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PubMedDate not supplied

The developmental profile of seizure genesis in the inferior collicular cortex of the rat: relevance to human neonatal seizures.

The ontogeny of seizure genesis within the inferior collicular cortex was characterized in rats ranging in age from 3 days old to adult. Brief electrical stimulation of the right inferior collicular cortex in 30-day-old rats evoked poststimulus wild running behavior that coincided with afterdischarge activity in the inferior collicular cortex but not in the adjacent occipital cortex. Similar electrical stimulation in 16-day-old rats produced poststimulus wild running and jumping behaviors, which also coincided with afterdischarge in the inferior collicular cortex. In 10- and 5-day-old rats, electrical stimulation of the inferior collicular cortex produced poststimulus locomotion and coincident afterdischarge activity, but unlike older rats the locomotor behaviors consisted of forelimb paddling, hindlimb treading, and rolling/curling movements of the torso. Identical behaviors can be electrically elicited in 3-day-old rats. Although many of the seizure characteristics appear to be similar among the different age groups, 5-day-old rats were more sensitive to low frequency stimulation than 16-day-old rats, who in turn were more sensitive than adult rats. Thus, the inferior collicular cortex is capable of generating seizure activity in rats as young as 3 days of age, providing a focal model of neonatal seizure genesis.

Age Factors↗

PubMed1986

Turtle hippocampal cortex contains distinct cell types, burst-firing neurons, and an epileptogenic subfield.

The dorsal and medial telencephalon of reptiles consists of a simple trilaminar cortex. The turtle dorsal cortex has been identified as a favorable physiological preparation that may bear a phylogenetic relationship to mammalian neocortex. While anatomical studies have likened the reptilian medial cortical region to mammalian hippocampus, its physiological properties have not been explored. We therefore used intracellular and extracellular recording techniques to examine the cellular and synaptic physiology of turtle "hippocampal" or medial cortex. Turtle medial cortex contains two principal classes of neurons, pyramidal cells and stellate neurons. Recordings with Lucifer yellow CH (LY)-filled microelectrodes allowed us to correlate the physiological properties of medial cortical neurons with their cellular morphology. Pyramidal neurons were situated in a single cellular layer and had spiny apical dendrites extending into the molecular layer. These cells fired relatively long-duration action potentials (APs) and showed frequency adaptation to suprathreshold current pulse injections. Stellate cells were usually found in the subcellular and molecular layers and had aspiny dendrites. In contrast to pyramidal cells, they fired brief APs and displayed no frequency adaptation. A discrete population of cells in the dorsal portion of medial cortex (DMC) was capable of bursting endogenously or in response to synaptic activation. Bursts usually contained an underlying slow depolarization and often occurred at regular intervals. Intracellular LY injections confirmed that these cells were pyramidal in morphology. Electrical stimulation of afferent fibers revealed that pyramidal cells and stellate neurons differed in their synaptic responses. In ventral medial cortex (VMC), afferent stimulation evoked a multiphasic response in most pyramidal cells, whereas stellate cells were synaptically excited. Orthodromic activation of DMC bursting cells resulted in a powerful excitation--often a short burst--and subsequent inhibition. Stellate neurons in DMC also had a biphasic synaptic response consisting of both an early excitation and a late inhibition. Experiments using intracellular chloride (Cl-) injection or focal bicuculline application suggested that part of the inhibitory component of the pyramidal cell synaptic response was dependent on a gamma-aminobutyric acid (GABA)-mediated increase in Cl- conductance. These results correlated with our immunohistochemical studies that revealed the presence of GABAergic neurons in medial cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1995

Monocyte chemoattractant protein-1 messenger RNA expression in rat ischemic cortex.

