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Compartmental protein expression of Tau, GSK-3beta and TrkA in cholinergic neurons of aged rats.

During aging basal forebrain cholinergic neurons (BFCNs) degenerate, and we hypothesize this to be the result of a degeneration of the cytoskeleton. As a corollary, retrograde transport of the complex of nerve growth factor (NGF) and its activated receptor phospho-TrkA (P-TrkA) is impaired. Using immunocytochemistry, we here compare young and aged rat brains in their subcellular localization of NGF and P-TrkA in relation to the compartmentalization of phosphorylation-dependent tau protein isoforms. Despite lower P-TrkA immunoreactivity in cortex and hippocampus of aged rats, NGF immunoreactivity was not altered in these areas, but was significantly lower in aged basal forebrain. In young animals, expression of tau isoforms and glycogen synthase kinase-3beta (GSK-3beta) was restricted to neuritic structures in cortex, hippocampus, and basal forebrain. In contrast, tau and GSK-3beta labeling was confined to cell bodies in aged rats. Since a somatic localization of phospho-tau is indicative of cytoskeletal breakdown, we suggest this to be the mechanism the breakdown of trophic support in aging BFCNs.

Acetylcholine↗

Compartmentation of energy metabolism in atrial myocardium of patients undergoing cardiac surgery.

The parameters of oxidative phosphorylation and its interaction with creatine kinase (CK)- and adenylate kinase (AK)-phosphotransfer networks in situ were studied in skinned atrial fibers from 59 patients undergoing coronary artery bypass surgery, valve replacement/correction and atrial septal defect correction. In atria, the mitochondrial CK and AK are effectively coupled to oxidative phosphorylation, the MM-CK is coupled to ATPases and there exists a direct transfer of adenine nucleotides between mitochondria and ATPases. Elimination of cytoplasmic ADP with exogenous pyruvate kinase was not associated with a blockade of the stimulatory effects of creatine and AMP on respiration, neither could it abolish the coupling of MM-CK to ATPases and direct transfer of adenine nucleotides. Thus, atrial energy metabolism is compartmentalized so that mitochondria form functional complexes with adjacent ATPases. These complexes isolate a part of cellular adenine nucleotides from their cytoplasmic pool for participating in energy transfer via CK- and AK-networks, and/or direct exchange. Compared to atria in sinus rhythm, the fibrillating atria were larger and exhibited increased succinate-dependent respiration relative to glutamate-dependent respiration and augmented proton leak. Thus, alterations in mitochondrial oxidative phosphorylation may contribute to pathogenesis of atrial fibrillation.

Adenine Nucleotides↗

Intracellular compartmentation of cardiac troponin T and its release kinetics in patients with reperfused and nonreperfused myocardial infarction.

In a previous study on the diagnostic efficiency of troponin T measurements in patients with suspected acute myocardial infarction (AMI), the authors found a high variability of troponin T serum concentration changes on day 1 in patients with AMI who underwent thrombolytic treatment. Therefore, the aims of the present study were to investigate the intracellular compartmentation of troponin T and to analyze the effects of AMI reperfusion on the appearance kinetics of cardiac troponin T in serum. Cardiac troponin T was measured with a newly developed bideterminant sandwich assay using cardiospecific, affinity-purified polyclonal antibodies and peroxidase-labeled monoclonal antibody. An unbound cytosolic troponin T pool was found in ultracentrifuged homogenates of myocardial tissue of different species ranging from 0.013 to 0.036 mg/g wet weight. The soluble troponin T molecule had electrophoretic properties identical to troponin T compartmented in the myofibrils. The clinical study group comprised 57 patients with AMI undergoing thrombolytic treatment. Blood flow to the infarct zone and point of time of reperfusion were tested by immediate and late angiography. The appearance of troponin T in serum on day 1 after the onset of AMI depended strongly on reperfusion and on duration of ischemia before reperfusion. Thus, in patients with early reperfused AMI, a marked peak in troponin T serum concentrations was found at 14 hours after the onset of pain. This early troponin T peak was absent in patients with AMI reperfusion occurring greater than 5.5 hours after the onset of pain and in patients with nonreperfused AMI. By contrast, the kinetics of troponin T release after the first day after AMI were unaffected by reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Potassium, sodium, and chloride content of isolated intact chloroplasts in relation to ionic compartmentation in leaves.

