode sites over a 7 x 7 mm2 area including most of somatosensory, auditory, and visual cortex in the right hemisphere of the rat. The unimodal AEP and VEP consisted of an archetypal response sequence representing a systematic spatial and temporal activation of primary and secondary sensory cortex. Spatiotemporal analysis of these waveforms indicated that they could be decomposed into a small number of spatial and temporal components; components that are related to patterns of specific and non-specific thalamocortical projections connecting the auditory and visual nuclei of the thalamus with primary and secondary auditory and visual cortex. These data suggest that the AEP and VEP complex are the cortical reflection of asynchronous activation of parallel thalamocortical projection systems. The areal distribution of the AEP and VEP also overlapped, primarily in secondary auditory and visual cortex, indicating that these regions contain populations of cells responding to either modality. Polymodal auditory-visual stimulation resulted in unique activation of two isolated populations of neurons positioned in secondary auditory and secondary visual cortex which were revealed by difference waveforms, computed by subtracting the sum of the AEP and VEP from the AVEP complex. Retrograde labeling of the polymodal zones indicated that they receive parallel thalamocortical projections primarily from non-specific auditory and visual thalamic nuclei including the medial and dorsal divisions of the medial geniculate nucleus (MGm and MGd), the suprageniculate nucleus (SGN), and the lateral posterior nucleus (LP). The polymodal zone in visual cortex also receives specific projections from the dorsal division of the lateral geniculate nucleus (LGd). These data conform to a general model of thalamocortical organization in which specific thalamic nuclei with a high degree of modality specificity make restricted projections to primary sensory cortex and parts of secondary sensory cortex, and association thalamic nuclei with a high degree of sensory convergence make more divergent cortical projections. Primary and secondary sensory cortex, as well as distinct zones of polysensory cortex appear to be activated in tandem via parallel thalamocortical projections. Thus, the cerebral cortex must have simultaneous access to both unimodal and polymodal sensory information.

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