BACKGROUND AND PURPOSE: Previously we demonstrated that focal cerebral ischemia results in an increased expression of several cytokines/chemokines that precede the infiltration of leukocytes into the ischemic cortex after focal stroke induced by occlusion of the middle cerebral artery (MCAO). Monocyte chemoattractant protein-1 (MCP-1) is a potent chemoattractant specific for monocytes. The aim of the present study was to examine whether MCP-1 messenger RNA (mRNA) is expressed in ischemic brain tissue after MCAO. METHODS: The expression of MCP-1 mRNA in the ischemic cortex was first identified by means of a sensitive reverse transcription and polymerase chain reaction technique. The time course of expression of MCP-1 mRNA in the ischemic and nonischemic cerebral cortex after both permanent MCAO and temporary MCAO (160 minutes) with reperfusion was then examined by means of Northern blot analysis. RESULTS: Almost no expression of MCP-1 mRNA was found in the sham-operated or nonischemic (contralateral) cortex. A significant increase in MCP-1 mRNA expression in the ischemic cortex was observed after either permanent or temporary MCAO. MCP-1 mRNA was elevated at 6 hours (4.4-fold increase over sham; n = 4), reached its highest expression from 12 hours to 2 days (22.7-fold at the peak level; P < .01), and remained elevated up to 5 days (5.6-fold; P < .01) after permanent MCAO. The profile of MCP-1 mRNA expression in the ischemic cortex after MCAO with reperfusion was similar to that of permanent MCAO except that MCP-1 mRNA was increased earlier (ie, 12.5-fold increase at 3 hours; n = 4; P < .01). Also, MCP-1 mRNA expression in the ischemic cortex after permanent MCAO was significantly greater in hypertensive rats than in two normotensive rats (n = 4; P < .05). CONCLUSIONS: The demonstration of induced MCP-1 mRNA expression early after focal ischemia suggests that MCP-1 may represent a locally expressed monocyte chemoattractant that plays an important role in monocyte infiltration into ischemic tissue and therefore may contribute to the tissue injury in ischemic stroke. Further studies must concentrate on identifying the induced expression of MCP-1 and its cellular localization in the ischemic brain when the appropriate antibodies become available.

Animals↗

PubMed2005

Stereoselective and region-specific induction of immediate early gene expression in rat parietal cortex by blockade of neurokinin 1 receptors.

Antagonists at neurokinin 1 (NK1) receptors are attracting attention as potential treatments for depressive states in light of their actions in behavioural models predictive of antidepressant properties, their modulation of corticolimbic monoaminergic transmission, and their influence upon neural plasticity. Here, we evaluated the influence of NK1 receptor blockade upon two immediate early genes, Arc and c-fos, implicated in mechanisms of synaptic plasticity. Administration of the selective NK1 receptor antagonist, GR 205,171 (40, but not 1, 5 or 10 mg/kg i.p.), elicited a pronounced elevation in mRNA encoding Arc in both outer and inner layers of the parietal cortex of rat brain. This action was region-specific inasmuch as Arc expression did not change in other cortical territories examined including frontal cortex, nor in CA1, CA3 and the dentate gyrus of the hippocampus. In comparison to GR 205,171, its less active isomer GR 226,206 (1-40 mg/kg) did not significantly modify Arc gene expression in parietal cortex or other cortical areas. GR 205,171 (40 mg/kg) also increased the abundance of c-fos mRNA in outer and inner parietal cortex and caused a corresponding increase in c-fos immunoreactivity in this region. GR 226,206 (40 mg/kg i.p.) had no effect on either c-fos mRNA or protein in parietal cortex. In conclusion, administration of GR 205,171 elicits a stereospecific increase in Arc and c-fos expression in rat parietal cortex but not in other cortical regions. These data suggest that the parietal cortex plays a role in the central actions of NK1 receptor antagonists.

Animals↗

PubMed1992

Melatonin signal transduction and mechanism of action in the central nervous system: using the rabbit cortex as a model.

