Although the neural location of the plaid motion coherence process is not precisely known, the middle temporal (MT) cortical area has been proposed as a likely candidate. This claim rests largely on the neurophysiological findings showing that in response to plaid stimuli, a subgroup of cells in area MT responds to the pattern direction, whereas cells in area V1 respond only to the directions of the component gratings. In Experiment 1, we report that the coherent motion of a plaid pattern can be completely abolished following adaptation to a grating which moves in the plaid direction and has the same spatial period as the plaid features (the so-called “blobs”). Interestingly, we find this phenomenon is monocular: monocular adaptation destroys plaid coherence in the exposed eye but leaves it unaffected in the other eye. Experiment 2 demonstrates that adaptation to a purely binocular (dichoptic) grating does not affect perceived plaid coherence. These data suggest several conclusions: (1) that the mechanism determining plaid coherence responds to the motion of plaid features, (2) that the coherence mechanism is monocular, and thus (3), that it is probably located at a relatively low level in the visual system and peripherally to the binocular mechanisms commonly presumed to underlie two-dimensional (2-D) motion perception. Experiment 3 examines the spatial tuning of the monocular coherence mechanism and our results suggest it is broadly tuned with a preference for lower spatial frequencies. In Experiment 4, we examine whether perceived plaid direction is determined by the motion of the grating components or the features. Our data strongly support a feature-based model.

In the turtle retina the peptides met-enkephalin (metENK), somatostatin (SS), neurotensin (NT), and the indoleamine serotonin (5-HT) modulate ganglion cell (GC) activity. The predominant action of the peptides is excitatory, generally enhancing spontaneous firing and light-evoked activity. In contrast, 5-HT usually inhibits these GC activities. MetENK has both direct synaptic input onto GC and indirect action possibly via a GABA inhibitory interneuron. The metENK actions appear mediated via a mu-opiate receptor; morphine and D-ala-metENK-amide (DALA), a stable analog of metENK, are agonists. Naloxone antagonizes the actions of metENK and its agonists. DALA occasionally inhibits GC. This inhibition is antagonized by picrotoxin, while concurrent excitatory action on GC is enhanced. DALA enhances GC response at high spatial frequencies; naloxone attenuates it. The enhancement by DALA suggests a narrowed receptive-field (RF) center, possibly due to changes in a GABA-mediated inhibitory surround. 5-HT inhibitory actions are also mediated via direct and indirect synaptic pathways. 5-methoxy-dimethyl-tryptamine and methoxy-phenyl-piperazine are agonists of 5-HT action. They are both specific 5-HT1 agonists. LSD (lysergic acid diethylamide) and cyproheptadine, which act on 5-HT2 receptors, antagonize 5-HT actions in this retina. Strychnine enhances GC activity, probably by antagonizing glycine-mediated inhibitory inputs. It does not block the inhibitory action of 5-HT, which suggests that the indirect 5-HT inhibition is not mediated via a glycinergic interneurone. 5-HT suppresses directional selectivity (DS) and attenuates high spatial frequencies in some GC. This may be mediated via inhibition of GABAergic amacrines subserving DS and the RF inhibitory surround.