The electrophysiological effects of N-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine(NMPTP), a chemical inducer of Parkinsonism in man and monkey, on the pigmented rabbit retina were determined under acute condition. The amplitude of the b-wave of the rabbit electroretinogram was affected, but both the implicit time and half-amplitude duration of it were not. The amplitude of the photopic b-wave was increased by 72.9 +/- 32.1% 5 hours after NMPTP administration(P[t]<0.05), Whereas the scotopic b-wave was decreased by 31.2 +/- 6.4% 4 hours after injection(P[t]<0.05). The above results suggest or support that: (1) the dopaminergic amacrine cells are related to the modulation of the b-wave of the rabbit electroretinogram. (2) during light adaptation, the dopaminergic amacrine cells uncouple the rod and cone systems in the inner plexiform layer and are involved in functions of the rod system. (3) the hypothesis that the function of tyrosine hydroxylase may be affected by NMPTP.
Adaptation, Ocular ; Amacrine Cells ; Haplorhini ; Parkinsonian Disorders ; Rabbits* ; Retina ; Tyrosine 3-Monooxygenase

Vasoactive intestinal polypeptide (VIP) is a neuroactive substance that is widely expressed in both non-mammalian and mammalian retinas. In this study, we immunocytochemically identified and investigated the VIP-containing neurons in the mouse retina, which has become an important model for the study of the structure and function of the mammalian retina, mainly because of the wide availability of transgenic animals. VIP immunoreactivity was observed in the somata of the amacrine cells in the inner nuclear layer (INL) and their varicose processes ramifying in strata 1 and 3 of the inner plexifrom layer (IPL). The distribution of VIP-immunoreactive (IR) amacrine cells showed a peak of 430 cells/mm2 in the central retina and minimum values of 50 cells/mm2 in the peripheral one. Double-label experiments demonstrated that all VIP-IR amacrine cells possessed GABA immunoreactivity. These results demonstrate that VIP-IR amacrine cells of the mouse retina make up a neurochemically and morphologically distinct subpopulation of the GABAergic amacrine cell population.
Amacrine Cells* ; Animals ; Animals, Genetically Modified ; gamma-Aminobutyric Acid ; Immunohistochemistry ; Mice* ; Neurons ; Retina* ; Vasoactive Intestinal Peptide*

We examined the morphological maturation of amacrine cells expressing neurokinin 1 (NK1) receptor, whose ligand is substance P, in the rat retina, focusing on the period from postnatal day 5 (P5) when the outer plexiform layer is formed, to postnatal day 13 (P13) when the eyes open, with immunohistochemistry using a specific antiserum against NK1 receptor, and we compared maturing NK1 receptor-immunoreactive (NK1 receptor-IR) amacrine cells with adult one. In the adult retina, numerous NK1 receptor-IR amacrine cells were located in the inner part of the inner nuclear layer (INL) adjacent to the inner plexiform layer (IPL), and their processes emerging from the somata branched and stratified at 1, 2, and 5 strata of within the IPL. NK1 receptor-IR amacrine cells were already observed at P5. The cell bodies were located in the inner INL away from the IPL and their processes branched and formed two distinct bands in the IPL. Afterwards, somata of NK1 receptor-IR amacrine cells moved toward the inner part of the INL, and thus, were located in the INL adjacent to the IPL. Their processes formed three distinct bands at P10 and then, at P13, three bands occupied the same strata as those of the adult, which were posed at 1, 2, and 5 strata of the IPL. During the postnatal development, most of NK1 receptor-IR amacrine cells directly extended one or a few primary dendrites toward the IPL and formed the strata. However, some of the labeled cells located at the outermost row had horizontal processes emerging from their primary dendrites, and these horizontal processes branched and formed plexuses in the INL. The NK1 receptor-IR amacrine cells with horizontal processes were frequently observed at P7, rarely at P10, and not at P13 and in the adult. These results indicate that the NK1 receptor-IR amacrine cells of the rat retina morphologically mature by way of migration of their somata within the INL and formation of distinct processes during postnatal development, and suggest that they morphologically and functionally complete the maturation process about the time of P13.
Adult ; Amacrine Cells* ; Animals ; Dendrites ; Humans ; Immunohistochemistry ; Rats* ; Retina* ; Substance P