The cortex of the rabbit (Oryctolagus cuniculus) is rich in melatonin binding sites, and particularly abundant is the parietal cortex. Consequently, we characterized the putative melatonin receptor in the parietal cortex by a series of in vitro ligand-receptor binding experiments and biochemical and electrophysiological studies. The in vitro saturation and competition experiments demonstrated that the binding in the crude cortical membrane preparations was of high affinity and specificity. Guanine nucleotides (GDP, GTP, and GTP gamma S) inhibited the specific 2-[125I]iodomelatonin binding in a dose-dependent manner. Coincubation with a nonhydrolyzable GTP analog provoked a shift in the binding affinity; the numerical values of the Kd increased from 20-30 to 200-600 pM. Melatonin, in nanomolar concentrations, was able to inhibit the forskolin-stimulated accumulation of cAMP in parietal cortex explants, and preincubation with pertussis toxin counteracted this effect of melatonin. Apparently, the melatonin binding site in the rabbit parietal cortex is linked to its second messenger via a pertussis toxin-sensitive G-protein, probably of the inhibitory Gi class, similar to what has been described for different parts of the brain of other vertebrates. The experiments on the spontaneous firing activity of single neurons in the third to fourth layer of the parietal cortex in anesthetized animals showed that melatonin and its potent agonist 2-iodomelatonin exhibited gamma-aminobutyric acid (GABA)-like effects and were able alone, in nanomolar concentrations, to significantly slow the neuronal firing activity. Moreover, both melatonin and 2-iodomelatonin potentiated the effect of GABA on the neuronal activity, leading to powerful inhibition of the tested neurons. Undoubtedly, the binding site in the rabbit parietal cortex possesses all of the characteristics of a functional receptor. We suggest that melatonin is involved in the control of fundamental cortical functions and that it acts in concert with GABA, one of the two major inhibitory neurotransmitters in the central nervous system.

Animals↗

PubMed2002

Protective effect of moutan cortex extract on acetaminophen-induced cytotoxicity in human Chang liver cells.

The aim of this study was to investigate the effect of Moutan Cortex on acetaminophen (AAP)-induced toxicity in human Chang liver cells. Cells were incubated with AAP (0-30 mM) to evaluate the drug's ability to reduce cytoviability. For the cells treated with 10, 20 and 30 mM AAP, LDH leakage was 39.8%, 49.0% and 57.6%, respectively. Administration of Moutan Cortex reduced cytotoxicity in a dose-dependent manner. Glutathione (GSH) concentration in human liver cells decreased significantly after exposure to 20 (p<0.05) and 30 mM (p<0.01) AAP, and increased (p<0.05) if incubated with AAP and Moutan Cortex. The ability of AAP to inhibit mitochondrial function and its counteraction by Moutan Cortex was also evaluated. Moutan Cortex showed dose-dependent increases in MTT metabolism and ATP levels in AAP-treated cells. The DNA content of AAP-treated cells increased with the treatment of Moutan Cortex. These observations demonstrate that Moutan Cortex may significantly attenuate AAP-induced toxicity. It can be considered a cytoprotective agent in this in vitro model of drug toxicity.

Acetaminophen↗

PubMed2006

The role of the dorsal vertebral cortex in the stability of transpedicular screws. A biomechanical study in human cadaveric vertebrae.

The aim of this biomechanical study was to investigate the role of the dorsal vertebral cortex in transpedicular screw fixation. Moss transpedicular screws were introduced into both pedicles of each vertebra in 25 human cadaver vertebrae. The dorsal vertebral cortex and subcortical bone corresponding to the entrance site of the screw were removed on one side and preserved on the other. Biomechanical testing showed that the mean peak pull-out strength for the inserted screws, following removal of the dorsal cortex, was 956.16 N. If the dorsal cortex was preserved, the mean peak pullout strength was 1295.64 N. The mean increase was 339.48 N (26.13%; p = 0.033). The bone mineral density correlated positively with peak pull-out strength. Preservation of the dorsal vertebral cortex at the site of insertion of the screw offers a significant increase in peak pull-out strength. This may result from engagement by the final screw threads in the denser bone of the dorsal cortex and the underlying subcortical area. Every effort should be made to preserve the dorsal vertebral cortex during insertion of transpedicular screws.

