Effects of ethanol on development of dorsal raphe transplants in oculo: A morphological and electrophysiological study
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Abstract The purpose of this project was to investigate ethanol influence on the development of serotonin‐containing (5‐HT) neurons of the dorsal raphe nucleus in rat. Fetal tissue of embryonic day 17 from the dorsal brainstem was grafted to the anterior chamber of the eye of adult albino rats. The experimental group was exposed to 16% ethanol in the drinking water, and the control group received water ad libitum. After 4 weeks, morphological and electrophysiological evaluations were performed. Immunohistochemical analysis showed that 5‐HT‐immunoreactive fibers from ethanol treated transplants had a disturbed outgrowth pattern into the host iris as compared to the control group. Furthermore, the outgrowth area and axon bundle formation was significantly greater in the control group than in the ethanol group. Electrophysiological recordings revealed a dose‐dependent biphasic effect of locally applied ethanol on transplanted monoaminergic neurons. Low doses of ethanol (0.5–3 mM)induced an increase in basal firing rate of control neurons, while higher doses (10–100 mM)caused inhibition. However, monoaminergic neurons in the ethanol group showed a decreased neuronal sensitivity to locally applied ethanol. The same dose of locally applied ethanol which produced an excitation of neuronal activity in the ethanol transplants produced an inhibition in the control grafts. The dose‐response curve was shifted to the right. The present results suggest that chronic ethanol exposure during early development leads to altered axonal outgrowth from brainstem 5‐HT neurons, as well as decreased sensitivity of these neurons to locally applied ethanol.Keywords:
Monoaminergic
Dorsal raphe nucleus
Melatonin, the hormone synthesized mainly by the pineal gland, is a key member of the complex monoaminergic signaling system, and a circadian regulator with pleiotropic functions. This ubiquitary lipophilic and hydrophilic molecule acts both at cellular and subcellular level, exerting anti-inflammatory, anti-oxidative and anti-apoptotic activities, extremely important in the nervous system, given its high vulnerability to oxidative injury. Melatonin deprivation and the consecutive chronodisruption are associated with multiple behavioural abnormalities, psychiatric disorders and neurodegenerative diseases. The present review summarizes the available information concerning the link between melatonin, monoaminergic neurotransmission and the pathophysiological bases of these conditions.
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Stress is known to activate distinct neuronal circuits in the brain and induce multiple changes on the cellular level, including alterations in neuronal structures. On the basis of clinical observations that stress often precipitates a depressive disease, chronic psychosocial stress serves as an experimental model to evaluate the cellular and molecular alterations associated with the consequences of major depression. Antidepressants are presently believed to exert their primary biochemical effects by readjusting aberrant intrasynaptic concentrations of neurotransmitters, such as serotonin or noradrenaline, suggesting that imbalances viihin the monoaminergic systems contribute to the disorder (monoaminergic hypothesis of depression). Here, we reviev the results that comprise our understanding of stressful experience on cellular processes, with particular focus on the monoaminergic systems and structural changes within brain target areas of monoaminergic neurons.
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Stress is known to activate distinct neuronal circuits in the brain and induce multiple changes on the cellular level, including alterations in neuronal structures. On the basis of clinical observations that stress often precipitates a depressive disease, chronic psychosocial stress serves as an experimental model to evaluate the cellular and molecular alterations associated with the consequences of major depression. Antidepressants are presently believed to exert their primary biochemical effects by readjusting aberrant intrasynaptic concentrations of neurotransmitters, such as serotonin or noradrenaline, suggesting that imbalances viihin the monoaminergic systems contribute to the disorder (monoaminergic hypothesis of depression). Here, we reviev the results that comprise our understanding of stressful experience on cellular processes, with particular focus on the monoaminergic systems and structural changes within brain target areas of monoaminergic neurons.
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Chronic Stress
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The present article describes functional development of monoaminergic synapses in the brain. Our recent findings on developmental changes of regional content, uptake, release of noradrenaline, dopamine, serotonin, specific binding of monoamines-related drugs and behavioral effects of these drugs were shown with aspect to the regulation mechanism in synaptic transmission.
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The physiological importance of the brainstem has made it one of the most studied structures of the central nervous system of mammals (in- cluding human). This structure receives somatic and visceral inputs and its neurons send motor efferences by means of the cranial nerves, which innervate the head, neck and sensory organs, and it mediates in several actions such as movement, pain, cardiovascular, respiratory, salivary, sleep, vigil and sexual mechanisms. Most of these actions are mediated by neuroactive substances denominated neuropeptides, which are short amino acid chains widespread dis- tributed in the nervous system, that play a role in neurotransmission, neuro- modulation (paracrine and autocrine actions), and act as neurohormones. In- creased study of these substances has taken place since the 1980s to shed light on both their potential role and the way that they mediate in the organism's different activities. Thus, our aim is a detailed review of available morphologic and physiologic data regarding some neuropeptides in the human brainstem. To such end, we will discuss aspects like: 1) the distribution of neuropeptides in the human brainstem; 2) their possible physiological actions in the human brainstem; 3) neuropeptide coexistences in the human brainstem; and 4) fu- ture research in neuropeptides in the human brainstem.
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消沉是破坏广泛地归因于在中央神经系统发信号的缺乏的 monoaminergic 的精神病学的混乱。然而，很临床的抗抑郁剂与很少延期提高 monoaminergic neurotransmission，但是 48 个星期要求到达治疗学的功效，建议消沉的 monoaminergic 假设是过分简化的悖论。与指向 monoaminergic 系统的抗抑郁剂相对照，对手 ketamine 生产的 N-methyl-D-aspartate 受体(NMDAR ) 的单个剂量快速(在 2 h 以内) 并且支撑(超过 7 天) 在处理抵抗的病人的抗抑郁剂功效。Glutamatergic 传播由 NMDAR 调停了为经验依赖者 synaptic 粘性是批评的并且学习，能被 monoaminergic 系统间接地修改的进程。为了更好理解新抗抑郁剂的行动的机制，希望 ketamine，我们考察并且比较 monoaminergic 和 glutamatergic 抗抑郁剂，与神经粘性上的强调。消沉的致病可以在可以用作目标的一个新班生产快速的抗抑郁剂效果的 glutamatergic 电路包含不适应的神经粘性。
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To study the significance of the pathological changes of axon and myelin sheath in injured brainstem.The neurofilament and myelin basic protein was demonstrated immunohistochemically,and the pathological changes of axons and myelin sheathes in human brainstem following trauma were observed.In the injured brainstem,irregular swelling and disconnecting axons could be found as early as 0 5h after injury, while pathological changes in myelin sheaths such as tortuous change,partial peeling off from axon and intermittent disappearance could be observed at 19～22h after injury.However,in the normal brainstem,there were no evident changes in axons and myelin sheaths.Pathological changes of axon and myelin sheath in brainstem would occur after trauma,which could be used for postmortem diagnosis of brainstem injury.
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The biochemical exploration in man is limited by ethical and technical factors. Results are contradictory and it is only by the mean of the antidepressants used as pharmacological tools that monoaminergic hypotheses have been made. The specificity of action of these drugs is very different from one substance to another and the post synaptic impact of the antidepressants is more important than it was thought before. Finally the monoaminergic hypothesis is too simple and cannot summarize the biochemical factors in depression.
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