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Intracellular recording techniques were used to
evaluate the effects of norepinephrine (NE) on the membrane
properties of superficial layer (stratum griseum superficiale
and stratum opticum) superior colliculus (SC)
cells. Of the 207 cells tested, 44.4% (N = 92)
were hyperpolarized by ≥3 mV and 8.7% (N =
18) were depolarized by ≥3 mV by application of NE.
Hyperpolarization induced by NE was dose dependent (EC50
= 8.1 μM) and was associated with decreased input resistance
and outward current which had a reversal potential of −94.0
mV. Depolarization was associated with a very slight rise
in input resistance and had a reversal potential of −93.1
mV for the single cell tested. Pharmacologic experiments
demonstrated that isoproterenol, dobutamine, and p-aminoclonidine
all hyperpolarized SC cells. These results are consistent
with the conclusion that NE-induced hyperpolarization of
SC cells is mediated by both α2 and β1
adrenoceptors. The α1 adrenoceptor agonists,
methoxamine and phenylephrine, depolarized 35% (6 of 17)
of the SC cells tested by ≥3 mV. Most of the SC cells
tested exhibited responses indicative of expression of
more than one adrenoceptor. Application of p-aminoclonidine
or dobutamine inhibited transsynaptic responses in SC cells
evoked by electrical stimulation of optic tract axons.
Inhibition of evoked responses by these agents was usually,
but not invariably, associated with a hyperpolarization
of the cell membrane and a reduction in depolarizing potentials
evoked by application of glutamate. The present in
vitro results are consistent with those of the companion
in vivo study which suggested that NE-induced
response suppression in superficial layer SC neurons was
primarily postsynaptic and chiefly mediated by both α2
and β1 adrenoceptors.
Single-unit recording and micropressure ejection
techniques were used to test the effects of norepinephrine
(NE) on the responses of neurons in the superficial layers
(the stratum griseum superficiale and stratum
opticum) of the hamster's superior colliculus
(SC). Application of NE suppressed visually evoked responses
by ≥30% in 75% of 40 neurons tested and produced ≥30%
augmentation of responses in only 5%. The decrement in
response strength was mimicked by application of the α2
adrenoceptor agonist, p-aminoclonidine, the nonspecific
β agonist, isoproterenol, and the β1
agonist, dobutamine. These agents had similar effects on
responses evoked by electrical stimulation of the optic
chiasm and visual cortex. The α1 agonist,
methoxamine, augmented the light-evoked responses of 53%
of 49 SC cells by ≥30%, but had little effect on responses
evoked by electrical stimulation of optic chiasm or visual
cortex. The effects of adrenergic agonists upon the glutamate-evoked
responses of SC cells that were synaptically “isolated”
by concurrent application of Mg2+ were similar to those
obtained during visual stimulation. Analysis of effects of NE on
visually evoked and background activity indicated that application
of this amine did not significantly enhance signal-to-noise
ratios for most superficial layer SC neurons, and signal-to-noise
ratios were in some cases reduced. These results indicate
that NE acts primarily through α2 and β1
receptors to suppress the visual responses of SC neurons.
Activation of either of these receptors reduces the responses
of SC neurons to either of their two major visual inputs
as well as to direct stimulation by glutamate, and it would
thus appear that these effects are primarily postsynaptic.
Administration of a single subcutaneous dose of
5,7-dihydroxytryptamine (5,7-DHT) to newborn hamsters results
in a significant increase in the density of serotoninergic
(5-HT) fibers in the superficial layers of the superior
colliculus (SC) and marked abnormalities in the uncrossed
retinotectal projection when these animals reach adulthood
(Rhoades et al., 1993). The present study was undertaken
to determine whether elevation of 5-HT in the developing
SC altered the visual representation in SC. Multi-unit
recordings from SC cells demonstrated that the overall
organization of the visual map in the superficial SC laminae
was normal and that the receptive-field sizes for unit
clusters were unchanged in the 5,7-DHT-treated animals.
However, when a combination of CNQX and MK-801 was directly
applied to the SC to block postsynaptic activity, the receptive
fields of unit clusters (presumably retinotectal axon terminals)
in the 5,7-DHT treated animals were significantly larger
than those in the normally reared hamsters. These results
are consistent with the conclusions that elevation of 5-HT
levels in the developing SC reduces the postnatal refinement
of the crossed retinotectal axons, and that mechanisms
operating within the SC may act to maintain normal sizes
for the receptive fields of its constituent neurons.
Immunocytochemistry and retrograde labeling were used to define the thalamic projections of calbindin- and parvalbumin-containing cells in superficial layers of the rat's superior colliculus (SC). Quantitative analysis revealed that 90.8 ± 2.2% (mean ± standard deviation) of the calbindin-immunoreactive neurons in the stratum griseum superficiale (SGS) projected to the dorsal lateral geniculate nucleus (LGNd) and that 91.3 ± 4.3% of calbindin-immunoreactive neurons in the stratum opticum (SO) projected to the lateral posterior nucleus (LP). In contrast, only 17.3 ± 2.5% of parvalbumin-immunoreactive neurons in the SGS were found to project to the LGNd and 16.5 ± 3.1% of the parvalbumin-immunoreactive SO cells were retrogradely labeled after LP injections. Few of the parvalbumin-immunoreactive neurons in either the SGS (7.2 ± 2.5%) or the SO (9.2 ± 2.5%) were GABA positive. The retrograde-labeling results suggest that parvalbumin-immunoreactive neurons in the rat's SO and SGS may either be primarily interneurons or have descending projections, while calbindin-containing cells are primarily thalamic projection neurons. These results are consistent with data from other rodents, but almost exactly the opposite of data that have been reported for the cat for these same populations of SC projection neurons. Such interspecies differences raise questions regarding the functional importance of expressing one calcium-binding protein versus another in a specific neuronal population.