Adolescent↗

PubMed1992

Possible role of cingulate cortex in regulating sexual behavior in male rats: effects of lesions and cuts.

The role of the cingulate cortex in regulating male sexual behavior was studied in testosterone propionate-treated castrated male rats. Males with lesions in the anterior part of the cingulate cortex showed lower levels of mount, intromission and ejaculation activities than sham-operated control males and males with lesions in the posterior part of the cingulate cortex or the frontal cortex. In male rats in which lateral connections of the anterior cingulate cortex were bilaterally interrupted by sagittal cuts, the sexual activity was much lower than in the control rats, being comparable to that of the anterior cingulate cortex lesion group, but transection of the anterior connections by a transverse cut made in the anterior part of the anterior cingulate had no effect. These results suggest that the anterior cingulate cortex and its lateral connections are critical in regulating male sexual behavior in male rats.

Animals↗

PubMed2005

Ventral frontal cortex morphology in adult males with isolated orofacial clefts: relationship to abnormalities in social function.

OBJECTIVE: In a previous magnetic resonance imaging (MRI) study, men with nonsyndromic clefts of the lip and/or palate (NSCLP) were found to have abnormalities in the structure of the frontal lobe of the brain. Moreover, many subjects with nonsyndromic clefts of the lip and/or palate have been described as being socially inhibited. A subregion of the frontal lobe, the ventral frontal cortex (VFC), has been shown to be related to social function. This study was designed to evaluate the morphology of the ventral frontal cortex in men with nonsyndromic clefts of the lip and/or palate, and the morphology's relationship to social function. METHODS: Subjects were 46 men with nonsyndromic clefts of the lip and/or palate and 46 sex matched controls. Social function was assessed using a standardized scale. The morphology of the ventral frontal cortex (composed of the orbitofrontal cortex [OFC] and the straight gyrus [SG]) was obtained from magnetic resonance imaging scans using the software BRAINS. RESULTS: After controlling for frontal lobe gray matter, the patient group had significant reductions in orbitofrontal cortex volume and area. The straight gyrus was not morphologically abnormal. Measures of orbitofrontal cortex morphology were significantly correlated to measures of social function--the greater the structural abnormality, the greater the social dysfunction. CONCLUSION: Compared with healthy controls, subjects with nonsyndromic clefts of the lip and/or palate showed morphologic abnormalities in the cortical surface anatomy of a brain region known to govern social function, the orbitofrontal cortex. Moreover, the structural abnormality in this brain region was directly correlated with social function.

Adult↗

PubMed2006

Alteration of 5-HIAA levels in frontal cortex and dorsal raphe nucleus in rats treated with combined administration of tryptophan and ethanol.

The present studies sought to investigate the effect of tryptophan alone or coadministration of tryptophan and ethanol on the interaction of central frontal cortex and dorsal raphe nucleus serotonergic functional activities by utilizing in vivo microdialysis. Tryptophan (50 mg/kg, i.p.) led to a significant increase in the levels of 5-HIAA, a metabolite of serotonin (5-HT), in the dorsal raphe nucleus, but not in the frontal cortex. Coadministration of tryptophan and ethanol caused very marked increases in 5-hydroxyindoleacetic acid (5-HIAA) levels in both the frontal cortex and the dorsal raphe nucleus, although ethanol (1.25 g/kg) did not change 5-HIAA levels in both areas. Moreover, the application of WAY100635 (10 muM), 5-HT(1A) antagonist, into the frontal cortex after coadministration caused a marked increase in 5-HIAA levels in the frontal cortex and a decrease in the levels in the dorsal raphe nucleus, although WAY100635 alone had no effect on these levels. This may suggest that WAY100635-induced increase of 5-HIAA levels in the frontal cortex resulted from negative feedback following the blockade of serotonergic 5-HT(1A) autoreceptors, and that this increase in 5-HIAA levels decreased 5-HIAA levels in the dorsal raphe nucleus by preventing the activation of dorsal raphe 5-HT(1A) autoreceptors. WAY100635 into the dorsal raphe nucleus did not significantly change 5-HIAA levels in both areas. This may indicate that the blockade of dorsal raphe 5-HT(1A) autoreceptors by WAY100635 resulted in unchanged 5-HIAA levels in the frontal cortex. Behavioral sign of teeth-chattering was markedly observed following the coadministration and in combination with WAY100635. These results may suggest that the increased 5-HIAA levels in both areas after coadministration are indicative of the interrelation via activation of serotonergic neurons, and that the increased levels are partly responsible for behavioral activation of rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMedDate not supplied

