Telencephalic enkephalinergic systems in the rat brain.
نویسندگان
چکیده
The comparative distribution of Leu-enkephalin and an enkephalin precursor fragment, BAM-22P, was studied in the rat telencephalon using immunocytochemical procedures. Although the enkephalins have previously been localized to telencephalic neurons, the use of high doses of colchicine in the present study has permitted the visualization of widespread enkephalin-containing systems in cortical-limbic regions. Rats were treated intraventricularly with colchicine (300 to 400 micrograms) to enhance the visualization of neuronal perikarya. Leu-enkephalin immunoreactivity was noted in perikarya as well as processes of neurons in many telencephalic regions including the olfactory bulb, parolfactory areas, olfactory tubercle, basal ganglia, nucleus accumbens, septal nuclei, amygdala, hippocampal formation, and several paleocortical regions such as the piriform, entorhinal, and cingulate cortex, as well as regions of the frontal, parietal, and occipital neocortex. In the majority of regions investigated, analysis of sections adjacent to those processed for Leu-enkephalin histochemistry showed BAM-22P immunoreactivity to be localized to perikarya and processes in the same region. These results suggest that brain enkephalin-positive neurons may possess mechanisms for enkephalin biosynthesis similar to those found in adrenal medullary enkephalin cells.
منابع مشابه
Modulation of quinolinic acid-induced depletion of striatal NADPH diaphorase and enkephalinergic neurons by inhibition of nitric oxide synthase.
The present study was designed to examine the role of nitric oxide (NO) in quinolinic acid (QUIN)-induced depletion of rat striatal nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase and enkephalinergic neurons. Intrastriatal injection of QUIN produced a dose-dependent decrease in NADPH diaphorase and enkephalin positive cells, with cell loss being evident following the injection of...
متن کاملNociceptive stimulation induces expression of Arc/Arg3.1 in the spinal cord with a preference for neurons containing enkephalin
BACKGROUND In pain processing, long term synaptic changes play an important role, especially during chronic pain. The immediate early gene Arc/Arg3.1 has been widely implicated in mediating long-term plasticity in telencephalic regions, such as the hippocampus and cortex. Accordingly, Arc/Arg3.1 knockout (KO) mice show a deficit in long-term memory consolidation. Here, we identify expression of...
متن کاملThe distribution of proenkephalin-derived peptides in the central nervous system of turtles.
The present study was carried out to examine if peptides similar to the various opioid peptide products of mammalian proenkephalin are present in the turtle central nervous system and to determine their distribution. Antisera against several enkephalin peptides were used: leucine-enkephalin (LENK), methionine-enkephalin (MENK), methionine-enkephalin-arg6-phe7 (MERF), methionine-enkephalin-arg6-...
متن کاملDecompensated hemorrhage activates serotonergic neurons in the subependymal parapyramidal region of the rat medulla.
According to prior evidence opioid and serotonin release by lower brain stem neurons may contribute to hemorrhage-induced sympathoinhibition (HISI). Here we seek direct evidence for the activation of opioidergic, GABAergic, or serotonergic neurons by severe hemorrhage in the medulla oblongata. Blood was withdrawn from awake rats (40-50% total volume) causing hypotension and profound initial bra...
متن کاملBDNF–TrkB signaling in striatopallidal neurons controls inhibition of locomotor behavior
The physiology of brain-derived neurotrophic factor signaling in enkephalinergic striatopallidal neurons is poorly understood. Changes in cortical Bdnf expression levels, and/or impairment in brain-derived neurotrophic factor anterograde transport induced by mutant huntingtin (mHdh) are believed to cause striatopallidal neuron vulnerability in early-stage Huntington's disease. Although several ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- The Journal of neuroscience : the official journal of the Society for Neuroscience
دوره 3 4 شماره
صفحات -
تاریخ انتشار 1983