Age-related changes in CREB binding protein immunoreactivity in the cerebral cortex and hippocampus of rats

Although the role of cAMP-response-element-binding protein (CREB) binding protein (CBP) in the neuroprotective mechanisms has been the focus of many studies, very little is known about the expression or function of CBP in aged brains. We have therefore examined age-related changes in CBP expression in the cerebral cortex and hippocampus with an immunohistochemical technique. In the cerebral cortex, the distribution patterns were not different between adult and aged groups, but the staining intensity of CBP was significantly decreased in aged rats. In the hippocampus, a distinct immunoreactivity pattern was observed in the CA1-3 areas and dentate gyrus. CBP immunoreactivity was significantly deceased in the pyramidal layer of CA1-3 regions in aged hippocampus. In the dentate gyrus of aged rats, significant decreases were also found in the granule cell layer and polymorphic layer. The first demonstration of age-related decreases in CBP expression in the cerebral cortex and hippocampus may provide useful data for investigating the pathogenesis of age-related neurodegenerative diseases and depression.     

Age-related changes in erythropoietin immunoreactivity in the cerebral cortex and hippocampus of rats

Although oxidative stress may influence the fluid properties of blood, resulting in a potential decrement in blood flow and oxygen delivery to the brain during aging, very little is known about age-related changes in Epo expression. Therefore, we examined age-related changes in Epo expression in the cerebral cortex and hippocampus with an immunohistochemical technique. In aged rats, there was a significant decrease in Epo immunoreactivity in the pyramidal cells in the cortical regions. In the hippocampus of adult rats, a distinct immunoreactivity pattern was observed in the CA1-3 areas and dentate gyrus. In aged hippocampus, Epo immunoreactivity was significantly deceased in the pyramidal layer of CA1 regions, and the granule cell layer of dentate gyrus. It was noted that there was distinct pattern of Epo immunoreactivity in the pyramidal layer of CA2-CA3 region of aged rats. Epo immunoreactivity was relatively strong, but was observed only in the periphery of the cytoplasm. The first demonstration of age-related decreases in Epo expression in the cerebral cortex and hippocampus may provide useful data for investigating the pathogenesis of age-related neurodegenerative diseases, suggesting that age-related decreases in Epo may contribute to degenerative events following age-related decreases in brain flow and oxygen supply.     

Immunohistochemical study on the distribution of nitrotyrosine and neuronal nitric oxide synthase in aged rat cerebellum

In the present study, we examined age-related changes in 3-nitrotyrosine (NT) and neuronal nitric oxide synthase (nNOS) in rat cerebellum using immunohistochemistry. No immunoreactivity for NT was found in any layers of adult cerebellar cortex. In aged cerebellar cortex, the most prominent labeling of NT was found in the Purkinje cell layers and molecular layers. In aged cerebellar nuclei, NT immunoreactivity was observed in the surrounding neuropil. In aged rat cerebellum, nNOS immunoreactivity was significantly decreased in the molecular layer, while it was slightly increased in the granular layer. Image analysis showed no significant age-related changes in nNOS immunoreactivity in the cerebellar nuclei. In summary, this report has demonstrated that NT increases with age in the cerebellum, and suggests that NO production by the neuronal form of NOS may not be the rate limiting step in NT formation in the aged brain. Further work is needed to examine the mechanisms underlying the increased immunoreactivity for NT, and the functional implications of this increase.     

Effects of insulin-induced hypoglycemia on somatostatin level and binding in rat cerebral cortex and hippocampus

The effects of severe insulin-induced hypoglycemia on somatostatin level and specific binding in the cerebral cortex and hippocampus were examined using 125I-Tyr11-somatostatin as a ligand. Severe insulin-induced hypoglycemia did not affect the level of somatostatin-like immunoreactivity in the brain areas studied. However, the number (but not the affinity) of specific somatostatin receptors was significantly decreased in membrane preparation from the hippocampus but not in the cerebral cortex at the onset of hypoglycemic coma (5-10 min). Administration of glucose at the onset of hypoglycemic coma brought about extensive recovery of hippocampal somatostatin receptor number. These results suggest that glucose modulates the somatostatin receptor in the rat hippocampus. The physiological significance of these findings remains to be clarified.     

