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PubMed1976

Patterns of cell and fiber distribution in the neocortex of the reeler mutant mouse.

In the neocortex of the reeler mutant mouse, there is inversion in the normal relative positions of polymorphic and pyramidal cells and of large with respect to medium-sized and small pyramidal cells. Granule cells are concentrated at a near-normal mid-cortical level in the mutant. As in the normal animal, and despite cell malposition in reeler, the principal tangential fiber system lies in the zone of polymorphic cells. Large fiber fascicles, known from experimental studies to be principally thalamo-cortical afferents, enter the tangential fiber system in the polymorphic cell zone of both reeler and normal neocortex. In the mutant these fascicles must traverse the full width of the cortex to reach this fiber system in its superficial location. In both normal and mutant animals single fibers, again principally thalamo-cortical afferents, pass from the principal tangertial fiber system to ramify in a fiber feltwork in the zone of granule cells. In the mutant these descend whereas in the normal animal they ascend. Also, as in the normal mouse, single fibers pass radially between all levels of the mutant cortex and the central white matter. Regional variations in the character, the pattern of distribution and the relative prominence of homologous cell and fiber elements are closely parallel in reeler and normal. This suggests that cell differentiation and the tangenital organization of reeler neocortex are normal despite cell malposition in the mutant.

Animals↗

PubMed1989

Corticotropin-releasing factor immunoreactivity in monkey neocortex: an immunohistochemical analysis.

Corticotropin-releasing factor (CRF) has been implicated in the pathophysiology of certain human neuropsychiatric disorders that affect neocortical function. However, the anatomical organization of CRF-containing structures in the expanded and highly differentiated primate neocortex has not been previously described. In this study, the distribution of CRF-immunoreactive neurons and processes was characterized in the neocortex of New World squirrel monkeys (Saimiri sciureus). Substantial regional differences were present in the density, laminar distribution, and morphological appearance of CRF-immunoreactive neurons. The greatest density of labeled neurons was present in anterior cingulate cortex. A wide range of intermediate densities of CRF-immunoreactive neurons was evident in the association regions of the prefrontal, parietal, and temporal cortices. The lowest numbers of CRF-immunoreactive neurons were observed in the primary visual and primary motor cortices. For example, the density of labeled neurons was nearly five times greater in the anterior cingulate cortex than in the precentral cortex. CRF-immunoreactive neurons were also distributed in at least four different laminar patterns. For example, in the agranular anterior cingulate cortex, labeled cell bodies were distributed throughout layers II, III, and V. In other regions, such as the posterior cingulate cortex, labeled neurons were present in layers II, III, and IV. In contrast, labeled neurons were predominantly present in layers II and superficial III of the visual cortex, whereas in the inferior temporal cortex, they were present predominantly in layer IV. Regional and laminar differences were also present in the relative distributions of the two major morphological types (as defined by cell body shape) of CRF-immunoreactive neurons. Vertically oriented oval neurons, which frequently had a single dendritic process arising from each somal pole, were most frequently found in layer III. In contrast, the labeled neurons in layers II and IV tended to have a round- or triangular-shaped soma. In layer IV of some association cortices, these multipolar neurons were associated with a high density of rod-like structures composed of large immunoreactive varicosities clustered together in vertical arrays. These structures were frequently found to be located immediately below the soma of pyramidal neurons. Comparison of these findings with Golgi impregnation studies strongly suggests that CRF is present in the soma and axonal cartridges of a subset of chandelier neurons. The heterogeneous distribution and morphological diversity of CRF-containing neurons suggest that CRF may mediate distinct functions in different regions and layers of monkey neocortex.

Animals↗

PubMed1989

Brain neocortex influence on the mononuclear phagocyte system.

The cerebral neocortex is known to modulate asymmetrically certain components of the immune system. It was previously shown that large ablation of the left cortex reduces B and T cell-mediated responses, whereas symmetrical right lesions enhance these responses. We have studied the immunomodulatory role of the brain cortex on the mononuclear phagocytic system. Resident and BCG-activated macrophages were investigated in female C3H/He mice at 8-10 weeks after right or left cortical ablation. After an intraperitoneal injection of BCG, the number of peritoneal macrophages was found to be lower in both right- and left-lesioned mice, the difference being stronger and more significant in left-lesioned animals than in sham-operated controls. Furthermore, the oxidative metabolism as assessed by chemiluminescence was depressed only in left-lesioned mice. On the other hand, cortical lesions were shown to have no effect on either the number or the endocytic activity of resident peritoneal macrophages. The possible implication of the brain neocortex on infectious diseases was assayed by using the Trypasonoma musculi model, in which macrophages are known to be effective in parasite eradication. Although the number of peritoneal macrophages was significantly depressed after left cortical lesions 11 days after T. musculi inoculation, the course of the infection was not modified significantly. Our results argue in favor of brain neocortex modulation of the mononuclear system.

