Biochemical evidence indicates that GABA and histamine may both be synthesized by barnacle photoreceptors (Koike & Tsuda, 1980; Timpe & Stuart, 1984; Callaway & Stuart, 1989b). We used antisera against GABA- and histamine-protein conjugates to determine whether the photoreceptors contain either or both of these antigens. Both antisera labeled all of the photoreceptors in each of the three ocelli. Histamine-like immunoreactivity was found throughout each photoreceptor cell but was most intense at their presynaptic terminals. Histamine-like immunoreactivity was blocked by preincubation of the antibody either with histamine or with a histamine-protein conjugate. GABA-like immunoreactivity was found in all parts of the photoreceptors including the cell body, axon, rhabdomeric dendrites, and presynaptic terminals. GABA-protein conjugates blocked the GABA-like labeling of the photoreceptors, while protein conjugates with histamine, L-glutamate, L-glutamine, β-alanine, and taurine did not. Histamine-like immunoreactivity in the supraesophageal ganglion was confined to the photoreceptor terminals and a second, loose plexus of endings in the main neuropil. GABA-like immunoreactivity, in contrast, was found in approximately twenty-five pairs of neurons of this ganglion. In the cirral nerves, which are expected to contain inhibitory motoneurons, unidentified axons also labeled with the GABA antiserum.

We tested the hypothesis that gamma-aminobutyric acid (GABA) is the transmitter released by barnacle photoreceptors onto postsynaptic cells (I-cells). GABA was applied to I-cells either by superfusion or by ejecting it with pressure from a pipette positioned close to the I-cell's soma. The I-cell's response to GABA was compared with its response to light (i.e. to the photoreceptors' transmitter) by recording intracellularly from its soma. Bath-applied (100 µm to 10 mM) and pressure-applied GABA (10 mM in pipette) hyperpolarizes I-cells by increasing their conductance, as does the photoreceptors' transmitter. The response to pressure-applied GABA consists of two components; both persist when Co2+ or Cd2+ are added to the saline to block synaptic transmission in the preparation, indicating that GABA affects the I-cell directly rather than affecting a presynaptic cell. GABA hyperpolarizes the I-cell when applied to the cell over the soma and ipsilateral arbor or over the contralateral arbor. The I-cells' responses to GABA and to light both depend on extracellular K+ and are affected by changes in intracellular and extracellular Cl−. However, picrotoxin and β-guanidinopropionic acid block the response to pressure-applied GABA but do not block the response to light even at an order of magnitude higher concentration. Thus, GABA is not likely to be the transmitter that causes the hyperpolarizing response of the I-cell. It may be a neuromodulator or the transmitter of an unknown input to the I-cell.

We tested the hypothesis that histamine is the transmitter released by barnacle photoreceptors. Median and lateral ocelli were incubated with 3H-histidine and found to synthesize 3H-histamine, identified by high-voltage electrophoresis. Synthesis could be blocked by the histidine decarboxylase inhibitor (S)-α-fluoromethylhistidine. Histamine was applied to 1-cells either by superfusion or by pressure ejection from a pipette (100 µM or 1 mM histamine) positioned close to the I-cell's soma. When bath-applied at concentrations ranging from 5–100 µM, histamine hyperpolarized the I-cell in a dose-dependent fashion and increased its conductance. At 100 µM, histamine abolished the I-cell's response to light. The response to a pulse of pressure-applied histamine was a hyperpolarization whose amplitude was graded with dose (determined by the duration of the pulse). This response persisted in concentrations of Co2+ and Cd2+ that blocked synaptic transmission from the photoreceptors. Cimetidine, an antagonist of mammalian H2 receptors, markedly decreased the cell's responses both to HA and to light at 100 µM and blocked both responses at 1 mM. Pyrilamine and triprolidine, H1 antagonists, had a complex effect on the I-cell's responses to histamine and to light. Neither H1 nor H2 antagonists, nor histamine itself, affected the voltage or light responses recorded in the presynaptic terminal region, or any phase of calcium-dependent action potentials induced in the terminal in the presence of tetraethylammonium ion. Thus, biochemical, immunocytochemical, and physiological evidence suggests that HA is the transmitter from these photoreceptors to the I-cells. Although gammaaminobutyric acid (GABA) is also present in the photoreceptors, it did not affect the I-cell's responses to light or to histamine when bath-applied at 100 µM. Thus, GABA does not appear to modulate transmission from the photoreceptor to the I-cell.