Region-specific alterations in insulin-like growth factor receptor type I in the cerebral cortex and hippocampus of aged rats

In the present study, we investigated age-related changes in IGF-I receptor localization in the cerebral cortex and hippocampus of Sprague-Dawley rats using immunohistochemistry. In the cerebral cortex of adult rats, weakly stained cells were seen in layers II-III and layer V/VI in several cortical regions. In aged rats, there was a significant increase in IGF-I receptor immunoreactivity in the pyramidal cells in the same cortical regions. In the hippocampus of adult rats, several moderately stained neurons were seen in CA1-3 areas and the dentate gyrus. Levels of IGF-I receptor protein increased substantially with age in the CA3 area of the hippocampus. Our first morphological data concerning the differential regulation of IGF-I receptors in aged cerebral cortex and hippocampus may provide insights into age-related changes in trophic support as well as basic knowledge required for the study of neurodegenerative diseases such as Alzheimer's disease.     

Age-related changes on monoamine turnover in hippocampus of rats

After pargyline treatment the turnover rates of dopamine (DA), noradrenaline (NA), 3,4-dihydroxyphenylacetic acid (DOPAC), serotonin (5-hydroxytryptamine (5-HT) and 5-hydroxy-3-indolacetic acid (5-HIAA) has been measured in control and aged hippocampus of the rats. In addition, the tyrosine hydroxylase (TH) activity and monoamine oxidase-A and monoamine oxidase-B activities have also been studied. The TH activity did not change in aged hippocampus as compared to controls. The monoamine oxidase-B:monoamine oxidase-A ratio increased in 26-month-old rats compared with controls. The turnover of DA, DOPAC and NA did not show significant changes while 5-HT synthesis, 5-HT accumulation rate and 5-HIAA turnover increased in aged rats. Serotonin fibers showed morphological dissimilarities between the hippocampus of young and aged rats using immunocytochemistry techniques. In aged rats aberrant serotoninergic fibers mainly appear in the molecular layer of the dentate gyrus and moleculare of the hippocampal CA1. It is suggested that the aberrant morphology of 5-HT fibers may reflect the local degeneration of serotoninergic hippocampal afferents during aging. Increase of 5-HT turnover in aged might be a signal of degeneration.     

Age-related and laminar-specific dendritic changes in the medial frontal cortex of the rat

Early hypotheses that normal brain aging involves widespread loss of neurons have been revised in light of accumulating evidence that, in most regions of the brain, the number of neurons is stable throughout adulthood and senescence. It is not clear, however, that all aspects of neuronal structure are similarly maintained, and anatomical changes are likely to contribute to age-related declines in cognitive function. The extent and pattern of dendritic branches is one likely target for age-dependent regulation since dendrites remain plastic into adulthood and since dendrites, as the site of most synapses, critically regulate neuronal function. This study quantified the dendritic extent and geometry of superficial and deep pyramidal neurons in the medial frontal cortex of Brown Norway rats from young adulthood through senescence. This region of cortex is of specific interest given its involvement in a variety of cognitive functions that change with age. In the present study, age-related changes in dendritic extent were found to occur with remarkable specificity. Superficial, but not deep, pyramidal neurons exhibited ongoing dendritic growth after 2 months-of-age and then dendritic regression after 18 months-of-age. Apical and basal dendrites were similarly regulated; in each arbor adult growth and regression were limited to terminal dendritic segments. The focal specificity of age-related changes suggests several possible regulatory mechanisms, including regional changes in trophic support and in neuronal activity. Although restricted to specific neuronal populations, dendritic regression in aged animals is likely to contribute to cognitive changes associated with senescence.     

Age-related changes in ultrastructural features of cathepsin B- and D-containing neurons in rat cerebral cortex