Animals↗

PubMed1994

Modulation of cellular excitability in neocortex: muscarinic receptor and second messenger-mediated actions of acetylcholine.

Muscarinic-type acetylcholine (ACh) receptor are involved in a variety of cortical functions. ACh "activates" neocortex; simultaneously modifying spontaneous subthreshold activity, intrinsic neuronal oscillations and spike discharge modes, and responsiveness to fast (putative glutamatergic) synaptic inputs. However, beyond the general involvement of muscarinic receptors, a mechanistic understanding of integrated cholinergic actions, and interactions with non-cholinergic transmission, is lacking. We have addressed this problem using intracellular recordings from the in vitro auditory neocortex. First, we investigated cholinergic modification of responses to the excitatory amino acid glutamate. ACh, or the muscarinic agonist methacholine, produced a lasting enhancement of glutamate-mediated membrane depolarizations. Muscarinic receptors of the M1 and/or M3 subtype, rather than M2 or nicotinic receptors, mediated this enhancement. Subsequently, we investigated whether second messenger systems contribute to observed muscarinic actions. Activation of protein kinase C with phorbol 12,13-dibutyrate (4 beta-PDBu), enhanced neuronal responses to glutamate. The effect of 4 beta-PDBu was attenuated by the kinase antagonist H7. Finally, we attempted to identify postsynaptic actions of endogenous ACh. Tetanic stimulation of cholinergic afferents elicited voltage-dependent effects, including reduced spike frequency adaptation and reduced slow afterhyperpolarization (sAHP) elicited by transmembrane depolarizing stimuli. These effects were mimicked by methacholine, enhanced by eserine, and antagonized by muscarinic receptor antagonists. These data suggest that cholinergic modulation in neocortex likely involves the integrated actions of diverse mechanisms, primarily gated by muscarinic receptors, and at least partly involving second messenger systems.

Acetylcholine↗

PubMed1991

A correlation between gene transcriptional activity and cerebral glucose metabolism in Alzheimer's disease-affected neocortex: cause or effect?

Our laboratory has measured mRNA pool sizes in neocortex afflicted with Alzheimer's disease (AD). We have observed a repression of gene expression in the temporal and parietal regions compared to age-matched control neocortex. These changes in messenger RNA pool size closely parallel the observed alterations in local cerebral metabolic rates for glucose (LCMR-g), as detected by positron emission tomography (PET). For example, deficits in both gene transcription and glucose metabolism appear to be the greatest in AD-affected superior temporal neocortex (Brodmann area 22) but are less apparent in the primary visual cortex (Brodmann area 17) or in the cerebellum. The unresolved question is whether changes in gene expression are the cause or effect of altered glucose metabolism. However, the non-random reductions in the pool size for certain neocortical mRNAs argue in favour of altered gene expression as the primary event.

Alzheimer Disease↗

PubMed1990

Differential effects of calcium channel antagonists (omega-conotoxin GVIA, nifedipine, verapamil) on the electrically-evoked release of [3H]acetylcholine from the myenteric plexus, phrenic nerve and neocortex of rats.

Electrically-evoked release of [3H]acetylcholine from autonomic neurons (myenteric plexus), motoneurons (phrenic nerve) and the central nervous system (neocortex) was investigated in the presence and absence of the calcium channel antagonists omega-conotoxin GVIA, nifedipine and verapamil, whereby the same species (rat) was used in all experiments. Release of [3H]acetylcholine was measured after incubation of the tissue with [3H]choline. omega-Conotoxin GVIA markedly reduced (70%) the evoked release of [3H]acetylcholine from the myenteric plexus of the small intestine (IC50: 0.7 nmol/l) with a similar potency at 3 and 10 Hz stimulation. An increase in the extracellular calcium concentration attenuated the inhibitory effect of omega-conotoxin GVIA. Release of [3H]acetylcholine from the rat neocortex was also inhibited (90%) by omega-conotoxin GVIA, but the potency was 19-fold lower (IC50: 13 nmol/l). However, the release of [3H]acetylcholine from the phrenic nerve was not reduced by omega-conotoxin GVIA (100 nmol/l) at 1.8 mmol/l calcium (normal concentration), whereas omega-conotoxin GVIA inhibited evoked [3H]acetylcholine release by 47% at 0.9 mmol/l calcium. Neither nifedipine (0.1 and 1 mumol/l) nor verapamil (0.1, 1 and 10 mumol/l) modified the evoked release of [3H]acetylcholine from the myenteric plexus and the phrenic nerve. Acetylcholine release from different neurons appears to be regulated by different types of calcium channels. N-type channels play the dominant role in regulating acetylcholine release from both the myenteric plexus and the neocortex, whereas acetylcholine release from motor nerves is regulated by calcium channel(s) not yet characterized.

