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Calcium-binding proteins in chemoreceptors of Xenopus laevis.

Calcium-binding proteins were investigated immunohistochemically in chemo-receptors of the olfactory epithelium and taste buds of the clawed frog, Xenopus laevis. Calmodulin-, S-100- and calbindin-immunoreactive material were found in sensory cells of the olfactory epithelium; however, parvalbumin-like material was absent in these cells. Taste buds of the palate showed calmodulin-, S-100- and parvalbumin-immunoreactive material in sensory cells, while calbindin-immunoreactive material in supporting cells. Merkel cells, surrounding the base of the taste buds in a ring-like manner, exhibited calmodulin- and S-100-immunoreactive material.

Animals↗

Stimulation of GABAergic neuron differentiation by NT-4/5 in cultures of rat cerebral cortex.

Primary cultures of fetal rat cortical cells were used to investigate trophic effects of neurotrophin-4/5 (NT-4/5) on GABAergic neurons. Chronic administration of NT-4/5 resulted in a significant increase in high-affinity GABA uptake and in a stronger immunohistochemical staining pattern and bigger cells size of neurons visualized by GABA immunohistochemistry. Brain-derived neurotrophic factor (BDNF) exerted similar actions. These effects were observed in cultures prepared from rat fetuses from embryonic day (ED) 15 and ED18. The total number of cells was marginally increased in ED15 but not ED18 cultures. NT-4/5 did not elevate uptake of excitatory amino acids. Administration of NT-4/5 and BDNF resulted in higher levels of the calcium binding protein, calbindin, in these cultures. Our findings suggest that subpopulations of cortical GABAergic and calbindin-expressing neurons respond to NT-4/5 during development.

Animals↗

Transient compartmental expression of a family of protein tyrosine phosphatases in the developing striatum.

The expression of a family of intracellular protein tyrosine phosphatases (STEP) was studied in the striatum of rats during ontogeny. Links between the formation of dopamine islands and STEP immunoreactive patches in the striatum were examined since previous work had suggested that STEP isoforms were selectively expressed in dopaminoceptive brain regions. STEP protein and mRNAs were distributed in a patchy manner during the first postnatal week. By 2 weeks, STEP immunoreactivity was homogeneous, indicating that both patch and matrix neurons express STEP by maturity. Two-color immunofluorescent staining was also performed to compare STEP with specific markers for patch and matrix. Tyrosine hydroxylase immunoreactive fibers from the substantia nigra form distinctive dopamine islands in the striatum during late embryonic development, and occupy the sites of future patches [23,37,38,54]. These fiber islands align with STEP immunoreactive neuronal patches during the first two postnatal weeks, suggesting that STEP is a marker for patch neurons in early postnatal development. When STEP's distribution was compared with other markers for patch (substance P) or matrix (calbindin), STEP co-localized with substance P in most striatal neurons on postnatal days 1 through 7. However, STEP was also expressed within a subset of calbindin-positive neurons in the lateral striatum, but not with these neurons elsewhere in the striatum. By adulthood, STEP colocalized with both markers. These results suggest that STEP is expressed first within patch neurons but not matrix, and subsequently within both. The expression of STEP may be triggered by the arrival of striatal afferents or other regulatory factors.

Animals↗

1,25-Dihydroxyvitamin D(3) receptors in developing dorsal root ganglia of fetal rats.

We observed immunostaining for the 1,25-dihydroxyvitamin D(3) receptor (VDR) and calbindin-D(28k) in neurons, but not glial cells, of fetal rat dorsal root ganglia (DRG) from days 13 through 21 of gestation. Dispersed cultures of DRG collected from rat fetuses at gestational day 15 also contained epitopes for VDR and calbindin-D(28k) in neurons, but not in glial cells. 1,25-Dihydroxyvitamin D(3), through VDR, may perform significant functions in the development of neuronal cells.

Animals↗

Identification of myenteric neurons which project to the mucosa of the guinea-pig small intestine.

Myenteric neurons which innervate the mucosa of the guinea-pig ileum were characterized by combining retrograde transport of DiI in vitro with immunohistochemistry. Of DiI-labelled myenteric neurons, 43% were immunoreactive for calbindin and substance P, 25% were immunoreactive for calbindin alone, and 18% were immunoreactive for substance P alone. These 3 classes of neurons had Dogiel Type II morphology and are probably sensory neurons. Two classes of probable secretomotor neurons were characterized by immunoreactivity for neuropeptide Y (4%) and vasoactive intestinal peptide (2%). These 5 classes of myenteric neurons represent over 90% of the retrogradely labelled myenteric neurons that project to the mucosa.