Autoradiography with 125I-neurotensin in normal and enucleated hamsters was used to define the distribution of receptors for this peptide in the superficial layers of the superior colliculus (SC). Neurotensin binding sites were densely distributed in the stratum griseum superficiale (SGS), and results from the enucleated animals indicated that they were not located on retinal axons. The effects of neurotensin on individual superficial layer cells were tested in single-unit recording experiments. Neurotensin was delivered via micropressure ejection during visual stimulation (n = 75 cells), or during electrical stimulation of either the optic chiasm (OX; n = 47 cells) or visual cortex (CTX; n = 29 cells). In comparison with control values, application of neurotensin decreased visual responses of all SC cells tested to 54.1 ± 34.9% (mean ± standard deviation; range of decrement 7.5 to 100%; nine cells showed no effect or an increase in visual activity, which for four of these was ≥30%). Neurotensin application also reduced responses to electrical stimulation of either OX or CTX, respectively, to 65.8 ± 36.5% of control values (range of decrement 2.6 to 97.4%; 12 neurons showed a weak increment ≤ 30%) and 68.0 ± 38.5% (range of decrement 3.3 to 100%; five cells showed no effect or an increment, in one case ≥ 30%). Of the 25 neurons tested with both OX and CTX stimulation, the correlation of evoked response suppression by neurotensin was highly significant (r = 0.70; P < 0.001). This suggests that the suppressive effects of neurotensin were common to both pathways. To test whether the inhibitory effects of neurotensin were presynaptic or postsynaptic, Mg2+ ions were ejected iontophoretically to abolish synaptic responses, and the neurons (n = 16) were activated by iontophoresis of glutamate and then tested with neurotensin. Neurotensin reduced the glutamate-evoked responses to an average 59.3 ± 37.9% of control values (range 2.3 to 92.5%; one cell showed an increment >30%). This result suggests that the site of action of neurotensin is most likely postsynaptic.
Neonatal subcutaneous administration of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) to hamsters results in a marked depletion of serotonin (5-HT) in cortex and an increase in the concentration of this amine in the superior colliculus (SC). To determine whether this increase was associated with an alteration in the synaptic organization of 5-HT-containing axons in the superficial gray layer of the SC, immunocytochemistry was combined with electron microscopy. In normal adult hamsters, only 4.0% of 500 5-HT-immunoreactive profiles make synaptic contacts in the superficial gray layer of the hamster's SC. In 5,7-DHT-treated animals, examination of 400 individual profiles indicated that 25.5% of 5-HT-positive profiles made synaptic contacts (P < 0.05). Given the recently demonstrated effect of 5-HT on retinotectal transmission in this species, the present results suggest that the functional organization of the SC may also be markedly altered in animals that sustain neonatal 5,7-DHT administration.
Superficial layer superior colliculus (SC) neurons were recorded extracellularly with multibarreled recording/ejecting micropipettes. Angiotensin II was delivered via micropressure ejection during visual stimulation (n = 215 cells), or during electrical stimulation of either the optic chiasm (OX; n = 150 cells) or visual cortex (CTX; n = 42 cells). Application of angiotensin II decreased visual responses of SC cells to 43.8% ± 30.7% (mean ± S.D.) and reduced responses to electrical stimulation of the OX and CTX to 58.6% ± 34.1% and 43.8% ± 30.7% of control values, respectively. Angiotensin II enhanced responses by at least 30% in only 6 cells (1.5%). Of the 35 neurons tested with both OX and CTX stimulation, the correlation of evoked response suppression by angiotensin II was highly significant (r = 0.69; P < 0.001). This suggests that the suppressive effects of angiotensin II were common to both pathways. To test whether the inhibitory effects of angiotensin II were presynaptic or postsynaptic, Mg2+ ions were ejected iontophoretically to abolish synaptic responses, and the neurons were activated by iontophoresis of glutamate and then tested with angiotensin II. Angiotensin II reduced the glutamate-evoked responses to an average 29.1% ± 21.1% of control values (n = 9 cells). This suggests that the site of action of angiotensin II is most likely postsynaptic. To identify which receptors were involved in these effects, angiotensin II was ejected concurrently with the AT1 antagonist Losartan (DUP753) or with either of two AT2 antagonists, CGP42112A or PD123177. Losartan antagonized the action of angiotensin II in 65.6% of the cells tested (n = 99) and CGP42112A and PD123177 had antagonistic effects in 58% (n = 65) and 60% (n = 5), respectively. Both classes of antagonists were tested in 29 cells; and there was no significant correlation between their effectiveness. These results suggest that both AT1, and AT2 receptors may independently mediate the suppressive effects of angiotensin II, and that collicular neurons may have either or both receptor subtypes.
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