Acetylcholine↗

PubMed1992

Projections from fetal neocortical transplants placed in the frontal neocortex of newborn rats. A Phaseolus vulgaris-leucoagglutinin tracing study.

Fetal rat neocortex grafted into lesion cavities made in the newborn rat neocortex can exchange multiple axonal connections with the host brain. Most previous studies demonstrating efferent transplant-to-host brain connections have used fluorescent retrograde tracers injected into the host brain (Castro et al. 1985, 1987; Floeter and Jones 1984; O'Leary and Stanfield 1989). Other studies have used anterograde axonal tracing with either tritium-labelled amino acids impregnating the transplant and its efferents (Floeter and Jones 1985) or horseradish peroxidase injected into the transplants (Chang et al. 1984, 1986). In the present study we used the anterograde axonal tracer Phaseolus vulgaris-leucoagglutinin (PHA-L) to examine in detail the course and termination of the efferent neocortical graft fibers. Twenty-six newborn rats had the right frontal cortex forepaw area removed by vacuum aspiration, while anesthetized by hypothermia. A piece of fetal frontal cortex 14-16 embryonic days old (E14-16) was immediately thereafter placed in the lesion, and the recipient rats allowed to survive for 5-7 months. At this time the rats were reoperated under sodium pentobarbital (Nembutal) anesthesia and the transplants iontophoretically injected with PHA-L. Two weeks later the animals were again anesthetized, perfused, and processed for PHA-L immunocytochemistry and routine histology. Analysis of acetylcholinesterase- (AChE) and Nissl-stained sections showed graft survival in 19 of the 26 animals used in this study. When these 19 brains were processed for PHA-L immunocytochemistry, 5 of them were found with certainty to have the PHA-L injection confined to the transplant. Based on these cases PHA-L-reactive fibers arising from labelled transplant neurons were traced into the ipsilateral host neocortex adjacent to the transplant and found to project through the subcortical white matter to the ipsilateral parietal neocortical area 1, and claustrum. Callosal fibers were traced to the contralateral frontal neocortical forelimb and parietal areas. Transplant fibers were also observed to descend through the caudate putamen in the dispersed fiber bundles of the internal capsule to distribute as terminal branches and varicose fibers within the mesencephalic periaqueductal gray, red nucleus, deep mesencephalic nucleus, and intermediate gray of the superior colliculus, as well as in the pontine gray. Similar fibers and terminations were present in the caudate putamen, the reticular, ventrobasal, centrolateral, posterior, and parafascicular thalamic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗

PubMed1983

Immunohistochemical demonstration of serotonin nerve fibers in the neocortex of the monkey (Macaca fuscata).

Using a peroxidase-antiperoxidase immunohistochemical method, the distribution of serotonin nerve fibers was studied in the neocortex of the monkey (Macaca fuscata). All layers of the neocortex showed evidence of serotonin fibers, both fine and thick. Unlike the distribution in rodents, different patterns of distribution were noted in each neocortex of the primate. Among the cortical areas--area 4, 3-1-2, 17, 18, 41 and 42--the primary visual cortex (area 17) contained the highest density of immunoreactive fibers, while the primary motor cortex (area 4) possessed the lowest concentration. The most outstanding finding was a dense and laminar distribution of serotonin fibers in area 17, particularly within the upper portion of layer IVc. In area 3-1-2, 18, 41 and 42, a fairly uniform density of immunoreactive fibers was observed across the six cortical layers, apart from a relatively dense plexus of fine serotonin fibers in layer IV.

Animals↗

PubMed1985

The distribution of plasma proteins in the neocortex and early allocortex of the developing sheep brain.