Animals↗

GABA-immunoreactive basal forebrain afferents innervate GABA-immunoreactive non-pyramidal cells in the cerebral cortex of the lizard Podarcis hispanica.

The basal forebrain projection to the cerebral cortex was studied in the lizard Podarcis hispanica by anterograde transport of Phaseolus vulgaris leucoagglutinin. After injections of the lectin into the septal-basal forebrain area, Phaseolus vulgaris leucoagglutinin-labelled fibres were mainly detected in the outer plexiform layer of the medial cortex and in the inner plexiform layer of the dorsal and dorsomedial cortices. Ultrathin sections from these areas were obtained and processed for postembedding immunogold staining for GABA. Most of the Phaseolus vulgaris leucoagglutinin-labelled boutons in the dorsal and dorsomedial cortical areas were GABA immunoreactive and all the double-labelled boutons established symmetric synaptic contacts on cell bodies and dendrites that were also found to be GABA immunoreactive in all cases. In contrast, Phaseolus vulgaris leucoagglutinin-labelled varicosities in the outer plexiform layer of the medial cortex made asymmetric synaptic contacts on GABA-immunonegative profiles and they were themselves negative for GABA. In double-labelled sections, GABA-, calbindin D28k- and neuropeptide Y-immunoreactive neurons were found to be innervated by multiple Phaseolus vulgaris leucoagglutinin-labelled varicosities in the dorsal and dorsomedial cortical areas, whereas in the medial cortex Phaseolus vulgaris leucoagglutinin-labelled fibres were not observed in contact with any subpopulation of GABAergic cells. The results demonstrate that in lizards the septal-basal forebrain projection to the cortex has a GABAergic component, which selectively terminates on GABAergic non-pyramidal cells including the neuropeptide Y- and the calbindin D28k-containing subpopulations. This synaptic organization is remarkably similar to that in mammals, and suggests that the mechanisms of control of the cortical activity by the basal forebrain have been highly preserved during phylogeny.

Afferent Pathways↗

Repeated asphyxia causes loss of striatal projection neurons in the fetal sheep brain.

Repeated episodes of cerebral hypoxia-ischemia can cause primarily striatal neuronal loss in the developing brain. We investigated the effect of repeated episodes of asphyxia on specific neuronal sub-populations of the basal ganglia in late-gestation fetal sheep. Asphyxia was induced in 10 fetal sheep (118-126 days gestation) by occluding the umbilical cord for 5 min. This procedure was repeated four times at 30 min intervals and the brains were fixed 3 days later for histopathology. Immunohistochemical markers were used to identify various populations of neurons in the striatum. Antibodies to calbindin were used to stain the GABAergic medium-sized striatal projection neurons and antibodies to somatostatin and parvalbumin to identify striatal interneurons. Striatal projection neurons to the globus pallidus were recognized by enkephalin immunoreactivity, while the striatonigral terminals were identified in the substantia nigra pars reticulata by substance P immunohistochemical labelling. The results showed a marked loss of calbindin staining in the striatum, evident by both reduced cell numbers and a decrease in neuropil staining. The number of parvalbumin immunoreactive cells was also reduced in the striatum, while somatostatin interneurons were selectively preserved. In addition, immunostaining for enkephalin in the globus pallidus and for substance P in the substantia nigra was markedly reduced. These results show that the stiatal GABAergic medium-sized projection neurons are severely affected by recurrent episodes of asphyxia. These findings are confirmed and extended by the results demonstrating that both the enkephalin/GABA striatopallidal and the substance P/GABA stiatonigral pathways are affected. The results of this study therefore suggest that the efferent striatal projections to the globus pallidus and to the substantia nigra may be involved in asphyxial episodes resulting in cerebral palsy.

Animals↗

Insulin-like growth factor I-immunoreactive peptide in adult human cerebellar Purkinje cells: co-localization with low-affinity nerve growth factor receptor.