[Structural organization of the prefrontal cortex in cats and differences between it and the same area in monkeys].

It has been demonstrated that similar to that in monkeys, prefrontal dorso-lateral cortex in cats significantly differs from the medio-basal cortex not only in the structure and level of differentiation, but also in its thalamic projections. In cats, definite topography in the distribution of projections from the medio-dorsal thalamic nucleus to the lobe pole cortex of the hemisphere was demonstrated which in general features is similar to the mode of projection of this nucleus in monkeys. This rendered it possible to homologize separate parts of the medio-dorsal thalamic nucleus and preforntal cortex in these animals. Together with these similarities, considerable differences were found as well. In cats, predominance of phylogenetically ancient medio-basal fields was noted, whereas in monkeys--the predominance of more young dorso-lateral fields was observed. In cats, parvocellular portion is absent from the medio-dorsal thalamic nucleus, its homologue being very small; therefore dorso-lateral cortex to which this portion of the nucleus is projected, is developed very poorly. In monkeys, this portion occupies up to 2/3 of the nucleus, dorso-lateral cortex being perfectly developed. These data suggest that progressive evolution of the prefrontal cortex, associated with a higher behavioural level, followed mainly the development of dorso-lateral surface, this development being closely related to the onset and projection of parvocellular portion of the medio-dorsal thalamic nucleus to this region.

Animals↗

PubMed1976

Conditional spore cortex-less mutants of Bacillus sphaericus 9602.

Lysine-requiring mutants of Bacillus sphaericus 9602 were isolated and classified into three groups by their mutation site in the pathway of lysine biosynthesis. The Group I mutant lacks meso-alpha, epsilon-diaminopimelic acid (meso-Dap) decarboxylase activity, but Group II and III mutants have a normal level of Dap decarboxylase activity. A Group II mutant makes dipicolinic acid from an intermediate in the lysine pathway, but Group III mutants do not. In the absence of meso-Dap in the culture, muramic lactam content in the spore cortex of Group II and III mutants is very low, compared to the wild type content. Addition of meso-Dap to the culture causes an increase of muramic lactam content. Since meso-Dap is detectable only in the spore cortex of B. sphaericus 9602, almost all of the muramic lactam in the spore is probably also located in the cortex. Group I mutants grown in the presence of L-lysine sporulate normally. Group II and III mutants produce oval and nonrefractile spores under the same conditions but the addition of meso-Dap to the culture results in the production of round and refractile spores. Thus, the presence of cortex in the spore is essential to give the round and refractile spores in B. sphaericus. The presence of cortex is also required for the accumulation of dipicolinic acid in the sporulating cells. Furthermore, 1-octanol resistance of the spore depends only on the presence of cortex but both cortex and dipicolinic acid are required for heat resistance of the spore.

Bacillus↗

PubMed1995

Extinction of conditioned eyelid responses requires the anterior lobe of cerebellar cortex.