The present study examines age-related changes in the subcellular localization of cathepsin B (cath B) and cathepsin D (cath D), as well as morphological features of the cathepsin-immunoreactive (ir) neurons in rat cerebral cortex. Sprague–Dawley rats were studied at 3 and 26 months. By immunoelectron microscopy cath B- or cath D-immunoreactivities were found in many, but not all, pyramidal neurons. In young rat cerebral cortical neurons, cath B was observed not only in lysosomal systems such as multivesicular bodies, dense bodies, and lipofuscin granules, but also in extralysosomal sites. By contrast, cath D was confined mainly to lysosomal systems in young rats. In aged rats, cath B showed a similar pattern in its subcellular localization compared to the young control, but some of the dense bodies containing cath B was closely apposed to the outer nuclear envelope. These cells exhibited a relatively normal appearance. Regardless of subcellular localization, approximately 10% of cath B-ir neurons displayed ultrastructural disturbances presumed to indicate an early stage of degeneration. The nucleus was indented, nuclear boundary was indistinct, nuclear pore structures appeared separately with high frequency, and the endoplasmic reticulum appeared to be affected. In addition to its presence in lysosomal structures, cath D-immunoreactivity in aged cerebral cortex was noted prominently in the cytosol as diffuse granules. About 37% of cath D-ir cells showed this age-related change. Among the neurons with the diffusely scattered form of cath D, approximately 70% of cells exhibited the degenerating features. These cells were characterized by large amounts of diffuse cath D, reduced cellular size, loss of the nuclear boundary, scattered nuclear pore structures, an often fragmentation of the nucleus, disturbances of endoplasmic reticular system, and in advanced stages, condensed nucleus and poor preservation of almost cytoplasmic organelles. Though some of these features were also found in cath B-ir neurons, findings of overt degeneration, such as fragmented and condensed nuclei and impaired almost cytoplasmic organelles, were generally not observed in cath B-ir neurons. In addition, lipofuscin aggregates containing cath D were observed frequently in the extracellular space close to sites of ruptured plasma membrane, whereas in the sections stained with anti-cath B antibodies, large-sized lipofuscin aggregates showed only very weak or no cath B-immunoreactivity at all. Taken together, the present results suggest that cath D and cath B may be regulated differently and play their specific roles in the aging of the brain, especially, the change in location of cath D from the lysosomal system to the cytosol in the aged brain may play an important role in age-related cell death.     

Serotonin distribution in rat cerebral cortex; radioenzymatic assays with thin-layer chromatography

Serotonin was measured in six different cortical regions of the rat by a specific and sensitive radioenzymatic assay which includes thin-layer chromatography in the last separation step. The indoleamine was found to be unevenly distributed throughout the cortical regions examined; and the highest concentrations were determined for the prefrontal and the occipito-temporal cortex lateral to the hypothalamus. These results correlate with anatomical and electrophysiological studies which support a modulatory role for the serotonin afferent innervation of the cerebral cortex.     

短暂性全脑缺血后大鼠海马CPP32 mRNA表达水平的动态变化

目的　观察短暂性全脑缺血后大鼠海马CPP32mRNA表达水平的动态变化 ,探讨缺血诱发神经元凋亡的机制。方法　将健康雄性SD大鼠 5 5只 ,随机分为自然组、假手术 6、12、2 4、4 8、72小时组 ,全脑缺血再灌注 6、12、2 4、4 8、72小时组 ,每组 5只。应用颈动脉负压分流法制作大鼠短暂性全脑缺血模型 ;应用荧光定量RT PCR方法测定大鼠海马组织CPP32mRNA的表达。结果　与自然组相比 ,假手术各组CPP32mRNA无显著性增高 ,而短暂性全脑缺血 6小时后CPP32mRNA的表达已有增加趋势 ,缺血后 12小时增加了 5 3% ,缺血后 2 4小时增加了 2 2 3% ,并维持在较高水平 ,缺血后 72小时有下降的趋势。结论　短暂性全脑缺血可诱导海马组织CPP32mRNA的表达 ,缺血 6小时其表达开始并逐渐增强 ,2 4小时达高峰 ,72小时有下降的趋势 ;CPP32的转录增强是缺血诱导神经元凋亡的重要机制之一     

Effects of subacute lead exposure on [H]MK-801 binding in hippocampus and cerebral cortex in the adult rat

We used the NMDA receptor non-competitive antagonist, [³H]MK-801, as a ligand for an autoradiographic study to determine the effects of lead on NMDA receptor in the rat brain. Adult male rats were administered lead acetate, 100 mg/kg, or sodium acetate, 36 mg/kg (control), by i.p. for 7 days. High lead levels were detected in blood (41.1 μg/dl) and in brain (16.7–29.4 μg/g). Concentrations of lead in brain regions were not significantly different. The [³H]MK-801 binding was heterogeneously distributed throughout the rat brain with the following order of binding densities: hippocampal formation>cortex>caudate-putamen>thalamus>brainstem. Lead exposure produced a significant decrease in [³H]MK-801 binding to the NMDA receptor in the hippocampal formation including CA2 stratum radiatum, CA3 stratum radiatum, hilus dentate gyrus and presubiculum, and in the cerebral cortex including agranular insular, cingulate, entorhinal, orbital, parietal and perirhinal areas. The hippocampal formation is known as a critical neural structure for learning and memory processes, whereas, cortical and subcortical regions have been demonstrated to be involved in the modulation of complex behavioral processes. The NMDA receptor has been demonstrated to play a key role in synaptic plasticity underlying learning and memory. Lead-induced alterations of NMDA receptors in the hippocampal formation and cortical areas may play a role in lead-induced neurotoxicity.     

