The release of gamma‐aminobutyric acid from horizontal cells of the goldfish (Carassius auratus) retina.

Abstract

Isolated horizontal cells from goldfish retinas were prepared by enzymatic dissociation using papain and separated from other cells by velocity sedimentation. In the intact retina, H1 horizontal cells possess a high‐affinity mechanism for accumulating gamma‐aminobutyric acid (GABA). This property is retained in isolated cells, which also release the accumulated GABA in response to depolarization by elevated external K+. L‐Glutamic acid and its analogues are highly effective at micromolar concentrations in eliciting the release of preloaded GABA from isolated cells. At saturating concentrations, L‐aspartic acid stimulates about one‐third as much release as L‐glutamic acid. In contrast, the D‐isomers of glutamate and aspartate are ineffective. In the intact retina, micromolar concentrations of L‐glutamic acid analogues are also capable of eliciting GABA release from H1 horizontal cells. Release of the accumulated GABA from isolated H1 cells is largely independent of external Ca2+ concentrations. In the intact retina, H1 horizontal cells also possess a K+‐stimulated GABA release mechanism that is independent of the Ca2+ concentrations in the medium. In addition, there appears to be a small but significant amount of [3H]GABA release that may be Ca2+ dependent. Under our conditions, [3H]GABA release from isolated cells is unaffected by external Na+ concentrations between 20 and 120 mM. However, concentrations of 10 mM or less significantly diminishes this release, with 70% curtailed in Na+‐free solutions. Our results, together with morphological observations by a number of other investigators, suggest that there may be two distinct mechanisms for GABA release from goldfish H1 horizontal cells: one being a conventional vesicular mechanism which is Ca2+ dependent, while the other is Na+ driven and Ca2+ independent. H1 horizontal cells in the intact goldfish retina release the accumulated GABA in response to brief incubations in darkness, which is known to be the natural stimulus that depolarizes these neurones.

Color opponency in cone-driven horizontal cells in carp retina. Aspecific pathways between cones and horizontal cells.

“…Since Ayoub and Lam (1984) found that/-glutamate yields a [SH]GABA release that is logarithmically related to the external Na + concentration, and since GABA is released in a carrier-mediated manner (Yazulla and Kleinschmidt, 1983), we used the following expression for the GABA release by the qHC:…”

“…A possible explanation for this controversy could be that another inhibitory transmitter is involved in the feedback from BHCs and THCs to cones. On the other hand, the absence of evidence for GABA in the BHCs and THCs might be due to a GABA concentration too low to be demonstrated in these cells.To find an expression for the feedback strength we have assumed that the membrane potential of the qHC, on which the GABA release depends, is controlled by a first-order low pass filter:where V e° is the driving force for the release of [GABA] from the qHC and @ is the time constant of the release and diffusion of GABA to the synaptic terminal of the photoreceptors.Since Ayoub and Lam (1984) found that/-glutamate yields a [SH]GABA release that is logarithmically related to the external Na + concentration, and since GABA is released in a carrier-mediated manner (Yazulla and Kleinschmidt, 1983), we used the following expression for the GABA release by the qHC:where [GABA] qHc is the GABA concentration, [GABA] i is the intracellular GABA concentration, and F, R, and T have their usual meanings. Finally, the GABA concentration near the nth cone, [GABA]", is determined by the total GABA release from the three types of HCs:…”

Cellular Neurophysiology of the Rat Suprachiasmatic Nucleus: Electrical Properties, Neurotransmission, and Mechanisms of Synchronization

“…in vitro studies (3)(4)(5)(6)(7). The correlation between the two hourly Whole-Cell Patch-Clamp Recordings.…”

“…In the which contains the mammalian biological clock (1, 2), exhibCa 2 +-free medium, MgCI 2 was substituted for CaCd 2 , and 0.1 its a circadian rhythm where peak activity occurs at the mM 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic middle of the light phase, even in a surgically isolated acid, a specific Ca 2 + chelator, was added. Blockade of hypothalamus (3) or in vitro brain slice (4)(5)(6)(7). Because these N-methyl-D-aspartic acid (NMDA), non-NMDA, and yamidata are derived from neuronal populations, they also imply nobutyric acid type A (GABAA) receptors was achieved by that the electrical activity generating the pacemaker is synbath application of 100 /AM DL-2-amino-5-phosphonopenchronized.…”

“…address two main issues: (i) How do SCN cells receive As at least some of the retinal input to SCN may and coordinate their temporal information within the be provided by axon collaterals projecting to other SCN? and (ii) How do SCN cells impose their visual regions," 6 the identity of the transmitter in circadian message on other neurons in the CNS? these other regions serves to elucidate further the The bilateral SCN is composed of about 20,000 identity of the retino-SCN transmitter.…”