Intact chloroplasts were isolated from spinach, sugarbeet, and pea leaves by a rapid procedure which included purification on a two-step Percoll gradient. The content of K+, Na+, and Cl- was determined together with the chloroplast volume from which the apparent concentration of these ions in the chloroplast was calculated. It was demonstrated by successive washing that K+ leaked out of the chloroplasts during isolation whereas Na+ and Cl- did not. For spinach and sugarbeet chloroplasts K+ was the predominant monovalent cation (160-200 mM) with Na+ present in lesser amounts (40-70 mM). Pea chloroplasts contained equal amounts of K+ and Na+ (40 mM). The Cl- concentration in the chloroplast was similar for the three species and was calculated to be near 100 mM. The Cl- concentration in the chloroplast was well above that of the leaf tissue implying accumulation of Cl- in the chloroplast. Qualitatively similar results were obtained for chloroplasts isolated by rapidly fractionating protoplasts of wheat and barley although the concentration of ions was lower than for the above three species. Spinach grown in 200 mM NaCl accumulated high levels of Na+ and Cl- in the leaves but K+ was decreased. The replacement of K+ by Na+ was also observed in the chloroplasts but the level of Cl- in the chloroplast was not greatly increased even at leaf Cl- in excess of 200 mM. Replacement of K+ by Na+ in the nutrient solution also resulted in replacement of K+ by Na+ both in the leaf and in the chloroplast. Spinach grown under Cl- deficiency showed a 70% decrease in growth and a similar decrease in leaf Cl- but the concentration of Cl- in the chloroplast was not significantly decreased. It is concluded that in most instances K+ is the dominant monovalent cation in chloroplasts, although replacement by Na+ can occur to some extent. Chloride is a major anion, being accumulated within the chloroplast at low leaf Cl- and excluded from the chloroplast at high leaf Cl-. Ionic compartmentation within the leaf cell appears to be regulated to maintain a relatively constant level of Cl- in the chloroplast.

Anions↗

Compartmentation of citrate in relation to the regulation of glycolysis and the mitochondrial transmembrane proton electrochemical potential gradient in isolated perfused rat heart.

Subcellular fractionation of tissue in nonaqueous media was employed to study metabolite compartmentation in isolated perfused rat hearts. The mitochondrial and cytosolic concentrations of citrate and 2-oxoglutarate, total concentrations of the glycolytic intermediates and rate of glycolysis were measured in connection with changes in the rate of cellular respiration upon modulation of the ATP consumption by changes of the mechanical work load of the heart. The concentrations of citrate and 2-oxoglutarate in the mitochondria were 16- and 14-fold, respectively, greater than those in the cytosol of beating hearts. The cytosolic citrate concentration was low compared with concentrations which have been employed in demonstrations of the citrate inhibition of glycolysis. In spite of the low activities reported for the tricarboxylate carrier in heart mitochondria, the cytosolic citrate concentration reacted to perturbations of the mitochondrial citrate concentration, and inhibition of glycolysis at the phosphofructokinase step could be observed concomitantly with an increase in the cytosolic citrate concentration. The delta pH across the inner mitochondrial membrane calculated from the 2-oxoglutarate concentration gradient and the mitochondrial membrane potential calculated from the adenylate distribution gave an electrochemical potential difference of protons compatible with chemiosmotic coupling in the intact myocardium.

Animals↗

Compartmental analysis of sulphate transport in Lemna minor L., taking plant growth and sulphate metabolization into consideration.

The compartmental analysis of sulphate transport in cells of Lemna plants has been performed, taking into account the growth of the samples and the metabolization of sulphate into organic thiocompounds during the course of the experiment. The results obtained form efflux and influx experiments are fully consistent with one another. Both unidirectional fluxes between the external medium and the cell wall are very large (order of magnitude of 1 MUMOL/h per g fresh weight of plants). All the other unidirectional fluxes, including the flux of sulphate metabolization, are much smaller (from about 10 to 60 nmol/h per g). Over 70% of the total sulphur of the plant corresponds to that incorporated into organic thio compounds, and over 25% to free sulphate in the vacuola. The pool of free sulphate in the cytoplasm is only about 1% of the total sulphur, and the sulphate content of the cell wall (free spaces) is also about 1%. Two remarks of general relevance have been made concerning the influx curves. First, these curves exhibit a long (several hours), quasi-stationary phase after the first few minutes of absorption, though the slope of this straight line does not correspond to the unidirectional flux of sulphate entry through the plasmalemma (from cell wall to cytoplasm). Second, the Lemna plants seem to be sensitive to the effect of "gas shock'.