The retina is a highly specialised part of the brain responsible for visual processing. It is well-laminated; three layers containing five different types of neurons are compartmentalised by two synaptic layers. Among the retinal layers, the inner nuclear layer (INL) is composed of horizontal, bipolar, and amacrine cell types. Bipolar cells form one sublayer in the distal half of the IPL, while amacrine cells form another sublayer in the proximal half, without any border-like structure. Here, we report that a plexiform layer-like structure exists temporarily in the border between the bipolar and amacrine sublayers in the INL in the rat retina during retinal development. This transient intermediate plexiform layer (TIPL) appeared at postnatal day (PD) 7 and then disappeared around PD 12. Most apoptotic cells in the INL were found near the TIPL. These results suggest that the TIPL may contribute to the formation of sublayers and the cell number limit in the INL.
Amacrine Cells ; Animals ; Apoptosis ; Brain ; Cell Count ; Neurons ; Rats ; Retina ; Retinaldehyde

The cellular localization of the GABA transporter-3 (GAT-3) was examined in the guinea pig retina by immunocytochemistry, using antisera against GAT-3. GAT-3 immunoreactivity was localized to cell bodies in the inner nuclear layer, and labeled processes were densely distributed in the inner plexiform layer (IPL) close to the ganglion cell layer. All GAT-3 labeled cells exhibited GAD65 immunoreactivity. In addition, 67% of GAT-3 labeled amacrine cells showed carbohydrate epitope CD15 immunoreactivity. These results indicate that GAT-3 is involved in modulating the rod pathway in the IPL of the guinea pig retina via presumptive A17 amacrine cells.
Amacrine Cells ; Animals ; gamma-Aminobutyric Acid* ; Ganglion Cysts ; Guinea Pigs* ; Guinea* ; Immune Sera ; Immunohistochemistry ; Retina*

Dopaminergic amacrine cells (DACs) are among the most well-characterized neurons in the mammalian retina, and their connections to AII amacrine cells have been described in detail. However, the stratification of DAC dendrites differs based on their location in the inner plexiform layer (IPL), raising the question of whether all AII lobules are modulated by dopamine release from DACs. The present study aimed to clarify the relationship between DACs and AII amacrine cells, and to further elucidate the role of dopamine at synapses with AII amacrine cell. In the rabbit retina, DAC dendrites were observed in strata 1, 3, and 5 of the IPL. In stratum 1, most DAC dendritic varicosities—the presumed sites of neurotransmitter release—made contact with the somata and lobular appendages of AII amacrine cells. However, most lobular appendages of AII amacrine cells localized within stratum 2 of the IPL exhibited little contact with DAC varicosities. In addition, double- or triple-labeling experiments revealed that DACs did not express the GABAergic neuronal markers anti-GABA, vesicular GABA transporter, or glutamic acid decarboxylase. These findings suggest that the lobular appendages of AII amacrine cells are involved in at least two different circuits. We speculate that the circuit associated with stratum 1 of the IPL is modulated by DACs, while that associated with stratum 2 is modulated by unknown amacrine cells expressing a different neuroactive substance. Our findings further indicate that DACs in the rabbit retina do not use GABA as a neurotransmitter, in contrast to those in other mammals.
Amacrine Cells* ; Dendrites ; Dopamine ; GABAergic Neurons ; gamma-Aminobutyric Acid ; Glutamate Decarboxylase ; Immunohistochemistry* ; Mammals ; Neurons ; Neurotransmitter Agents ; Retina* ; Synapses