It has been proposed that Insulin-like growth factor I is involved in the development, growth and maintenance of the central nervous system possibly interacting with other trophic factors. High levels of insulin-like growth factor I have been detected in the cerebellum during development and adulthood suggesting a specific role for insulin-like growth factor I in this brain area. While there is ever increasing data regarding the cell types containing endogenous insulin-like growth factor I in the rat brain, no information on the human brain is yet available. In the present study we sought to analyse the precise location of insulin-like growth factor I peptide in the adult human cerebellum using a specific antiserum against recombinant human insulin-like growth factor I. After immunocytochemistry, numerous Purkinje cells exhibited intense positive staining occupying the cell soma, dendrites and dendritic spines as well as axons. Occasionally, immunoreactive Purkinje cell axons were arciform and exhibited bulbous dilatations along their proximal length. Putative recurrent collaterals of Purkinje cell axons were also insulin-like growth factor I reactive. Double-staining immunocytochemistry in the same sections consistently showed, as expected, co-expression of insulin-like growth factor I and calbindin, although a few calbindin containing Purkinje cells lacked insulin-like growth factor I immunostaining suggesting there are insulin-like growth factor I positive Purkinje cell subsets in the human cerebellum. In addition, co-expression of insulin-like growth factor I and low-affinity nerve growth factor receptor-immunoreactive protein was found in a subpopulation of insulin-like growth factor I positive Purkinje cells. The results of this study prove the presence of insulin-like growth factor I immunoreactivity in a Purkinje cell subpopulation of the adult human cerebellum suggesting that insulin-like growth factor I may participate in paracrine or autocrine regulatory systems in the adult human brain.

Adult↗

Distribution of limbic system-associated membrane protein immunoreactivity in primate basal ganglia.

The limbic system-associated membrane protein is a 64,000-68,000 mol.wt molecule known to be preferentially expressed by neurons in limbic structures of rats and cats. The present immunohistochemical study describes the distribution of this protein in the basal ganglia of Macaca fascicularis. The ventral striatum of the cynomolgus monkey displays a very intense immunostaining, whereas the dorsal striatum is much more weakly stained, except for some small zones scattered in the caudate nucleus and, to a lesser extent, in the putamen. These protein-rich zones are in register with striosomes, as visualized on adjacent sections immunostained for calbindin. At pallidal levels, immunostaining for the protein is observed only in the subcommissural regions, at the ventromedial tip of the internal pallidum, and in the caudoventral portion of the external pallidum. At nigral levels, the immunostaining is highly heterogeneous with a marked decreasing rostrocaudal gradient. The staining is most intense in nigral regions that receive striatal inputs and are enriched with calbindin. Nigral sectors populated by dopaminergic neurons, as visualized on adjacent sections immunostained for tyrosine hydroxylase, are largely devoid of immunoreactivity. In contrast, the immunostaining is uniformly intense in the ventral tegmental area. This study provides the first neuroanatomical evidence for teh existence of the limbic system-associated membrane protein in primate brain. It reveals that this glycoprotein is distributed in a highly heterogeneous manner in primate basal ganglia, where it preferentially labels regions that are anatomically and functionally linked to the limbic system.

Animals↗

An experimental model for the non-invasive trans-synaptic induction of nitric oxide synthase in Purkinje cells of the rat cerebellum.

Nitric oxide synthase and its product nitric oxide are believed to be significantly involved in neuronal degeneration associated with various excitotoxic events and in some acute and chronic neuropathological disease states. The synchronous activation of inferior olive neurons by the drug harmaline is known to produce tremorogenic activity in rats via increased stimulation of the olivocerebellar system. Following subcutaneous or intraperitoneal injection (15, 30 or 60 mg/kg) of harmaline and survival intervals of three days or more, NADPH-diaphorase histochemistry and nitric oxide synthase immunocytochemistry revealed nitric oxide synthase induction in Purkinje cells of the cerebellar vermis and paravermis, but not the lateral hemispheres. Double labeling with NADPH-diaphorase and calbindin revealed that induced Purkinje cells contain calbindin and that induced Purkinje cells are not necessarily associated with regions of Purkinje cell degeneration. The induction of nitric oxide synthase in a subpopulation of Purkinje cells may reflect a protective response of selected Purkinje cells to overstimulation of specific olivocerebellar projections. This is the first experimental model for the non-invasive induction of nitric oxide synthase in central nervous system neurons and as such may provide a useful tool for studying the induction of nitric oxide synthase associated with excitotoxic events.

Amino Acid Sequence↗

Pattern of neuronal death in the rat hippocampus after status epilepticus. Relationship to calcium binding protein content and ischemic vulnerability.