Biological Transport↗

Compartmentation of phosphorylated precursors of phospholipid biosynthesis in cultured neuroblastoma cells.

The continuous turnover of membrane phospholipids requires a steady supply of biosynthetic precursors. We evaluated the effects of decreasing extracellular Na+ concentration on phospholipid metabolism in cultured neuroblastoma (N1E 115) cells. Incubating cultures with 145 to 0 mM NaCl caused a concentration-dependent inhibition of [32P]phosphate uptake into the water-soluble intracellular pool and incorporation into phospholipid. Phospholipid classes were differentially affected; [32P]phosphate incorporated into phosphati-dylethanolamine (PE) and phosphatidylcholine (PC) was consistently less than into phosphatidylinositol (PI) and phosphatidylserine (PS). This could not be attributed to decreased phospholipid synthesis since under identical conditions, there was no effect on arachidonic acid or ethanolamine incorporation, and choline utilization for PC synthesis was increased. The effect of Na+ was highly specific since reducing phosphate uptake to a similar extent by incubating cultures in a phosphate-deficient medium containing Na+ did not alter the relative distribution of [32P]phosphate in phospholipid. Of several cations tested only Li+ could partially (50%) replace Na+. Incubation in the presence of ouabain or amiloride had no effect on [32P]phosphate incorporation into phospholipid. The differential effects of low Na+ on [32P]phosphate incorporation into PI relative to PC and PE suggests preferential compartmentation of [32P]phosphate into ATP in pools used for phosphatidic acid synthesis and relatively less in ATP pools used for synthesis of phosphocholine and phosphoethanolamine, precursors of PC and PE, respectively. This suggestion of heterogeneous and distinct pools of ATP for phospholipid biosynthesis, and of potential modulation by Na+ ion, has important implications for understanding intracellular regulation of metabolism.

Animals↗

Nutritional effects on precursor uptake and compartmentalization of intracellular pools in relation to RNA synthesis.

The effects of nutritional variables on the processing of exogenous precursors into RNA was examined. General nutritional deprivation, or asparagine depletion, led to significant changes in the absolute pool sizes, especially of ATP, UTP and CTP. Fluctuations were found depending on the elapsed time after the nutritional perturbations occurred, and the cell density of the cultures. Depletion of the medium by 28 h of growth, or 1 h of guinea pig asparaginase action, led to considerable inhibition of the conversion of exogenous uridine to CTP by the cells. A series of experiments indicated that in 6C3HED lymphoma cells the uridine nucleotide pool which provided the immediate precursors to RNA (denoted UTP-NA) behaves as a small compartment in rapid equilibrium with exogenously supplied nucleosides. The resemblance to the compartmentation model described by Plagemann (Plagemann, P.G.W. (1972) J. Cell Biol. 52, 131-146 and (1971) J. Cell. Physiol. 77, 241-258) for rat hepatoma cells was close. The UTP-NA pool of the 6C3HED cells constitutes no more than 5% of the cellular UTP pool and is relatively slow in equilibrating with the general cell pool. Correction of the rates of incorporation of isotope into RNA by using some function of the whole cell UTP specific activity to normalize the pool effects, was shown to be invalid.

Adenosine Triphosphate↗

Evidence for compartmentation of uridine nucleotide pools in rat hepatoma cells.

Interaction between the de novo and salvage pathways of pyrimidine metabolism was studied in a line of rat hepatoma cells by co-labelling with [14C]-uridine and [3H]orotate. A difference in the ratio of 14C/3H between CTP and UTP in acid-soluble nucleotide pool was reflected in the corresponding ratios in CMP and UMP in RNA, with uridine labelling cytidine nucleotides relatively more effectively than orotate. These results are not compatible with the concept of a single UTP pool, and a new model for pyrimidine anabolic pathways, based on compartmentation of de novo from salvage pathways, is proposed.

