To test our present quantitative knowledge of nicotinic transmission, we reconstruct the postsynaptic conductance change that results after a presynaptic nerve terminal liberates a quantum of acetylcholine (ACh) into the synaptic cleft. The theory assumes that ACh appears suddenly in the cleft and that is subsequent fate is determined by radial diffusion, by enzymatic hydrolysis, and by binding to receptors. Each receptor has one channel and two ACh binding sites; the channel opens when both sites are occupied and the rate-limiting step id the binding and dissociation of the second ACh molecule. The calculations reproduce the experimentally measured growth phase (200 microseconds), peak number of open channels (2,000), and exponential decay phase. The time constant of the decay phase exceeds the channel duration by approximately equal to 20%. The normal event is highly localized: at the peak, two-thirds of the open channels are within an area of 0.15 micrometer 2. This represents 75% of the available channels within this area. The model also simulates voltage and temperature dependence and effects of inactivating esterase and receptors. The calculations show that in the absence of esterase, transmitter is buffered by binding to receptors and the postsynaptic response can be potentiated.

The visual capacity of the common barn owl (Tyto alba) was studied by quantitative analysis of the retina and optic nerve. Cell counts in the ganglion cell layer of the whole-mounted retina revealed a temporal area centralis with peak cell density of 12,500 cells/mm² and a horizontal streak of high cell density extending from the area centralis into the nasal retina. Integration of the ganglion cell density map gave an estimated total of 1.4 million cells for the ganglion cell layer. Electron microscopy of a single, complete section of the optic nerve revealed a bimodal fiber diameter spectrum (modes at 0.3 and 0.9 µm; bin width = 0.2 µm), with diameters ranging from 0.15 µm (unmyelinated) to 6.05 µm (myelinated, sheath included). The total axon count for the optic nerve was estimated from sample counts to be about 680,000 axons (25% unmyelinated). Therefore, roughly half of the cells in the retinal ganglion cell layer do not send axons into the optic nerve. With certain assumptions the data predict a visual spatial acuity for barn owls on the order of 8 cycles/degree, a value similar to the known behaviorally measured acuities of masked owls (10 cycles/degree) and domestic cats (6 cycles/ degree).

Long-term potentiation of hippocampal excitatory synapses is often accompanied by an increase in the probability of spiking to an EPSP of fixed strength (E-S potentiation). We used computer simulations of a CA1 pyramidal neuron to test the plausibility of the hypothesis that E-S potentiation is caused by changes in dendritic excitability. These changes were simulated by adding "hot spots" of noninactivating voltage-sensitive Ca2+ conductance to various dendritic compartments. This typically caused spiking in response to previously subthreshold synaptic inputs. The magnitude of the simulated E-S potentiation depended on the passive electrical properties of the cell, the excitability of the soma, and the relative locations on the dendrites of the synaptic inputs and hot spots. The specificity of the simulated E-S potentiation was quantified by colocalizing the hot spots with a subset (40 of 80) of the synaptic contacts, denoted "tetanized," and then comparing the effects of the hot spots on these and the remaining (untetanized) synaptic contacts. The simulated E-S potentiation tended to be specific to the tetanized input if the untetanized contacts were, on average, electrically closer to the soma than the tetanized contacts. Specificity was also high if the tetanized and untetanized contacts were segregated to different primary dendrites. The results also predict, however, that E-S potentiation by this mechanism will appear to be nonspecific (heterosynaptic) if the synapses of the untetanized input are sufficiently far from the soma relative to the tetanized synapses. Experimental confirmation of this prediction would support the hypothesis that changes in postsynaptic excitability can contribute to hippocampal E-S potentiation.

Autoradiographic analysis of the primary retinal projections in the thornback guitarfish reveals both contralateral and ipsilateral projections to diencephalic, pretectal, and tegmental nuclei and the optic tectum. A total of 12 retino-recipient cell groups receive ipsilateral as well as contralateral inputs.

A homolog of the Edinger-Westphal nucleus of other vertebrates is described in two species of serranid basses of the genus Paralabrax, a group possessing a wide range of ocular accommodation but lacking a pupillary reflex to light. The nucleus was found by retrograde labeling from the ciliary ganglion and lies dorsolateral to the ipsilateral oculomotor nucleus. The nucleus consists of 60 to 100 neurons with an average soma diameter of about 20 microns in animals weighing 70 to 150 g. Electrophysiological experiments support the identification. Microstimulation of the nucleus evokes contraction of the ipsilateral lens retractor muscle and slight constriction of the caudal ipsilateral iris. Multi- and single-unit recordings in the nucleus reveal spontaneous firing (about 30 spikes/s in single units), the rate of which decreases during visually-evoked lens retractor relaxations (accommodation to near stimuli). Recordings of muscle fiber activity in the lens retractor show essentially the same behavior, which suggests that the ciliary ganglion and neuromuscular junctions simply relay impulses with little if any synaptic integration. The existence of a discrete Edinger-Westphal nucleus devoted largely to accommodation makes Paralabrax a good model system for the further tracing of central accommodation control pathways.