We test the hypothesis that the cerebellar cortex is required for the extinction of conditioned eyelid responses in rabbits trained using standard Pavlovian delay procedures. Following 10 daily training sessions during which rabbits achieved asymptotic performance, lesions of the ipsilateral hemisphere of the cerebellar cortex were made by aspiration. The target of these lesions was the anterior lobe, as suggested by previous observations that this region is necessary for the learning-dependent timing of conditioned eyelid responses (Perrett et al., 1993). We report that anterior lobe damage, as indicated by disrupted response timing and confirmed by tissue analysis, produces severe deficits in conditioned response extinction. Postlesion responses show no significant decline over ten training sessions, whereas response timing and extinction are unaffected by lesions that do not include the anterior lobe. These conditioned responses that do not extinguish display stimulus specificity, excluding the possibility that they are unlearned responses unmasked by cerebellar cortex lesions. These observations suggest that Pavlovian eyelid conditioning is mediated by synaptic plasticity in at least two sites and the anterior lobe of the cerebellar cortex influences one of these sites during extinction. Based on these and previous data, we propose the hypothesis that eyelid conditioning can involve plasticity in both the cerebellar cortex and interpositus nucleus and that plasticity in the nucleus is controlled by input from Purkinje cell activity in the cortex. This hypothesis is consistent with observations that the cerebellar cortex may not always be required for the expression of conditioned responses, but it is necessary for response timing and for extinction.

Animals↗

PubMed1998

Perirhinal cortex ablation impairs visual object identification.

Impairments in both recognition memory and concurrent discrimination learning have been shown to follow perirhinal cortex ablation in the monkey. The pattern of these impairments is consistent with the hypothesis that the perirhinal cortex has a role in the visual identification of objects. In this study we compared the performance of a group of three cynomolgus monkeys with bilateral perirhinal cortex ablation with that of a group of three normal controls in two tasks designed to test this hypothesis more directly. In experiment 1 the subjects relearned a set of 40 familiar concurrent discrimination problems; the stimuli in each trial were digitized images of real objects presented in one of three different views. After attaining criterion they were tested on the same problems using similar, but previously unseen, views of the objects. In experiment 2 the subjects were tested on their ability to perform 10 of these familiar discriminations with each problem presented in the unfamiliar context of a digitized image of a unique complex scene. The subjects with ablations were significantly impaired on both tasks. These results demonstrate that the role of the perirhinal cortex is not restricted to memory, and they support the hypothesis that the perirhinal cortex is involved in visual object identification. We suggest that the perirhinal cortex is crucially involved in processing coherent concepts of individual objects. A deficit of this nature could underlie the pattern of impairments that follow perirhinal cortex damage in both visual object recognition memory and visual associative memory.

Animals↗

PubMed1997

Regional differences in synaptogenesis in human cerebral cortex.

The formation of synaptic contacts in human cerebral cortex was compared in two cortical regions: auditory cortex (Heschl's gyrus) and prefrontal cortex (middle frontal gyrus). Synapse formation in both cortical regions begins in the fetus, before conceptual age 27 weeks. Synaptic density increases more rapidly in auditory cortex, where the maximum is reached near postnatal age 3 months. Maximum synaptic density in middle frontal gyrus is not reached until after age 15 months. Synaptogenesis occurs concurrently with dendritic and axonal growth and with myelination of the subcortical white matter. A phase of net synapse elimination occurs late in childhood, earlier in auditory cortex, where it has ended by age 12 years, than in prefrontal cortex, where it extends to midadolescence. Synaptogenesis and synapse elimination in humans appear to be heterochronous in different cortical regions and, in that respect, appears to differ from the rhesus monkey, where they are concurrent. In other respects, including overproduction of synaptic contacts in infancy, persistence of high levels of synaptic density to late childhood or adolescence, the absolute values of maximum and adult synaptic density, and layer specific differences, findings in the human resemble those in rhesus monkeys.

Auditory Cortex↗

PubMed2003

Co-release of noradrenaline and dopamine from noradrenergic neurons in the cerebral cortex induced by clozapine, the prototype atypical antipsychotic.

