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Alteration of serotonin (5‐HT) levels influences developing thalamocortical afferents (TCAs) in primary somatosensory cortex (SI) of rats and mice. The 5‐HT1Breceptor, present on TCAs during the first postnatal week, may be involved in these effects. The present study asked whether administration of 5‐nonyloxytriptamine (NNT), a selective 5‐HT1Breceptor agonist, affects TCA organization in rat SI. Littermates were injected five times daily (5×/day), with either 0.1 mg/kg NNT or vehicle from birth to postnatal day 6 (P‐6). Animals were killed on P‐6, and their brains were processed for high‐performance liquid chromatography (HPLC), cytochrome oxidase (CO) histochemistry, cresyl violet, or demonstration of TCAs by placement of 1,1′‐dioctadecyl‐3,3,3′′,3′‐tetra‐methylindocarbocyanine perchlorate (Di‐I) on thalamocortical radiations. At P‐6, NNT treatment decreased 5‐HT levels slightly compared with controls, although this difference was not statistically significant. In NNT‐treated rats, the Di‐I‐labeled vibrissae‐related pattern showed a range of effects, from fusion of patches related to mystacial vibrissae in treated animals to a less distinct vibrissae‐related pattern in SI barrelfield compared with controls. Staining for CO and Nissl stain in layer IV of SI showed a similar range of abnormalities. These results indicate that the agonist action of NNT at the 5‐HT1Breceptor causes TCA disorganization in rat barrel field cortex in the absence of elevated 5‐HT. J. Comp. Neurol. 425:130–138, 2000. © 2000 Wiley‐Liss, Inc.

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.

1. Visual response properties of superior collicular neurones were investigated in golden hamsters reared from birth to adulthood in a stroboscopic environment.

1. The response characteristics of visual, somatosensory, and auditory neurones in the golden hamster's superior colliculus were investigated.