Animals↗

Compartmentation of intestinal drug sulphoconjugation. Incorporation of luminal and contraluminal [35S]sulphate into 1-naphthol by the isolated mucosa of guinea pig jejunum and colon.

Compartmentation of 1-naphthol metabolism was inferred from the metabolite pattern and distribution in the isolated mucosa of guinea pig intestine mounted in a flux chamber (Sund and Lauterbach, Arch Pharmacol Toxicol 58: 74-83, 1986). To verify the existence of these compartments the dependence of [35S]sulphate incorporation into 1-naphthol sulphate on the side of administration of 1-naphthol and [35S]sulphate was determined. Isolated mucosae were pre-equilibrated with [35S]-sulphate (5 x 10(6) cpm/mumol, 1 mM) for 30 min and subsequently incubated for 15 min with 50 microM 1-naphthol. The three 1-naphthol sulphate fractions (luminal side, blood side and tissue) were assayed by HPLC and liquid scintillation counting; their specific activity was calculated as percentage of the specific activity of the inorganic sulphate administered. 1-Naphthol glucuronide was also measured. In jejunal experiments: after luminal administration of 1-naphthol, 1-naphthol sulphate appeared almost exclusively in the luminal solution; its specific activity approached 70% and 3%, when [35S]sulphate was added to the luminal and blood side, respectively. After introducing 1-naphthol and [35S]sulphate on the blood side, a high and similar specific activity of 50-60% was observed in all three 1-naphthol sulphate fractions (luminal and blood side, tissue) though adding [35S]sulphate to the lumen side decreased the specific activity to 10-20%. In experiments on colonic mucosa: a specific activity both of luminal and blood side 1-naphthol sulphate of more than 50% was observed with blood side [35S]sulphate irrespective of the side of 1-naphthol administration. When [35S]sulphate was placed on the luminal side the specific activity of blood side 1-naphthol sulphate dropped to only 3%, and that of luminal 1-naphthol sulphate ranged between 6% and 20%. Supplementary experiments in which mucosae were exposed to 1-naphthol and [35S]sulphate for 45 min without preincubation showed a tendency to decrease the lumen: blood distribution ratio of 1-naphthol sulphate. However, the general pattern of 1-naphthol sulphate specific activity remained unchanged. The experiments provide further evidence that the jejunal conjugation of phenolic drugs is being performed in two major compartments, which are accessible from the lumen ("luminal compartment") and blood ("systemic compartment") side. The luminal compartment seems practically inaccessible to blood side sulphate as is the systemic compartment for luminal 1-naphthol. In the colonic mucosa, a major "systemic compartment" receiving its sulphate from the blood side is the site for most of the events, but a minor "luminal compartment" seems to be involved as well.

Animals↗

Compartmentation of amino acid metabolism in the rat dorsal root ganglion; a metabolic and autoradiographic study.

The incorporation of radioactivity into glutamate, glutamine, GABA and other amino acids was followed after incubation of desheathed rat dorsal root ganglia in media containing [14C]glucose or [14C]acetate. The results indicated that [14C]glucose was incorporated into a large pool of glutamate, but that this glutamate pool did not synthesize glutamine or GABA to any great extent. [14C]Acetate, on the other hand, was incorporated into a small glutamate pool which was readily converted to glutamine, and which synthesized GABA to a greater extent than the large pool. Light microscopic autoradiography of ganglia incubated with [14C]glucose or [14C]acetate confirmed that the small pool labelled by acetate was probably associated with satellite glial cells, while the large pool was located within the ganglion neurons. The results are discussed within the context of previous work on compartmentation of glutamate metabolism in the central nervous system.

Acetates↗

Alterations in the compartmentalized metabolism of glutamic acid with changed cerebral conditions.

Data obtained from combined determinations of the nervous tissue content of glutamic acid, taurine and glutamine were examined in terms of the well established concept of a compartmentalized metabolism for glutamic acid. Three different situations associated with altered cortical conditions were studied: cortical hyperexcitability induced by cobalt epilepsy (mouse); chronic stimulation of the optic tectum by light adaptation (fish); and anatomic alteration of the optic tectum following unilateral enucleation (fish). All 3 situations appear to cause a reduction in the ability of glial elements to capture free glutamic acid released from neuronal structures. However, the underlying causes for such an insufficiency seem to differ in each instance. In epilepsy the release of glutamic acid and taurine exceeds the glial capture rate; during chronic stimulation of a normal cortex a diminished glial uptake rate for both amino acids seems apparent; anatomical degenerative changes seem to diminish especially the glutamine retention capacity of the cortex, possibly in combination with a reduced glial taurine uptake.