Partial lesions of striate cortex were made in newborn and adolescent or young adult macaque monkeys, one newborn squirrel monkey, and adult squirrel and owl monkeys. After survival times ranging from 3 1/2 weeks to 8 years, the retinas were examined for transneuronal retrograde ganglion cell loss and retinal projections to the dorsal lateral geniculate nucleus, and other targets were examined for changes. After lesions in infant macaque monkeys and long postoperative survivals, nearly 80% of the ganglion cells were lost in the altered portions of the retinas. The degeneration appeared to be exclusively of ganglion cells projecting to the parvocellular layers of the lateral geniculate nucleus, and the loss of this class of cell appeared to be complete or nearly complete for the affected portions of the retina. Cases with shorter survivals showed that nine-tenths of the potential loss occurred within 6 months, and about half of the potential loss took place within one month. In cases where lesions were placed in adolescent and young adult macaque monkeys, the loss also was of ganglion cells projecting to the parvocellular layers. However, the rate of cell loss was slower so that little or no cell loss was apparent after six months, and only one-third to three-fourths of the potential loss occurred within 12–14 months. A cell loss of 22% was measured in the altered portions of the retina of a squirrel monkey lesioned as an infant and surviving for 6 months, but no regions of ganglion cell loss were apparent in the retinas of owl and squirrel monkeys lesioned as adults and surviving as long as two or more years.

We conclude that nearly 80% of the ganglion cells project to the parvocellular layers in macaque monkeys, and that the ultimate survival of these ganglion cells depends on the presence of target neurons in the parvocellular layers. Age is important in that the loss of ganglion cells proceeds rapidly in infant macaque monkeys, but slowly in older animals. Infant New World monkeys, judging from one squirrel monkey, are also susceptible to ganglion cell loss, although apparently at a rate comparable to older macaque monkeys. Finally, adult New World monkeys do not appear to be susceptible to ganglion cell loss. These age and species differences in rates of loss and susceptibility to loss challenge a “sustaining collateral” hypothesis proposed earlier (Weller et al., 1979), and suggest alternatives and modifications.

The number of subregions in the activity profiles of simple cells varies in different cells from 2–8; that is, the number of cycles in the weighting function varies from 1–4. The distribution of receptive-field (RF) sizes at eccentricities of 0-6 deg are clustered at half-octave intervals and form a discrete distribution with maxima at 0.62, 0.9, 1.24, 1.8, 2.48, and 3.4 deg. The spatial frequencies to which the cells are tuned are also clustered at half-octave intervals, forming a discrete distribution peaking at 0.45, 0.69, 0.9, 1.35, 1.88, 2.7, 3.8, and 5.6 cycles/deg. If we divide the RF sizes by the size of the period of the subregions, then the average indices of complexity (really existing) or the number of cycles in the weighting function form (after normalization) the sequences: 1, 1.41, 2.0, 2.9, 4.15.

The relation between the bandwidth of the spatial-frequency characteristic and the optimal spatial frequency is in accordance with predictions of the Fourier hypothesis. The absolute bandwidth does not change with the number of cycles/module. This means that inside the module the absolute bandwidth does not change with the number of the harmonic. The results allow us to suggest the following. A module of the striate cortex, which is a group of cells with RFs of equal size projected onto the same area of central visual field, accounts for the Fourier description of the image. The basis functions of the module are composed of four harmonics only, irrespective of size and position of the module.

Besides linear cells (sinusoidal and cosinusoidal elements), the module contains nonlinear cells, performing a nonlinear summation of the responses of sinusoidal and cosinusoidal elements. Such cells are characterized by an index of complexity which is more than the number of cycles in the weighting function and by marked overlap of ON and OFF zones. The analysis of organization suggests that the cells can measure the amplitude and phase of the stimulus.

We examined the role of the lateral suprasylvian (LS) cortex in motion perception by testing the ability of three cats to detect moving targets and to discriminate differences in stimulus direction and speed before and after making bilateral ibotenic acid lesions in LS. The lesions had little or no effect on contrast sensitivity for detecting moving sinusoidal gratings. Moreover, we found no deficits in discriminating opposite directions of motion: the cats discriminated grating directions at threshold contrasts. All three cats, however, showed permanent deficits in discriminating differences in speed and in flicker rate. The deficits were most pronounced at higher temporal and spatial frequencies and at lower contrasts. This result suggests that LS plays an important role in the analysis of stimulus speed. It appears that information needed for discriminating opposite directions of motion may be signalled by visual areas outside LS.

The trajectory of retinal projections and the location of retinorecipient nuclei in the quail brain was examined after application of horseradish peroxidase (HRP) either to the cut end of the optic nerve or following intraocular injection of HRP. Retinal projections to the hypothalamus, dorsalateral anterior thalamus (rostralateral part, magnocellular part, and lateral part), lateral anterior thalamus, lateroventral geniculate nucleus, lateral geniculate intercalated nuclei (rostral and caudal parts), ventrolateral thalamus, superficial synencephalic nucleus, external nucleus, tectal gray, diffuse pretectal area, pretectal optic area, ectomammillary nucleus, and optic tectum were revealed. Retinal projections observed in quail were compared with results obtained in other avian species and considered in relation to possible anatomic pathways underlying photoperiodism and circadian rhythms.