Neuroscience research
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Neuroscience research · May 1998
Comparative StudyEffect of WAY-100135 on the hippocampal acetylcholine release potentiated by 8-OH-DPAT, a serotonin1A receptor agonist, in normal and p-chlorophenylalanine-treated rats as measured by in vivo microdialysis.
The mechanisms involved in the enhancement of acetylcholine (ACh) release in the rat hippocampus by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a serotonin (5-HT)1A receptor agonist, were investigated using in vivo microdialysis. Administration of p-chlorophenylalanine (PCPA, 300 mg/kg, i.p.), a tryptophan hydroxylase inhibitor, 3 days before the dialysis experiments reduced the hippocampal 5-HT content to 30% of that in saline-treated rats, but did not affect basal ACh release in the hippocampus. 8-OH-DPAT administered systemically (0.5 mg/kg, s.c.) or applied locally (30 microM) into the hippocampus through the dialysis probe significantly enhanced the release of ACh in the hippocampus of PCPA-treated rats to the same degree as that in saline-treated rats. ⋯ These results suggest that the modification of endogenous 5-HT release via the 5-HT1A autoreceptor is not involved in the 8-OH-DPAT-induced increase of hippocampal ACh release, and that the increase of ACh release induced by locally applied 8-OH-DPAT involves mainly hippocampal postsynaptic 5-HT1A receptor stimulation. In addition, a possibility that subtypes of 5-HT receptors other than the 5-HT1A receptor, probably 5-HT7 receptor in the septum as well as postsynaptic 5-HT1A receptor in the hippocampus, are involved in the increased hippocampal ACh release induced by systemically administered 8-OH-DPAT is discussed.
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Neuroscience research · Apr 1997
Macrophages/microglia as 'sensors' of injury in the pineal gland of rats following a non-penetrative blast.
The pineal gland of adult rats was examined immunohistochemically and electron microscopically following exposure of the animals to a single blast equivalent to 110 kg TNT explosive. The most dramatic feature in rats killed at 7, 14 and 21 days after the blast was the upsurge of a large number of macrophages/microglia intensely immunostained with OX-42, OX-18, OX-6 and ED1 antibodies. These antibodies recognise the complement type three (CR3) receptors, major histocompatibility complex class I and class II (MHC I and MHC II) antigens and monocyte/macrophage antigens. ⋯ Ultrastructural study confirmed a wider occurrence of perivascular macrophages/microglia after the blast and the cells were laden with massive amounts of phagosomes resembling degenerating pinealocyte processes. It is concluded that the seemingly quiescent macrophages/microglia present normally in pineal gland were activated by the external blast force. The induced changes including the increase in cell numbers and endocytosis, however, were reversible in longer surviving animals.
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Neuroscience research · Oct 1996
Comparative StudyDense GABAergic input on somata of parvalbumin-immunoreactive GABAergic neurons in the hippocampus of the mouse.
GABAergic neurons in the hippocampus proper are greatly diverse in their morphological and physiological features. In the present study we examined whether or not they are also diverse regarding the density of GABAergic input on their somata. GABAergic neurons were immunocytochemically identified with antibodies against glutamic acid decarboxylase (GAD), and the densities of GAD-immunoreactive (GAD-IR) boutons that abutted on GAD-IR somata were estimated by conventional light microscopic, combined light and electron microscopic, and confocal laser scanning microscopic analyses. ⋯ Furthermore, the majority of GAD-IR boutons on PV-IR somata in the stratum pyramidale were also PV-IR. Bilateral transection of the fimbria-fornix, which was supposed to remove GABAergic afferents from the septum, had only partial effects on the densities of PV-IR boutons on PV-IR somata, indicating these PV-IR boutons mainly originated from intrinsic PV-IR neurons. These observations indicate the dense mutual connection between PV-IR GABAergic neurons through perisomatic synaptic contacts, particularly in the stratum pyramidale.
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Neuroscience research · Aug 1996
Peripheral axotomy induces increased expression of neurotensin in large neurons in rat lumbar dorsal root ganglia.
In normal rat lumbar 4 and 5 dorsal root ganglia (DRGs) a few large neurons expressed neurotensin-like immunoreactivity (LI). Twenty hours after crushing the lumbar 4 and 5 dorsal roots or the sciatic nerve, accumulations of neurotensin-LI were seen in many nerve fibers on the ganglionic side of both crushes, indicating a significant centrifugal transport of neurotensin under normal circumstances. A distinct increase in expression of neurotensin (peptide and mRNA) was observed in many large neuron profiles in the ipsilateral lumbar 4 and 5 DRGs two days after unilateral sciatic nerve transection. ⋯ Neurotensin-LI only sometimes colocalized with neuropeptide Y-LI, another peptide known to be upregulated in large DRG neurons. These two peptides may therefore partly be localized in different populations of large DRG neurons. The present results show that, in contrast to the nerve injury-induced general downregulation of neurotensin systems in the superficial dorsal horn and of neurotensin receptor mRNA expression in DRGs as shown in previous studies, axotomy causes upregulation of expression of neurotensin peptide in some large DRG neurons.
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Neuroscience research · Jun 1996
Comparative StudyThe role of cholinergic systems in the expression of morphine withdrawal.
Both oxotremorine and physostigmine both in doses ranging from 25 to 100 micrograms/kg produced dose-dependent attenuation of withdrawal jumping and potentiation of 'wet dog' shakes, burrowing, hypothermia and body weight loss precipitated by naloxone (1 mg/kg, i.p.) in morphine-dependent mice. On the other hand, atropine sulphate (2-20 mg/kg) dose-dependently attenuated all naloxone precipitated withdrawal symptoms except withdrawal hypothermia which was further potentiated. However, the peripherally acting derivative atropine methyl nitrate (2-10 mg/kg) also attenuated all naloxone-induced withdrawal symptoms except jumping, which was not significantly modified. ⋯ Withdrawal body weight loss was dose-dependently attenuated but 'wet dog' shakes, burrowing and hypothermia were markedly potentiated by hyoscine. Our results suggest that a combination of central muscarinic activation and peripheral muscarinic blockade can partially ameliorate precipitated morphine withdrawal. Differences observed between atropine and hyoscine with regard to their modifying effects on withdrawal symptoms may be explained on the basis that the drugs may be acting on the different subpopulations of the muscarinic receptor or through non-cholinergic systems.