The pathogenesis of abnormal cytoarchitecture in the cerebral cortex and hippocampus of the mouse treated transplacentally with cytosine arabinoside

Summary Pregnant mice were treated with cytosine arabinoside on days 13.5 and 14.5 of pregnancy. Brains of the offspring were studied histologically. The matrix layer of the embryonic brains was extensively destroyed 12h after the injection of cytosine arabinoside, but regenerated partially on day 17 of gestation. In the cerebral cortex of 1-, 3-, and 5-day-old treated mice, abnormal clusters of young neurons were found on the surface of the developing cerebral cortex. Some clusters still had a supply of immature neurons from the remnants of the regenerated matrix layer. After 20 days, the clusters became gradually indistinct, although some vestigial groups of neurons were observed even after 120 days. In the hippocampus of young mice, the pyramidal cells decreased in number and were disarranged. Heterotopic pyramidal cell masses were found in the stratum radiatum and in the molecular layer of the dentate gyrus. Apical dendrites of pyramidal cells exhibited abnormal arborization. It was demonstrated by³H-thymidine autoradiography that young neurons in the abnormal clusters in the cerebral cortex were those produced in the matrix layer regenerated after the destructive change by cytosine arabinoside.Supported in part by grant no. 81-11-03 from NCNMMD of the Ministry of Education, Health, and Welfare, Japan     

Age-related changes in calbindin-D28k,calretinin, and parvalbumin-immunoreactive neurons in the human cerebral cortex

Calbindin-D(28k) (CB), calretinin (CRT), and parvalbumin (PV) are high-affinity cytosolic calcium (Ca(2+)) binding proteins (CBP) that have been found to regulate intracellular calcium concentrations in neurons through their buffering capacity and to protect neurons from insults that induce elevations of intracellular Ca(2+). In earlier studies we observed a substantial and neurochemically specific loss of CB from the human basal forebrain cholinergic neurons (BFCN) in the course of normal aging. In the present experiments we expanded our investigation of age-related changes in calcium binding proteins in the human brain by investigating the status of CB-, CRT-, and PV-positive neurons in 17 cortical areas. There was a trend toward a decrease in the number of CB-immunoreactive neurons in all areas studied. However, this trend reached significance in only 4 areas in which the loss of CB-positive neurons ranged between 20 and 46%. Immunoreactivity for CRT was also decreased in many areas and this difference reached significance in three regions (26-37%). Cortical neurons displaying PV immunoreactivity did not show an age-related change. Comparison with other neurochemically specific cortical neurons indicated a similar age-related loss of nonphosphorylated neurofilament and NADPH-d activity in only a few cortical areas. In contrast, neuronal acetylcholinesterase activity was increased in a few cortical areas. These observations indicate that loss of CBP-positive neurons occurs in restricted cortical regions and is not a specific change as other neurochemically specific neurons also display restricted age-related changes. Furthermore, the age-related changes in cortical CBP-positive neurons appear to be considerably smaller than similar changes in the BFCN. The age-related depletion of CBPs is likely to deprive neurons from the capacity to buffer intracellular calcium and thus to leave them vulnerable to pathological processes that can cause increased intracellular calcium and lead to their degeneration.     

Age-related changes in brain microanatomy: Sensitivity to treatment with the dihydropyridine calcium channel blocker darodipine (PY 108-068)

The influence of aging and of treatment with the dihydropyridine Ca²⁺ antagonist darodipine (PY 108-068) on the age-related microanatomical changes of rat brain were studied in male Wistar rats treated from the 18th to the 24th month of age with an oral dose of 5 mg/kg/day of darodipine. Twelve-month-old untreated rats were used as an adult reference group. A decreased number of nerve cells and of alkaline phosphatase-positive capillaries and an increased lipofuscin deposition were observed in the frontal and occipital cortex, in the hippocampus, and in the cerebellar cortex of rats of 24 months in comparison with 12-month-old animals. The number of nerve cells was higher in the occipital cortex and in the hippocampus, but not in the frontal cortex and in the cerebellar cortex, of darodipine-treated rats in comparison with age-matched untreated animals. Lipofuscin deposition is reduced in all the brain areas investigated. The density of alkaline phosphatase-reactive capillaries is also increased in the frontal and occipital cortex and in the hippocampus of aged rats treated with darodipine. The above results suggest that treatment with darodipine is able to counter some microanatomical changes occurring in the brain of aged rats and involving not only microvascular parameters. The occipital (visual) cortex and the hippocampus were the cerebral areas more sensitive to treatment with darodipine. The possible relevance of these findings is discussed.     