Animals↗

Role of microtubules in the cytoplasmic compartmentation of neurons.

We have examined the role of microtubules (MTs) in the development and maintenance of the cytoplasmic compartmentation of ribosomes in cultured embryonic chick sensory neurons. Control neurons show a sharp cytoplasmic demarcation between the ribosome-rich/MT-deficient 'translational' cytoplasm of the perikaryon and the ribosome-deficient/MT-rich 'expressional' cytoplasm of the axon-like neurites. Neurites treated with 1.0 microgram/ml nocodazole for 15-20 min show in addition to the depolymerization of MTs a clear loss of the cytoplasmic demarcation between the soma and neurite. We found a decreasing density of ribosomes with increasing distance from the soma in the nocodazole treated neurites. Ribosomes, as confirmed by their diameter and sensitivity to ribonuclease treatment, populated the first 100 microns of neurites at roughly the same density as found in the soma (150-300 ribosomes per microns2 in 50 mm longitudinal thin sections). The second 100 microns contained a lower density of ribosomes than the first, 20-60 per microns2, but still higher than controls. Distances past 200 microns were devoid of unambiguous ribosomes. Neurites amputated between 50 and 150 microns from the soma then treated with nocodazole contained a dense population of ribosomes in the proximal segment still attached to the soma, but few or none in the distal segment. We interpret these findings as evidence that ribosomes are able to move from the soma down the neurite after MT disassembly.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Role of microtubules in the cytoplasmic compartmentation of neurons. II. Endocytosis in the growth cone and neurite shaft.

We investigated the role of microtubules in the compartmentation of motility and endocytosis in the neurite shaft and growth cone of cultured chick sensory neurons. As reported previously by Letourneau and Ressler (J. Cell Biol., 98 (1984) 1355-1362), stimulating microtubule polymerization with taxol inhibits growth cone motility. In neurons that had grown for 18-30 h, taxol treatment caused growth cones to round up forming an obvious varicosity (taxol bulb) at the terminal. Removal of taxol allowed nearly immediate resumption of cortical motility in all 17 neurons observed by time-lapse videomicroscopy. However, only one of the 17 neurites was observed to elongate measurably even after 5 h of observation. In 14 cases taxol was rinsed out and the concentration of nerve growth factor was increased 10x, 11/14 neurites retracted within the next hour. Endocytic activity was investigated by incubating control and taxol treated neurons in either cationized ferritin or horseradish peroxidase for 30 min. The number and area of label-containing vesicles was measured along with the total area of the growth cone or taxol bulb. We found that taxol treatment caused a 7-fold decrease in the ratio of the area of the labeled vesicles to the area of growth cone or taxol bulb. Conversely, in neurite shafts, normally relatively quiescent with respect to endocytosis, those regions devoid of microtubules in both control and nocodazole-treated cells contained a high concentration of label-containing vesicles. We conclude that the presence of microtubules plays a role in regulating endocytic activity by the overlying cell cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaloids↗

Dark-induced changes in activity and compartmentalization of retinal calmodulin kinase in the rat.

Calmodulin kinase (CaM kinase) activity and immunoreactivity were measured in the cytosol and crude synaptic membranes of light- and dark-adapted rat retinas. Dark adaptation increased the calcium-independent CaM kinase activity 2.7 times and calcium-stimulated activity 3.9 times in membrane fractions. Dark adaptation also increased membrane-bound CaM kinase immunoreactivity 2.4 times. In the cytosol, dark adaptation increased calcium- and calmodulin-independent kinase activity 3.3-fold but did not enhance calcium- and calmodulin-dependent activity. Soluble CaM kinase immunoreactivity was decreased by 13% by dark exposure. These changes in enzyme activity and immunoreactivity are likely due to changes in the endogenous state of autophosphorylation and compartmental concentrations of CaM kinase and may represent translocation of CaM kinase from cytosol to membranes. CaM kinase may have an important role in modulating visual processes.

