Laminar distribution and sources of catecholaminergic input to the optic tectum of the pigeon (Columba livia)

Abstract

A combined immunohistochemical and retrograde tracing approach was used to characterize the catecholaminergic innervation of the optic tectum (TeO), the major target of retinal projections in many avian species. Giemsa counterstaining was employed to determine precisely the laminar localization of immunoreactive fibers and presumptive terminals. The TeO of the pigeon is densely innervated by fibers immunoreactive for tyrosine hydroxylase (TH), which are most heavily distributed to the superficial layers of its dorsal and anterior portions. Within the dorsal-anterior tectum, TH-immunoreactive processes are particularly dense in retinorecipient layers 4 and 7 and in layer 5a. As in the mammalian superior colliculus, the bulk of the catecholaminergic innervation of the pigeon TeO reflects inputs, presumably noradrenergic, originating in the locus coeruleus and nucleus subcoeruleus. However, the catecholaminergic innervation of the pigeon TeO shows several features distinct from those reported for the mammalian superior colliculus. These include an input from a pretectal TH-positive cell group unknown in mammals and the presence of residual TH immunoreactivity after administration of the noradrenergic neurotoxin DSP-4. Moreover, the pattern of TH-immunoreactive fibers in pigeon TeO indicates more laminar and regional specialization within this structure than has been reported for the catecholaminergic innervation of the superior colliculus in mammals.

Cerebellar and spinal projections of the coeruleus complex in the duck: A fluorescent retrograde double-labeling study

“…The observation that noradrenergic inputs gate sensory processing in avian visual system (Broyles and Cohen, 1985;Elmslie and Cohen, 1990) and the functional significance given to the regional and laminar patterns of the Co complex noradrenergic inputs to the pigeon optic tectum (Rodman and Karten, 1995) are consistent with this suggestion.…”

“…However, on the basis of their connectivities and location, we may presume the noradrenergic nature of many if not all FB and DY retrogradely labeled cells since, according to the chemoarchitectonic subdivision of the avian Co complex, noradrenergic neurons are confined to the caudal parts of the LCo and SCo (Bailhache and Balthazart, 1993;Moons et al, 1995;Rodman and Karten;1995, von Bartheld andBothwell, 1992;von Bartheld et al, 1995).…”

“…Because of the mingling of FB and DY labelings, the caudal portions of the LCo and dSCo cannot be subdivided into distinct anatomical cellular groups. Moreover, in birds these regions of the Co complex contain noradrenergic neurons projecting to the optic tectum (Rodman and Karten, 1995) and to many diencephalic as well as telencephalic fields (Kitt and Brauth, 1986). …”

“…The caudal parts of the LCo and SCo contain noradrenergic perikarya (Fuxe and Ljunggren, 1975;Yamamoto et al, 1977;Guglielmone and Panzica, 1984;Dubé and Parent, 1981;von Bartheld and Bothwell, 1992;Bailhache and Balthazart, 1993;Bottjer, 1993;Moons et al, 1995;von Bartheld et al, 1995), which project to many telencephalic and diencephalic structures (Tohyama et al, 1974;Brauth et al, 1978;Kitt and Brauth, 1986), to the optic tectum (Rodman and Karten, 1995), and to the spinal cord as far as the lumbar region (Cabot et al, 1982;Gross and Oppenheim, 1985;Webster and Steeves, 1988). Therefore, at least the caudal part of the avian Co complex may be homologous to the mammalian Co complex both from histochemical and anatomical aspects (Moons et al, 1995;von Bartheld et al, 1995).…”

Neurotoxic effects of DSP-4 on the central noradrenergic system in male zebra finches

“…The noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) is widely used to lower brain NE to investigate the functions of the central noradrenergic system [7,11,12,55,64]. When administered systemically in rats, DSP-4 crosses the blood-brain barrier and causes rapid, profound, long-term decreases in NE and markers of noradrenergic function in the cortex but leaves hypothalamic NE function relatively unaltered [39,58].…”