The pattern of hippocampal cell death has been studied following hippocampal seizure activity and status epilepticus induced by 110-min stimulation of the perforant pathway in awake rats. The order of vulnerability of principal cells in the different hippocampal subfields--as determined by silver impregnation--was found to be very similar to the pattern found in ischemia; i.e., dentate hilus greater than CA1, subiculum greater than CA3c greater than CA3a,b greater than dentate granule cells. The hilar somatostatin-containing cells were the most vulnerable cell type, whereas all other subpopulations of nonprincipal neurons--visualized by immunocytochemistry for the calcium binding proteins parvalbumin and calbindin--were remarkably resistant. Pyramidal cells in the CA3 region containing neither of the examined calcium binding proteins were more resistant to overexcitation than CA1 pyramidal cells, most of which do contain calbindin. This indicates that no simple relationship exists between vulnerability in status epilepticus and neuronal calcium binding protein content, and that local and/or systemic hypoxia during status epilepticus may be responsible for the ischemic pattern of cell death.

Animals↗

Estradiol enhances light-induced expression of transcription factors in the SCN.

The suprachiasmatic nucleus of the hypothalamus (SCN) is the master clock that regulates circadian and seasonal rhythms. Among these, the SCN regulates the phasic release of hormones and provides for the timing of the preovulatory luteinizing hormone (LH) surge necessary for ovulation in females. There is little evidence, however, of sex hormone effects on mechanisms underlying SCN function. This study examined the effects of exogenous administration of estradiol on the light-induced expression of transcription factors in the SCN of female rats. Ovariectomized (OVX) female rats were given estradiol or cholesterol implants and perfused 48 h later. Half of the animals were sacrificed 1 h after the regular onset of light within the colony. The rest had the lights go on 2 h prior to the regular time and perfused 1 h later. Collected brains were sliced and sets of SCN sections were processed for immunoreactivity (ir) detecting the Fos, pCREB, egr-1, CREB binding protein (CBP), and calbindin-D (28K) proteins. Following quantification, statistical analyses demonstrated that estradiol enhanced Fos and p-CREB-ir in the SCN of females that experienced a 2-h phase advance. The phase advance also enhanced calbindin and egr-1-ir, but the expression of these proteins was not affected by estradiol. These results demonstrate that estradiol enhances the levels of transcription factors that precede the expression of clock gene proteins in the SCN in response to advances in the onset of environmental light. These data support the hypothesis that steroid hormones play an important role in the fine tuning of the clock in the face of environmental changes in daylight.

Animals↗

Chromogranin peptides in Alzheimer's disease.

Synaptic disturbances may play a key role in the pathophysiology of Alzheimer's disease. To characterize differential synaptic alterations in the brains of Alzheimer patients, chromogranin A, chromogranin B and secretoneurin were applied as soluble constituents for large dense core vesicles, synaptophysin as a vesicle membrane marker and calbindin as a cytosolic protein. In controls, chromogranin B and secretogranin are largely co-contained in interneurons, whereas chromogranin A is mostly found in pyramidal neurons. In Alzheimer's disease, about 30% of beta-amyloid plaques co-labelled with chromogranin A, 20% with secretoneurin and 15% with chromogranin B. Less than 5% of beta-amyloid plaques contained synaptophysin or calbindin, respectively. Semiquantitative immunohistochemistry revealed a significant loss for chromogranin B- and secretoneurin-like immunoreactivity in the dorsolateral, the entorhinal, and orbitofrontal cortex. Chromogranin A displayed more complex changes. It was the only chromogranin peptide to be expressed in glial fibrillary acidic protein containing cells. About 40% of chromogranin A immunopositive plaques and extracellular deposits were surrounded and pervaded by activated microglia. The present study demonstrates a loss of presynaptic proteins involved in distinct steps of exocytosis. An imbalanced availability of chromogranins may be responsible for impaired neurotransmission and a reduced functioning of dense core vesicles. Chromogranin A is likely to be a mediator between neuronal, glial and inflammatory mechanisms found in Alzheimer disease.

Aged↗

Induced cerebral hypothermia reduces post-hypoxic loss of phenotypic striatal neurons in preterm fetal sheep.