Adaptation, Physiological↗

The compartmentalization of the monkey and rat cerebellar cortex: zebrin I and cytochrome oxidase.

The cerebellar cortex of mammals is composed of parasagittal zones that encompass the afferent inputs, the efferent corticonuclear and corticovestibular projections, and a number of intrinsic molecular markers. One such marker is the polypeptide antigen zebrin I that is recognized by monoclonal antibody (mab) Q113. In rodents, zebrin I immunocytochemistry reveals an array of parasagittal Purkinje cell compartments. In the present study, zebrin I has been used to reveal the molecular heterogeneity of the cerebellar cortex in the squirrel monkey (Saimiri sciureus). As in rodents, zebrin I is Purkinje cell specific in the primate cerebellum and not all Purkinje cells are immunoreactive. Immunocytochemistry on frontal or horizontal sections reveals a system of bands of zebrin I+ cells extending through the vermis of both anterior and posterior lobes. A midline (P1+) band and two more lateral bands (P2+ and P3+) are found in all lobules. The situation in the paravermis and hemispheres is similar, with alternating zebrin I+ and zebrin I- compartments, but the complex lobulation obscures the precise band pattern: it seems probable that 4 additional bands are present in the hemispheres, as in rodents. Comparison of rat and monkey cerebellums suggests that the cortex has expanded in primates by the growth of the same individual bands found in rats rather than by the addition of supplementary compartments. The zebrin I compartmentalization revealed by using mab Q113 is reproducible from individual and thus provides a stable frame of reference that has been used to compare the different chemoarchitectonic patterns found in the cerebellar cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Developmental expression, compartmentalization, and possible role in excitotoxicity of a putative NMDA receptor protein in cultured hippocampal neurons.

The mechanisms regulating the expression and localization of excitatory amino acid (EAA) neurotransmitter receptors in neurons of the developing mammalian brain, and roles for these receptors in the plasticity and degeneration of neural circuits are not well understood. We previously isolated and characterized a 71 kDa glutamate binding protein (GBP) from rat brain, and have recently obtained evidence that this GBP is a component of a functional N-methyl-D-aspartate (NMDA) receptor-ion channel complex. We have now used antibodies to this putative NMDA receptor protein to examine its expression and localization, and consequences of its activation in cultured embryonic (18 day) rat hippocampal neurons. Immunocytochemistry and Western blots using monoclonal antibodies to the GBP demonstrated an increase in GBP-positive neurons and their staining intensity with time in culture. GBP was localized to the somata and dendrites of pyramidal-like neurons and was sparse or absent in the axons. The expression and compartmentalization of GBP occurred in isolated neurons indicating that direct cell interactions were not required for these processes. Cell surface staining for GBP occurred in patches on the soma and dendrites. The developmental expression of GBP immunoreactivity closely paralleled the expression of sensitivity to NMDA neurotoxicity. There was a direct relationship between GBP immunoreactivity and neuronal vulnerability to glutamate-induced degeneration; vulnerable neurons stained heavily whereas resistant neurons showed either low levels of staining or no staining. Finally, a GBP antiserum greatly reduced NMDA neurotoxicity (but not kainate neurotoxicity). Taken together, these findings demonstrate the expression of presumptive NMDA receptors within a subpopulation of embryonic hippocampal neurons, and their segregation to the soma and dentrites of pyramidal neurons. This spatial distribution of glutamate receptors among and within neurons is likely to play important roles in regulating the structure of neural circuitry during development, and may also be an important determinant of selective neuronal vulnerability in pathological conditions.

Animals↗

Compartmentalization of parvalbumin immunoreactivity in the human striatum.

The distribution of parvalbumin in the basal ganglia was studied in eight human brains using immunohistochemical techniques and the pattern of staining was compared to the distribution of enkephalin immunoreactivity in adjacent sections. The results showed a heterogeneous pattern of parvalbumin immunoreactivity in the caudate nucleus and putamen; this pattern of staining was characterized by irregularly shaped patches of low parvalbumin immunoreactivity dispersed against a background matrix of moderate-to-high immunoreactive staining. These parvalbumin-poor patches in the caudate nucleus and putamen aligned with the enkephalin-rich striosomes. These results show that parvalbumin immunoreactivity in the human striatum has the same compartmental mosaic organization as other neurochemical markers in the mammalian striatum.

Adolescent↗