The role of acetylcholine as an excitatory neurotransmitter is well established, and cholinergic neurons appear to play an important role in the mammalian retinae. Though it has been reported that certain conventional and displaced amacrine cells are consistently labeled with anti-choline acetyltransferase antiserum in the mammalian retinae, little has been studied on the synaptic circuitry of cholinergic neurons to clarify mechanism of its action in the visual processing of the mammalian retinae. This study was conducted to localize cholinergic neurons and to define their synaptic circuitry in the rat retina by immunocytochemical method using anti-choline acetyltransferase antiserum. The results were as follows: 1. Cholinergic neurons of the rat retina were conventional amacrine cells located in the inner nuclear layer and displaced amacrine cells in the ganglion cell layer. 2. Cholinergic amacrine cells were branched in the middle of the sublamina a of the inner plexiform layer, and cholinergic displaced amacrine cells branched in the sublamina b, forming one prominent band, respectively. 3. Presynaptic processes to cholinergic amacrine cell processes were axon terminals of invaginating and flat cone bipolar cells, and unlabelled amacrine cell processes in the inner plexiform layer. Postsynaptic dyads at the ribbon synapses of axon terminals of cone bipolar cells were cholinergic amacrine cell process and dendrite of ganglion cell, cholinergic amacrine cell process and unlabelled amacrine cell process and cholinergic amacrine cell process and cholinergic amacrine cell process. In addition, cholinergic amacrine cell process formed postsynaptic monoad at the ribbon synapse. 4. Cholinergic amacrine cell processes made output conventional chemical synapses onto the dendrites of ganglion cells, unlabelled amacrine cell processes and cholinergic amacrine cell processes in the inner plexiform layer. These results demonstrate that (1) cholinergic neurons are conventional amacrine cells and displaced amacrine cells of which somata are located in the inner nuclear layer and ganglion cell layer, respectively, (2) cholinergic conventional amacrine cells are involved in OFF pathway, and cholinergic displaced amacrine cells play an important role in ON pathway in visual processing of lightness, and (3) acetylcholine released from cholinergic neurons by light excites directly ON and OFF ganglion cells or indirectly ON and OFF ganglion cells via non-cholinergic amacrine cells.
Acetylcholine ; Amacrine Cells ; Animals ; Choline O-Acetyltransferase ; Cholinergic Neurons* ; Dendrites ; Ganglion Cysts ; Neurotransmitter Agents ; Presynaptic Terminals ; Rats* ; Retina* ; Synapses

In the retina, dopaminergic cells express the receptor for brain-derived neurotrophic factor (BDNF), which is known to be retrogradely transported from higher center to the retina. This study was conducted to identify the effect of optic nerve transaction on the dopaminergic cells in the rat retina by immunocytochemistry using antityrosine hydroxylase (TH) antiserum. In the control retina, we found two types of TH-immunoreactive amacrine cells, type I and type II, in the inner nuclear layer (INL) adjacent to the inner plexiform layer (IPL). The type I amacrine cell varicosities formed ring-like structures in contact with AII amacrine cell somata in stratum 1 of the IPL. In the axotomized retinas, TH-labeled processes formed loose networks of fibers, unlike the dense networks in the control retina, and the ring-like structures were disrupted. Our data suggest that retrogradely transported neurotrophic factor affects the expression of TH immunoreactivity in the axotomized rat retina and may therefore influence the retinal dopaminergic system.
Amacrine Cells ; Animals ; Axotomy* ; Brain-Derived Neurotrophic Factor ; Immunohistochemistry ; Optic Nerve ; Rats* ; Retina* ; Retinaldehyde ; Tyrosine 3-Monooxygenase

An excitatory neurotransmitter glutamate is engaged in slow transmission by activating the secondary signal transduction pathway through metabotropic receptors of the target cells. The present study has been investigated the localization of group I (mGluR1 and mGluR5) and II (mGluR2/3) metabotropic glutamate receptors in the retina and their altered expression patterns following long-term diabetes using immunohistochemistry, in order to clarify the involvement of the slow transmission of glutamate in diabetic retinopathy. Insulin-dependent diabetes was induced by a single intravenous injection of streptozotocin. Experimental periods were set at 1, 4, 12 and 24 weeks after the onset of diabetes. MGluR1 and mGluR5 were expressed in the outer plexiform layer, 1, 3, and 5 strata of the inner plexiform layer, and the photoreceptor layer in the retina at normal state. In the early periods of diabetes, the expression pattern of group I receptors was no large change. The expression level in the photoreceptor layer of 12 and 24 weeks diabetic retinas was increased, while that in the IPL was decreased. MGluR2/3 was expressed in the amacrine cells, in the displaced amacrine cells, and in two bands in the inner plexiform layer at normal retina. In later diabetic periods, the expression level of mGluR2/3 was increased in the two bands especially. These results demonstrate that diabetes induces the activation of I and II mGluRs in the retina, and may suggest the involvement of slow transmission of glutamate via metabotropic receptors in progression of diabetic retinopathy.
Amacrine Cells ; Animals ; Diabetic Retinopathy ; Glutamic Acid ; Immunohistochemistry ; Injections, Intravenous ; Neurotransmitter Agents ; Rats* ; Receptors, Metabotropic Glutamate* ; Retina* ; Signal Transduction ; Streptozocin