Perinatal hypoxic-ischemic injury of the basal ganglia is a significant cause of disability in premature infants. Prolonged, moderate cerebral hypothermia has been shown to be neuroprotective after experimental hypoxia-ischemia; however, it has not been tested in the preterm brain. We therefore examined the effects of severe hypoxia and the potential neuroprotective effects of delayed hypothermia on phenotypic striatal neurons. Preterm (0.7 gestation) fetal sheep received complete umbilical cord occlusion for 25 min followed by cerebral hypothermia (fetal extradural temperature reduced from 39.4+/-0.3 degrees C to 29.5+/-2.6 degrees C) from 90 min to 70 h after the end of occlusion. Hypothermia was associated with a significant overall reduction in striatal neuronal loss compared with normothermia-occlusion fetuses (mean+/-SEM, 5.5+/-1.2% vs. 38.1+/-6.5%, P<0.01). Immunohistochemical studies showed that occlusion resulted in a significant loss of calbindin-28 kd, glutamic acid decarboxylase isoform 67 and neuronal nitric oxide synthase-immunopositive neurons (n=7, P<0.05), but not choline acetyltransferase-positive neurons, compared with sham controls (n=7). Hypothermia (n=7) significantly reduced the loss of calbindin-28 kd and neuronal nitric oxide synthase, but not glutamic acid decarboxylase-immunopositive neurons. In conclusion, delayed, prolonged moderate head cooling was associated with selective protection of particular phenotypic striatal projection neurons after severe hypoxia in the preterm fetus. These findings suggest that head cooling may help reduce basal ganglia injury in some premature babies.

Animals↗

Pattern differentiation of excitatory and inhibitory synaptic inputs on distinct neuronal types in the rat caudal nucleus of the tractus solitarius.

Region- and size-specific neuronal organizations of the caudal nucleus of the tractus solitarius (cNTS) were investigated, followed by analyses of excitatory and inhibitory synaptic input patterns onto specific cell types by patch clamp recordings and immunoelectron microscopy. Cell size distribution and numerical density of cNTS neurons were examined in subregions at levels of the area postrema. In the subpostremal and dorsomedial subnuclei, characterized by the presence of dense glutamatergic and sparse GABAergic somata, small calbindin neurons constituted 42% of the total cells. The medial subnucleus contained large numbers of glutamatergic, GABAergic, and catecholaminergic somata and large tyrosine hydroxylase-containing cells constituted 13% in this region. In total, small neurons (<150 microm2) represented about 80% of the cell population in the cNTS. Predominant excitatory postsynaptic currents were observed in the adult small neurons, while inhibitory postsynaptic currents were more evident in larger neurons, irrespective of subnuclear location. This distinct differentiation of postsynaptic current patterns was not evident in neonates. GABAergic synapses were more frequently associated with dendrites of large catecholaminergic cells (73%) than with those of small calbindin-containing cells (10%) in adults. These results indicate that differential synaptic input patterns were developmentally established in distinct small and large neurons.

Animals↗

Differential disruption of nuclear volume and neuronal phenotype in the preoptic area by neonatal exposure to genistein and bisphenol-A.

Changes in the volumes of sexually dimorphic brain nuclei are often used as a biomarker for developmental disruption by endocrine-active compounds (EACs). However, these gross, morphological analyses do not reliably predict disruption of cell phenotype or neuronal function. In the present experiments, we used a more comprehensive approach to assess whether postnatal exposure to the EACs genistein (GEN) or bisphenol-A (BIS) affected the development of two sexually dimorphic brain regions in male rats: the anteroventral periventricular nucleus of the hypothalamus (AVPV) and the sexually dimorphic nucleus of the preoptic area (SDN). In addition to nuclear volumes, we also measured the number of immunopositive calbindin neurons in the SDN and the activational patterns of gonadotropin-releasing hormone (GnRH) neurons, a neuronal population that is functionally linked to the AVPV. In rats, exposure of the neonatal male brain to endogenous estrogen, aromatized from testicular testosterone, is essential for the proper sexual differentiation of these endpoints. Thus, we hypothesized that exposure to BIS and GEN during this critical period could disrupt brain sexual differentiation. Animals were given four subcutaneous injections of sesame oil (control), 250 microg GEN, or 250 microg BIS at 12 h intervals over postnatal days (PND) 1 and 2, gonadectomized on PND 85, and treated sequentially with estrogen and progesterone to stimulate Fos expression in GnRH neurons, a marker for their activation. A cohort of age-matched ovariectomized (OVX) females that were given the same hormone treatment in adulthood served as a positive control group. SDN volume was unchanged by treatment, but the number of calbindin neurons in the SDN was significantly increased by both BIS and GEN. GEN, but not BIS, demasculinized male AVPV volume, but patterns of GnRH neuronal activation were not affected by either compound. These results suggest that acute exposure to EACs during a critical developmental period can independently alter nuclear volumes of sexually dimorphic nuclei and their phenotypic profiles in a region specific manner.