Age-related changes of VIP, NPY and somatostatin-immunoreactive neurons in the cerebral cortex of aged rats

Recent studies have explored certain changes with aging of neurons containing neuropeptides. The degree of loss of vasoactive intestinal polypeptide (VIP)-, neuropeptide Y (NPY)- and somatostatin-containing neurons in the aged CNS has not yet been established with certainty however, and available data is often contradictory. Changes with aging of VIP- and NPY-containing neurons were demonstrated by immunocytochemistry in this study. A major loss of VIP-immunoreactive (ir) neurons in aged rat brain was observed in the frontal cortex area 3, parietal cortex area 1, hindlimb area, temporal cortex area 1 and 2, monocular part of occipital cortex area 1, occipital cortex area 2, and retrosplenial cortex. VIP-ir cells in the frontal cortex areas 1 and 2, parietal cortex area 2, forelimb area, binocular part of the occipital cortex area 1, and the dentate gyrus were moderately decreased. The axis of VIP neurons in the aged group showed an irregular orientation tendency, especially in layers II and III. Major loss of NPY-ir neurons in aged rat brain were observed in the retrosplenial cortex, frontal cortex areas 1 and 2, parietal cortex areas 1 and 2, occipital cortex areas 1 and 2, the temporal cortex, hippocampus proper and cingulate cortex. Loss of NPY-ir neurons was observed mostly in layers V and VI. The number and length of dendritic branches also appeared to have decreased and shortened in the aged group. There were only slight decreases of somatostatin-ir cell numbers in the parietal and occipital cortex of the aged group. These results indicate the involvement of VIP and NPY-ir neurons in the aging process of cerebral cortex, and provide the morphological evidence for the decreased number of VIP and NPY neurons by immunocytochemistry in each area of cerebral cortex of aged rats. © 1997 Elsevier Science B.V. All rights reserved.     

c-fos protooncogene expression in rat hippocampus and entorhinal cortex following tetanic stimulation of the perforant path.

The elevated expression of the c-fos protooncogene has been proposed to be a marker of cell activation leading to a long term cellular response. In this communication we compared the c-fos mRNA accumulation in the hippocampus (i.e. postsynaptic cells) and entorhinal cortex (i.e. presynaptic cells) following high (tetanic) and low frequency electrical stimulation of the perforant path. Using Northern blot analysis we have found that high frequency stimulation elevates c-fos expression in both hippocampus and entorhinal cortex, and the increase of c-fos mRNA levels in the entorhinal cortex is less pronounced, but longer lasting, than in the hippocampus. Slight increase of c-fos mRNA levels has been also observed in low frequency treated animals in the entorhinal cortex, but not in the hippocampus. These findings raise the question about differences in mechanisms involved in c-fos activation in both parts of the brain after stimulation which evokes long term potentiation (LTP) of synaptic efficacy.     

丁苯酞对缺血大鼠大脑皮质中钙通道Cav1.3表达的影响

目的探讨丁苯酞对脑缺血大鼠大脑皮质中钙通道Cav1.3表达的影响及其脑保护作用的机制。方法雄性Wistar大鼠36只,随机分为假手术组、缺血对照组和丁苯酞治疗组,每组12只。采用免疫组织化学方法和蛋白质印迹法分别检测各组大鼠大脑皮质中钙通道Cav1.3表达的情况。采用TUNEL法观察大鼠大脑皮质内细胞凋亡的情况。结果与缺血对照组比较,丁苯酞治疗组大鼠大脑皮质中钙通道Cav1.3表达有所增加(P0.05),但仍低于假手术组(P0.05),大脑皮质中凋亡神经元数量丁苯酞治疗组明显少于缺血对照组但多于假手术组(P0.05)。结论丁苯酞可以抑制缺血造成的脑皮质中钙通道Cav1.3表达的减少,减少缺血后大脑皮质中的神经元凋亡。     