The histogenesis of the cerebral neocortex and early allocortex of the sheep has been described and, using an immunohistochemical technique, five plasma proteins have been identified in the telencephalic wall and their distribution followed during its differentiation. The development of the neocortex was studied from 18 days gestation, when the neural tube was still open, to 120 days, when the adult structure was established. A primordial plexiform layer was formed above the ventricular zone by 25 days and by 35 days this layer was divided by the differentiating cortical plate into an outer marginal zone and an inner subplate zone. The appearance of the subventricular and intermediate zones by 50 days gestation completed the formation of the neocortical layers. The differentiation of the allocortex was generally less advanced than the neocortex up to 40 days gestation, when the primordium of the pyramidal layer was beginning to develop. The five plasma proteins identified, fetuin, alpha-fetoprotein, albumin, transferrin and alpha 1-antitrypsin, are quantitatively the most important in the csf and plasma of the sheep fetus. Fetuin was the earliest plasma protein to be detected in the brain and it was also the most widespread; positive staining for this protein was seen in cells and fibres of all layers as they differentiated and could still be identified in some mature neurons at 120 days. alpha-Fetoprotein and albumin had a limited distribution, appearing in cells in the developing cortical plate for a short period early in gestation (35-40 days), but mainly confined to the ventricular zones later and barely detectable by 80 days gestation. Transferrin appeared to have a different distribution, being detected in fibres first in the primordial plexiform layer and then in the marginal and subplate zones, only later being identified in cells of the cortical plate. From their distribution it is suggested that fetuin and transferrin may play an important role in the differentiation of the cortex and the establishment of correct connections between fiber systems and migrating cells at certain stages of development. alpha 1-Antitrypsin was only found in a few cells during a restricted period of gestation. All five plasma proteins were identified in precipitated csf and plasma at most ages examined, although at 18 days gestation albumin, transferrin and alpha 1-antitrypsin and at 120 days, alpha-fetoprotein, could not be detected.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1978

Autoradiographic study of early neurogenesis in rat neocortex.

The early neurogenesis of rat neocortex was analysed by means of light and electron microscopic autoradiography. It was found that the very first preneurons originate probably as early as ED 11. They are the horizontal cells of Cajal-Retzius. The peak of their formation is on ED 13 (surface index estimated on ED 17 after injection of 3H-thymidine on ED 13:21, after injection on ED 12:4, after injection on ED 15:5), WHereas no Cajal-Retzius cells could be found to have originated after ED 15. Theses cells are the developmentally most advanced of the neocortex. The cells second in date of origin and maturation are preneurons which presumably correspond to the presumptive neurons of Layer VII (VI b), and begin to originate on ED 12. The end of their formation could not be defined owing to a lack of ultrastructural differences to other, younger preneurons in later gestational stages. These two cell types are the first cellular components of the primordial plexiform layer (Marin-Padilla, 1978) or pallial anlage (Rickmann, 1977), demonstrating an outside-in gradient within this layer, and are separated by the formation of the cortical plate. This could be proven by their simultaneous labelling above and below the cortical plate after administration of 3H-thymidine before ED 15. These results confirm the hypothesis of a dual origin of the mammalian neocortex (Marin-Padilla, 1978).

Animals↗

PubMed1991

Empirical comparison of the MEG and EEG: animal models of the direct cortical response and epileptiform activity in neocortex.

This review directly addresses the appropriateness of the dipole model as a physical representation of neocortical sources produced by evoked and spontaneous epileptiform activity in neocortex. Three dimensional electrical measurements of cellular currents in rat sensory neocortex are compared to the extracranial magnetic fields these currents produce. Comparisons are performed for the direct cortical response (DCR) evoked by electrical stimulation of the cortical surface, and for evoked and spontaneous interictal and ictal discharge of the penicillin focus in the same animal preparation. Our data support the hypothesis that evoked and epileptiform magnetic fields result from intradendritic currents oriented perpendicular to the cortical surface. Furthermore, magnetic fields can be detected from epileptic foci smaller than 3 x 3 mm2. This work provides an empirical foundation for physical models with which to interpret noninvasive neuromagnetic recordings of epileptic discharge in human focal seizure disorders. The dipole approximation appears to be appropriate for the interpretation of magnetic field phenomena in neocortex.

Animals↗

PubMed1976

[The predominantly unilateral influence of the posterior hypothalamus on the neocortex].

