The optic tecta of surgically produced threeeyed tadpoles were chronically exposed to the N-methyl-Daspartate (NMDA) receptor antagonist aminophosphonovaleric acid (APV), or to NMDA itself, to assess the influence of NMDA receptor/channels on the eye-specific segregation of retinal ganglion cell (RGC) terminals that occurs whenever two retinas innervate one tectal lobe. Exposure of the tectum to the active isomer of APV produces desegregation of the RGC terminals without blocking electrical activity in the afferents or altering their terminal arbor morphology. Exposure to the inactive isomer of APV causes no perturbation of the normal stripe pattern. APV-induced desegregation is completely reversible within 2 weeks of removal of the APV. In addition, exposure of the optic tectum to NMDA results in stripes with sharper borders and fewer forks and fusions than untreated animals. These results suggest that the NMDA receptor/ channel plays a role in eye-specific segregation in the three-eyed tadpole.Studies on the establishment of topography in the central visual pathway suggest that retinotopic maps develop by a two-step process, whereby a coarse projection of afferents onto target neurons is followed by a dynamic sorting of relative synaptic positions based on stabilization of coactive afferent terminals. The same cellular mechanisms are believed to be involved in the formation of ocular dominance columns in the visual cortex (1-3), where inputs driven by left and right eyes converge within the same cortical layer. A model system in which to study the fine-tuning of synaptic positions is provided by implanting a supernumerary eye primordium into embryonic Rana pipiens. In surgically produced three-eyed tadpoles, retinal ganglion cells (RGCs) from the normal and supernumerary eyes project to the same optic tectum and their terminals segregate into highly stereotyped ocular dominance stripes (4, 5). Despite asymmetric patterns of retinal and tectal cell proliferation (6-8), both retinotopy and eye-specific segregation are maintained throughout the 3-6 months of larval development by a constant shifting of RGC terminals over the tectal surface (1, 9). Consequently, the mechanisms responsible for fine-tuning the retinotectal projection operate continuously throughout larval life, presumably by selectively increasing the lifetimes of coactive connections (10, 11). In the three-eyed frog, disruption of the fine-tuning mechanisms is detectable as a gradual degradation of the stripe pattern (9, 12).Studies using tetrodotoxin (TTX) to block RGC action potentials have demonstrated that afferent activity is required for the refinement of both the retinotopic projection and eye-specific segregation (13-17). It is thought that retinal inputs confer their neighbor relations to the target neurons by virtue of their highly correlated action potentials (10,11,(18)(19)(20)(21) We report that chronic application of aminophosphonovaleric acid (APV), a specific antagonist of the NMDA receptor/channel (34), to the optic tectum ...
Leech swimming is produced by the antiphasic contractions of dorsal and ventral longitudinal muscles that travel rearward along the animal and propel it forward. Research over the past three decades has focused on identifying the underlying neuronal circuit and mechanisms that produce and control this coordinated movement pattern. Investigations have also tested whether leech swimming is modifiable, both by experience and by neuromodulators. One outcome has been the identification of several functional classes of neurons associated with swimming. Systematic analysis of the interactions between these neurons had led to the elucidation of a neuronal circuit that adequately accounts for the generation of the swim motor program cord. The swim motor program appears to be produced by a chain of coupled segmental oscillators whose intrinsic properties and intersegmental connections ensure the coordinated expression of swimming along the nerve cord. In addition, neurons identified in the head ganglion comprise two parallel, but opposite-acting, systems that control the initiation of swimming in response to sensory input. Also, the pathway by which body wall stimulation initiates swimming shows a simple form of learning, that is habituation. Repeatedly stroking the leech body wall decreases both the probability of initiating swimming and the length of elicited swim episodes. Finally, the biogenic amine serotonin, which is found in the nerve cord, affects leech swimming in a number of ways. Serotonin's modulation of swimming is due, in part, to its effect of the membrane properties of swim-initiating interneurons and several swim motor neurons.
We have assessed the role of activity in the adult frog visual system in modulating two aspects of neuronal plasticity: neurotransmitter expression and topographic map maintenance. Chronic treatment of one tectal lobe with the non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione decreased the percentage of substance P-like immunoreactive (SP-IR) tectal cells in the untreated lobe while disrupting topographic map formation in the treated one. Treatment with the NMDA receptor antagonist d-(-)-2-amino-5-phosphonovaleric acid (d-AP-5) disrupted the topographic map but had no affect on SP-IR cells. These results indicate that maintenance of the topographic map is dependent on direct input from the glutamatergic retinal ganglion cells, whereas substance P (SP) expression is being regulated by a pathway that relays activity from one tectal lobe to the other. Such a pathway is provided by the cholinergic nucleus isthmi, which is reciprocally connected to the ipsilateral tectum and sends a projection to the contralateral one. Mecamylamine and atropine, antagonists of nicotinic and muscarinic receptors, respectively, were used together to block all cholinergic activity or alone to block receptor subclass activity. All three treatments decreased SP expression and disrupted the topographic map in the treated tectal lobe. We conclude that both SP expression and topographic map maintenance in the adult optic tectum are activity-dependent processes. Although our results are consistent with the maintenance of the topographic map through an NMDA receptor-based mechanism, they suggest that SP expression is regulated by a cholinergic interaction that depends on retinal ganglion cell input only for its activation.
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