依达拉奉对局灶性脑缺血大鼠神经功能恢复及海马病理形态学改变的影响

目的 探讨大鼠局灶性脑缺血后神经功能恢复及海马病理形态学改变,评价依达拉奉的干预作用.方法 126只雄性SD大鼠随机分为3组:假手术组(A组,6只),生理盐水组(B组,MCAO后6h、12h、24h、48h、72h、5d、7d7时点,各6只),依达拉奉处理组(C组,同B组),术后即刻予以依达拉奉干预.行神经功能缺损评分测定;TTC染色观察脑梗死体积改变;用HE染色方法观察病理形态学改变.结果 术后进行神经缺损评分发现,由于麻醉和手术创伤的影响,假手术组术后出现6～24h神经功能减退.与假手术组相比,在6～24h时间段盐水组神经功能下降明显(P＜0.05).依达拉奉组神经功能明显好于盐水组(P＜0.05).术后7d盐水组和依达拉奉组神经功能基本恢复.同时,在依达拉奉组和盐水组中,缺血24h脑梗死体积最大;与盐水组相比,术后6～24h依达拉奉组脑梗死体积明显减小(P＜0.05).HE染色显示术后6h在脑缺血区神经元细胞无明显改变,6h后缺血区脑组织逐渐出现肿胀与坏死;在依达拉奉组,脑水肿和神经元坏死病理损害明显较轻,在假手术组,脑组织无明显改变.结论 依达拉奉具有改善神经功能缺损、缩小脑梗死体积和减轻缺血性病理损害程度的作用;研究还提示依达拉奉对缺血性脑卒中早期神经功能恢复具有十分重要的临床意义.     

Prefrontal cortex and hippocampus in posttraumatic functional recovery: spatial delayed alternation by rats subjected to transection of the fimbria-fornix and/or ablation of the prefrontal cortex

Lesions of the prefrontal cortex and the hippocampus often lead to impairment of the same behavioural tasks (e.g., allocentric as well as egocentric spatial orientation and spatial delayed alternation). In case of allocentric and egocentric spatial orientation we have previously found that the two structures mutually contribute to the posttraumatic functional recovery of such tasks. We therefore presently tested the hypothesis that this would even be true in case of spatial delayed alternation. The acquisition of a spatial delayed alternation task in a T-maze was studied in four groups of rats: animals in which the fimbria-fornix had been transected bilaterally, rats who had received bilateral ablations of the anteromedial prefrontal cortex, animals in which both of these structures had been lesioned, and a sham operated control group. All three lesion groups demonstrated an impaired task acquisition. The group given prefrontal cortical lesions in isolation underwent a complete functional recovery. Both of the fimbria-fornix transected groups were significantly impaired even when compared to the group given prefrontal cortical ablations in isolation. The two fimbria-fornix lesioned groups did, however, exhibit levels of functional recovery. The group in which both structures had been lesioned demonstrated a task acquisition, which was significantly inferior to that of the group given fimbria-fornix transections in isolation. After completion of the task acquisition period, all animals were subjected to two behavioural challenges including a session on which the duration of the inter-trial delay was doubled. This expansion of the inter-trial delay rather selectively impaired the task performance of the group given fimbria-fornix transections in isolation. Consequently, both during the acquisition period and in one of the challenges a differentiation of functional recovery was seen between the combined lesioned group and the group given fimbria-fornix lesions only. This indicates that even in case of a spatial delayed alternation task the prefrontal cortex normally contributes significantly to mediation of posttraumatic functional recovery after isolated lesions of the fimbria-fornix. The results are discussed in the context of models of posttraumatic functional recovery.     

Parvalbumin-immunoreactive neurons in the cerebral cortex of the lizardPodarcis hispanica

An antibody against the calcium binding protein parvalbumin selectively labels a set of neurons in the cerebral cortex of lizards. Golgi-like immunostained bipolar, multipolar and pyramid-like neurons appear mainly located in the inner plexiform layers. Parvalbumin-immunoreactive (PARV-IR) puncta are concentrated in the cell layer of the dorsal and dorsomedial cortices showing a basket-like distribution. The morphology and distribution of PARV-IR neurons and puncta overlap GABA-immunostaining in the cerebral cortex of lizards. Thus, it is likely that PARV-IR neurons are a subset of the cortical GABAergic neurons of lizards.