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.