High-frequency electrical stimulation of the-posterior hypothalamus applied 10-20 days after the sectioning of the brain stem at the level of the anterior frontal margins of the anterior coliculus results in the preferential activation of the ipsilateral neocortex. When unilateral lesions are placed in the posterior hypothalamus, the predominance of synchronous activity in the ipsilateral neocortex is observed. In the premesencephalic preparations, weak single electrical stimulation of the posterior hypothalamus provokes spindles in the ipsilateral portions of the frontal cortex. At more intensive single stimulation of the posterior hypothalamus there occurs diffuse appearance of spindles in different neocortical areas. Besides the preferential unilateral effect, the influence of the posterior hypothalamus is more prominent in the frontal than in the occipital regions of the cortex. It is suggested that the posterior hypothalamus exerts its influence on the neocortex through the thalamic nuclei.

Animals↗

PubMed1992

Effect of ACTH, adrenalectomy and the combination treatment on the density of 5-HT2 receptor binding sites in neocortex of rat forebrain and 5-HT2 receptor-mediated wet-dog shake behaviors.

The effect of ACTH and/or adrenalectomy on serotonin (5-HT)2 receptor binding sites was evaluated in the neocortex of rat forebrain. One day after the adrenalectomy or sham operation, ACTH (50 micrograms/day) was injected subcutaneously into adult male SD rats for 10 consecutive days. Saturation analysis showed that subchronic ACTH treatment significantly increased the Bmax values for 3H-ketanserin binding without any change in the Kd values. Moreover, this ACTH-induced increase in the Bmax values was prevented by adrenalectomy. The concentrations of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) measured by HPLC-ECD were not altered by these manipulations. Ten-day administration of corticosterone (20 and 50 mg/kg) also increased 5-HT2 receptor density in the neocortex of rat forebrain. 5-HT2 (and 5-HT1C) receptor agonist, (+/-)DOI-induced wet-dog shakes in ACTH and/or adrenalectomy-treated rats were also examined. Ten-day administration of ACTH enhanced (+/-)DOI-induced wet-dog shakes and this increase was prevented by adrenalectomy. These results indicate that subchronic adrenocorticotropin-adrenal axis activation of rats increases both the number of 5-HT2 receptors in neocortex of forebrain and the wet-dog shake responses induced by (+/-)DOI.

Adrenalectomy↗

PubMed1994

Redistribution of glutamate and GABA in the cerebral neocortex and hippocampus of the Mongolian gerbil after transient ischemia. An immunocytochemical study.

The redistribution of glutamate and GABA in postischemic brains was examined immunocytochemically using the gerbil model of unilateral 1 h cerebral ischemia. In the cerebral neocortex, the majority of neurons underwent recovery processes after 5 h of recirculation, while neurons in the hippocampus were irreversibly damaged. Glutamate-like immunoreactivity (LI) was highly increased in the degenerating hippocampal CA3 pyramidal cells after recirculation, while in the neocortex and the hippocampal CA1 sector, the pyramidal cells showed only slightly increased glutamate-LI. GABA-LI-positive punctae in the neuropil, corresponding to neuronal processes of GABAergic neurons, were accentuated after recirculation both in the cerebral neocortex and the hippocampus. Although the astrocytes on the nonischemic side showed neither glutamate-LI nor GABA-LI, the swollen astrocytes and their foot processes, which were observed after recirculation, often showed strong glutamate-LI and GABA-LI. These data suggest (1) the accumulation of glutamate or glutamate-like substances, especially in the CA3 pyramidal cells, (2) the excitation of the GABAergic neurons and their subsequent uptake of GABA, and (3) the sequestration of the extracellular neurotransmitters by astrocytes in the postischemic period.

Animals↗

PubMed1999

Does the perireticular thalamic nucleus project to the neocortex?

This study defines several features of the early connections of the developmentally transient perireticular thalamic nucleus of rats. The neocortex of developing rats was injected with either DiI, biotinylated dextran, WGA-HRP (wheatgerm agglutinin conjugated-horseradish peroxidase), fluorescent latex beads or cholera toxin subunit B (CTB) and their brains were processed for tracer detection with standard methods. In general, tracer injections into various regions of the developing neocortex revealed no labelled neurones within the perireticular nucleus, although some of these tracers (WGA-HRP, dextran) labelled many of the amoeboid microglial cells that are found within this nucleus. There were, however, many retrogradely labelled neurones in a region adjacent to the perireticular nucleus, within the nucleus basalis of the basal forebrain (medial edge of globus pallidus). Their identity was confirmed as neurones of the nucleus basalis since they were all were similar in morphology and somal size to neurones that were immunoreactive to NGFr (nerve growth factor receptor), an antigen found only among neurones of the nucleus basalis and basal forebrain. Moreover, double labelling experiments revealed that most, if not all, of the cortically labelled neurones were NGFr-immunoreactive also. Thus, in conclusion, our results suggest that the perireticular nucleus does not project to the neocortex; the only neurones in the general vicinity of the perireticular nucleus that have a cortical projection form part of the nucleus basalis.