RATIONALE: Clozapine has been shown to increase extracellular dopamine (DA) and noradrenaline (NA) in the medial prefrontal cortex (mPFC). A recent study of ours suggested that extracellular DA in the PFC originates not only from dopaminergic but also from noradrenergic terminals, its release being controlled by alpha(2)-adrenoceptors. OBJECTIVES: Since clozapine binds to alpha(2)-adrenoceptors, the possibility that it might co-release DA and NA was studied. METHODS: By means of microdialysis coupled to HPLC with electrochemical detection, the effect of clozapine on extracellular DA and NA in the mPFC, densely innervated by DA and NA, was compared to that in the occipital cortex, equally innervated by NA but receiving few DA projections. RESULTS: Extracellular NA was found to be the same in the two cortices, consistent with homogeneous NA innervation. On the other hand, extracellular DA in the occipital cortex was only 29% lower than in the mPFC, in spite of the scarce dopaminergic innervation in the occipital cortex. Clozapine (10 mg/kg IP) increased extracellular DA and NA not only in the mPFC (by about 320% and 290%, respectively) but also in the occipital cortex (by 560% and 230%, respectively). Administration of the alpha(2)-agonist clonidine (0.15 mg/kg) reversed the effect of clozapine in both cortices, while the D(2)-agonist quinpirole (0.1 mg/kg IP) was ineffective. CONCLUSIONS: The results suggest that clozapine, by inhibiting alpha(2)-adrenoceptors, co-releases DA and NA from noradrenergic terminals in the occipital cortex and that the same mechanism might be responsible for the concomitant increase of the two monoamines in the mPFC.

Adrenergic alpha-Agonists↗

PubMed1975

The effects of monocular deprivation on synaptic terminals in the visual cortex of rabbits. A quantitative electron microscopic study.

The effect of prolonged (7 month) monocular deprivation (right eye sutured) on the density of synapses (NA) and the number of synaptic vesicles (Nves) in the visual cortex of rabbits is studied. The results can be summarized as follows: (1) No changes (NA and Nves) are observed in the non-deprived hemisphere (visual areas I and II, motor cortex) as compared to control animals. (2) NA has not changed, as compared to control animals, in the binocular field of the deprived visual cortex. (3) A significant rise in NA, as compared to control animals, is observed in the monocular field of area I and in the motor cortex of the deprived cortex. This rise is similar to that found after recovery from prolonged dark rearing. (4) The increase in NA is mainly restricted to the laminae I-II, indicating that, most likely, we are not dealing with an increase in specific visual afferents. (5) The deprived visual cortex shows a significant decrease (16%) in NVes. This decrease is less pronounced than after dark rearing (40%). This probably points to the fact that eye suturing does not fully prevent light penetration. The results are discussed in the light of recent discussions on the plasticity of synapses and the effect of retinal input on the development of the visual system.

Animals↗

PubMed1976

Catecholamines released from cerebral cortex in the cat; decrease during sensory stimulation.

In an attempt to determine the functional role of catecholamine (CA) nerve terminals in cerebral cortex the release of endogenous norepinephrine (NE) and dopamine (DA) into superfusates from visual and somatosensory cortex of the cat have been measured by a sensitive radiometric enzymatic assay based on the methylation of CA by catechol-O-methyltransferase (COMT) in the presence of a [3H]-methyl donor and followed by resolution of 3H derivatives through a series of organic extractions. In the flaxedilized animal maintained under local anaesthesia with artificial respiration the concentration of CA measured in 30-min superfusates was fairly constant in a given experiment under basal conditions without sensory stimulation, but varied widely from one experiment to another. Variations in NE were often independent of those for DA. For visual cortex the average basal release of NE in experiments was 20.09 +/- 3.64 pg/min/sq.cm while the average for DA was 34.01 +/- 7.62 pg/min/sq.cm. In all experiments intermittent visual stimulation (15/sec) produced a significant reduction in release rate averaging about 42% for NE and 64% for DA in visual cortex. The reduction was relatively non-specific since visual or somatic sensory stimulation produced a decrease in release from both visual and somatic sensory cortical areas. Since it has been shown that there is a relatively non-specific increase in acetylcholine (ACh) release from sensory cortex during stimulation, it is proposed that ACh may regulate CA release at presynaptic CA terminals in the cortex as it does in the periphery. A marked increase in CA release observed on perfusing with nicotine or atropine is consistent with this hypothesis.

Acetylcholine↗