The role of glycine as an inhibitory neurotransmitter is well established, and glycinergic neurons appear to play an important role in the mammalian retinae[Ikeda & Sheardown, 1983 ; Bolz et al., 1985]. Though it has been reported that certain conventional and displaced amacrine cells and a few of bipolar cells are consistently labeled with anti-glycine antiserum in the mammalian retinae so far[W ssle et al., 1986 ; Pourcho & Goebel, 1987 ; Davanger et al., 1991 ; Yoo & Chung, 1992], little has been studied on the synaptic circuitry of glycinergic neurons to clarify mechanism of its action in the visual processing of the mammalian retinae. This study was conducted to localize glycinergic neurons and to define their synaptic circuitry in the rat retina by immunocytochemical method using anti -glycine antiserum. The results were as follows : 1. Glycinergic neurons of the rat retina were conventional and displaced amacrine cells, interstitial cells and bipolar cells. 2. Glycinergic amacrine cells could be subdivided into two types, that is, A II amacrine cells and other amacrine cells, according to their ultrastructures. Glycinergic A II amacrine and other amacrine cell processes comprised postsynaptic dyad at the ribbon synapse of rod bipolar axon terminals in the sublamina b of the inner plexiform layer of the retina. Glycinprgic A II amacrine cell processes made gap junctions with axon terminals of unlabeled invaginating cone bipolar cells in the sublamina b, and made chemical synapses onto axon terminals of unlabeled flat cone bipolar cells and onto dendrites of ganglion cells in the sublamina a of the inner plexiform layer. In the sublamina b of the inner plexiform layer, g1ycinergic amacrine cell processes were postsynaptic to axon terminals of unlabeled invaginating cone bipolar cells, and made chemical output synapses onto axon terminals of unlabeled invaginating cone bipolar and rod bipolar cells and onto the dendrites of ganglion cells. Such cases that pre- and post-synaptic processes of glycinergic amacrine cell processes were non- glycinergic amacrine cell processes were frequently observed throughout the inner plexiform layer. In some cases, glycinergic amacrine cell processes receiving synaptic inputs from other glycinergic amacrine cell process made synaptic outputs onto the non-glycinergic or glycinergic amacrine cell processes. 3. Glycinergic bipolar cells could be subdivided into invaginating and flat cone bipolar cells. Postsynaptic dyads of cone bipolar cells at the ribbon synapses were non-glycinergic amacrine and amacrine cell processes, glycinergic amacrine and amacrine cell processes, glycinergic amacrine and non-glycinergic amacrine cell processes, and dendrite and dendrite of ganglion cells. These results demonstrate that [1] glycinergic A II amacrine cell receiving synaptic input from rod bipolar cells inhibit flat cone bipolar cells and OFF ganglion cells via chemical synapse, and excite ON cone bipolar cells via electrical synapse ; thereby visual information in the darkness can be transmitted to ON ganglion cells via ON cone bipolar cells, and [2] glycine released from glycinergic neurons inhibits directly ON and OFF ganglion cells or indirectly ON and OFF ganglion cells via non-glycinergic amacrine or bipolar cells.
Amacrine Cells ; Animals ; Darkness ; Dendrites ; Electrical Synapses ; Ganglion Cysts ; Gap Junctions ; Glycine ; Neurons* ; Neurotransmitter Agents ; Presynaptic Terminals ; Rats* ; Retina* ; Synapses