Animals↗

PubMed1979

Histological and neurochemical effects of fetal treatment with methylazoxymethanol on rat neocortex in adulthood.

Forebrain microencephaly results when developing rats are exposed to methylazoxymethanol acetate (MAM) at 15 days of gestation (DG). This potent alkylating agent is selectively cytotoxic for dividing cells. Since distinct neuronal populations in neocortex vary greatly with respect to timing of mitotic activity during gestation, it was predicted that some groups would be differentially reduced by treatment. Histological examination of neocortex from treated rats grown to adulthood revealed major losses of laminae II--IV with relative preservation of deeper layers. The atrophic adult neocortex was further characterized by assay of several defined pre- and postsynaptic neurochemical markers. Total markers for GABAergic neurons were greatly reduced (glutamate decarboxylase -71%, [3H]GABA synaptosomal uptake -63% and endogenous GABA -59%). Total [3H]GABA binding to cortical membranes was reduced 67%. Total [3H]glutamate synaptosomal uptake and endogenous glutamate were reduced 71% and 65% respectively. In contrast, total presynaptic markers for noradrenergic innervation were minimally altered but concentration of tyrosine hydroxylase, [3H]norepinephrine synaptosomal uptake and endogenous norepinephrine were increased by 275%, 130% and 133%, respectively. Concentration of cholinergic presynaptic markers was also increased (choline acetyltransferase +97%, endogenous acetylcholine +64%) in atrophic cortex, but to a lesser degree than for noradrenergic innervation. Specific binding of muscarinic cholinergic antagonist [3H]quinuclidinyl benzilate and the beta-adrenergic receptor antagonist [3H]dihydroalprenolol was reduced 25% and 29% respectively in treated cortex. Thus, MAM treatment at 15 DG severely reduces intrinsic neuronal populations including GABAergic and glutamatergic neurons, and produces a shrunken cortex relatively hyperinnervated by noradrenergic and cholinergic neurons. MAM-induced microencephaly is a useful model system for producing relatively selective lesions of telencephalic neurons and for study of altered neurochemical relationships following developmentally incurred brain damage.

Acetylcholine↗

PubMed1981

Spreading depression induced by microinjection of enkephalins into the hippocampus and neocortex.

The opioid peptides Leu-enkephalin, Met-enkephalin and D-Ala2-Met-enkephalinamide were injected at various concentrations into the neocortex and hippocampus of rats to examine their effects on EEG activity and DC potentials. All three compounds were found to elicit spreading depression (SD) in both structures. Higher doses of Met-enkephalin were required to elicit SD as well as seizure activity. In the hippocampus the wave of SD was frequently preceded by seizure activity which was antagonized by naloxone pretreatment (40 mg/kg i.p.). Naloxone also prevented Leu-enkephalin-induced SD in the neocortex (but not in the hippocampus) and Met-enkephalin-induced SD in the hippocampus (but not in the neocortex). It failed to block SD elicited by D-Ala2-Met-enkephalinamide in both structures. Some of the various reported behavioral effects of intracranial injections of enkephalins could be artefacts of hippocampal and/or cortical spreading depression.

Animals↗

PubMed1983

The evoked release of endogenous amino acids from tissue prisms of human neocortex.

The K+-evoked release of 13 amino acids has been determined from tissue prisms of neocortex from patients of various ages, and from rats. Prisms were prepared from various regions of human neocortex obtained at neurosurgery. Upon depolarization aspartate, glutamate and gamma-aminobutyrate (GABA) were shown to be preferentially released. The efflux of glutamate was calcium-dependent. Prisms prepared from human neocortex obtained shortly after death also exhibited preferential K+-induced release of putative amino acid transmitters. Absolute concentrations released into the media were similar to those found for neurosurgical samples. Comparison of the release data for rat and human samples revealed that the efflux of aspartate, glutamate and GABA occurred to a greater extent from rat brain preparations. The K+-evoked release of glutamate from human samples showed a significant linear increase from 12 to 68 years of age.

Aged↗