Brain research
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Adult male Sprague-Dawley rats were injected in the right cerebral hemisphere with the neurotoxin 6-hydroxydopamine (6-OHDA) at a site which interrupted the noradrenergic axons ascending from the locus coeruleus (LC). Distal to the injection site ('posterior cortex'), levels of norepinephrine (NE), dopamine-beta-hydroxylase (D beta H) and tyrosine hydroxylase (TH) fell to 39-42% of control levels ipsilateral to the lesion over the first 25 days, while contralateral levels fell to 32-73% of control during this time. These changes were paralleled by a 63% decrease in the high affinity uptake of [3H]NE in the ipsilateral posterior cortex at 12 days after the lesion. ⋯ Transport of D beta H fell to 7-40% of control from 2 to 24 days and rose to 160% of control by 3 months after the lesion. TH transport was decreased to only 61% of control only at 24 days and returned to control levels by 3 months. These studies document that there is independent regulation of the metabolism of the NE synthetic enzymes, D beta H and TH, during the degeneration and subsequent regeneration or collateral sprouting of injured distal axons of LC noradrenergic neurons.
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Spikes with bimodal and occasional trimodal latencies were recorded from neurons in the olfactory bulb of rabbits in response to lateral olfactory tract (LOT) stimulation at one site. Among neurons with bimodal spike latencies, two types have to be distinguished. In the case of type I neurons long-latency second-mode spikes were suppressed by short-latency first-mode spikes. ⋯ In the multiple collision test the c-l deviations from the lowest c-l value of each neuron ranged for axonal spikes between 0.0 and 0.7 ms (n = 25), with 38% not exceeding 0.1 ms and 81% not exceeding 0.4 ms. Spikes activated via axon collaterals had c-l deviations between 0.0 and 2.0 ms (n = 13). The c-l deviations above 2 ms were remote from other values and considered to be possibly inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)