Animals↗

Differences in the suprachiasmatic nucleus and lower subparaventricular zone of diurnal and nocturnal rodents.

Diurnal and nocturnal species are profoundly different in terms of the temporal organization of daily rhythms in physiology and behavior. The neural bases for these divergent patterns are at present unknown. Here we examine functional differences in the suprachiasmatic nucleus (SCN) and one of its primary targets in a diurnal rodent, the unstriped Nile grass rat (Arvicanthis niloticus) and in a nocturnal one, the laboratory rat (Rattus norvegicus). Grass rats and laboratory rats were housed in a 12:12 light:dark cycle, and killed at six time points. cFos-immunoreactive rhythms in the SCN of grass rats and laboratory rats were similar to those reported previously, with peaks early in the light phase and troughs in the dark phase. However, cFos-immunoreactivity in the lower subparaventricular zone (LSPV) of grass rats rose sharply 5 h into the dark phase, and remained high through the first hour after light onset, whereas in laboratory rats it peaked 1 h after light onset and was low at all other sampling times. Daily cFos rhythms in both the SCN and the LSPV persisted in grass rats, but not in laboratory rats, after extended periods in constant darkness. In grass rats, the endogenous cFos rhythm in the LSPV, but not the SCN, was present both in calbindin-positive and in calbindin-negative cells. Cells that expressed cFos at night in the region of the LSPV in grass rats were clearly outside of the boundaries of the SCN as delineated by Nissl stain and immunoreactivity for vasopressin and vasoactive intestinal peptide. The LSPV of the grass rat, a region that receives substantial input from the SCN, displays a daily rhythm in cFos expression that differs from that of laboratory rats with respect to its rising phase, the duration of the peak and its dependence on a light/dark cycle. These characteristics may reflect the existence of mechanisms in the LSPV that enable it to modulate efferent SCN signals differently in diurnal and nocturnal species.

Animals↗

Monoaminergic markers in the optic tectum of the domestic chick.

The avian optic tectum has become a reliable model system to study the basic mechanisms that underlie the computation of visual stimuli. Many aspects of its cytoarchitecture, chemoarchitecture, connectivity and development are thoroughly characterized. However, knowledge about its monoaminergic innervation is still incomplete. As a prerequisite to understand a possible functional role of the monoaminergic neurotransmitters, the serotonergic, noradrenergic, and dopaminergic innervation of the optic tectum as well as the distribution of serotonin 2A receptors, the dopamine- and cAMP-regulated phosphoprotein DARPP-32 and calbindin D-28K was studied in domestic chicks by immunohistochemical techniques. Serotonergic, noradrenergic, and tyrosine hydroxylase positive axons and axon terminals were present in all layers of the optic tectum. Generally, the highest densities of serotonergic, noradrenergic, and tyrosine hydroxylase positive fibers were found in the superficial tectal layers 1-8, whereas only moderate densities of serotonergic, noradrenergic, and tyrosine hydroxylase positive fibers became obvious in the deep tectal layers 9-15. Serotonergic fibers were particularly abundant in layers 4, 5a and 7 and serotonin 2A receptors in layer 13. Noradrenergic fibers were densest in layers 4 and 5a, whereas tyrosine hydroxylase positive fibers showed a slightly different distribution pattern with additional dense labeling in layer 7. As revealed by double-labeling immunohistochemistry, serotonergic fibers were closely related to the cell bodies of calbindin-positive horizontal cells in layer 5b and tyrosine hydroxylase positive fibers often contacted DARPP-32+ dendritic shafts in layers 9 and 10. These findings indicate that the catecholaminergic innervation of the optic tectum consists of a noradrenergic and a dopaminergic component and that the noradrenergic, serotonergic, and dopaminergic system may be potentially involved in the modulation of retinal input in the superficial layers of the optic tectum as well as in the modulation of tectal output via the deep tectal layers.

Animals↗