THE STRESS-INDUCED RESPONSE OF THE SEPTOHIPPOCAMPAL CHOLINERGIC SYSTEM - A VECTORIAL OUTCOME OF PSYCHONEUROENDOCRINOLOGICAL INTERACTIONS
THE STRESS-INDUCED RESPONSE OF THE SEPTOHIPPOCAMPAL CHOLINERGIC SYSTEM - A VECTORIAL OUTCOME OF PSYCHONEUROENDOCRINOLOGICAL INTERACTIONS
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DOI：
10.1016/0306-4530(87)90002-3
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发表时间：
1987-01-01
影响因子：
3.7
通讯作者：
GILAD, GM
中科院分区：
文献类型：
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作者：
GILAD, GM
大量的数据表明，中隔海马胆碱能系统参与了对压力的适应性反应。这部分边缘系统胆碱能突触末端的神经递质调控机制在应激反应中发生适应性变化，应激后恢复缓慢。最初的应激诱导反应的特征是在几分钟内激活海马胆碱能末端，表现为高亲和力胆碱摄取和新合成乙酰胆碱释放的快速和短暂升高。这种胆碱能系统对压力的反应受到神经元和激素刺激的影响。在中隔聚集的几个神经系统中，多巴胺能中边缘系统的末端被发现选择性地参与对压力的早期反应。通过激动剂和拮抗剂对多巴胺能神经传递的药物干预，揭示了中隔多巴胺能末梢的强直抑制作用的变化可以调节海马胆碱能末梢对应激的反应。在大剂量促肾上腺皮质激素或皮质酮治疗后，观察到海马胆碱能终端的激活与短期应激后相似。此外，糖皮质激素而非促肾上腺皮质激素可以直接促进乙酰胆碱的释放，但仅从兴奋终端释放。这表明压力诱导的中隔-海马系统的激活可能继发于垂体-肾上腺皮质激素水平的升高，而不是直接由其引起。然而，在应激条件下，糖皮质激素水平的升高可能会调节受刺激的海马胆碱能末梢的活动。总之，这些发现支持了这样一种观点，即中隔-海马胆碱能系统的应激诱导反应代表了神经元和激素刺激的综合输出，这些刺激将应激信号传递到大脑边缘区域。
Considerable data have emerged which strongly indicate that the septohippocampal cholinergic system is involved in the adaptive response to stress. Neurotransmitter regulatory mechanisms in cholinergic synaptic terminals of this part of the limbic system undergo adaptive changes in response to stress and recover slowly after stress. The initial stress-induced response is characterized by activation of hippocampal cholinergic terminals within minutes, as indicated by a rapid and transient elevation in high affinity choline uptake and increased newly synthesized acetylcholine release. The response of this cholinergic system to stress is influenced by both neuronal and hormonal stimuli. Among the several neuronal systems converging in the septum, terminals of the dopaminergic mesolimbic system have been found to be selectively involved in the early response to stress. Pharmacological interference with dopaminergic neurotransmission, with agonist and antagonist treatments, revealed that changes in the tonic inhibitory influence of septal dopaminergic terminals can modulate the response of hippocampal cholinergic terminals to stress. A similar activation of hippocampal cholinergic terminals as after short-term stress was observed after treatments with a large dose of either adrenocorticotropic hormone or corticosterone. Furthermore, glucocorticoids and not adrenocorticotropic hormone can directly enhance acetylcholine release, but only from excited terminals. This indicates that stress-induced activation of the septo-hippocampal system may occur secondary to, but not directly by, increased levels of pituitary-adrenocortical hormones. Yet, it is possible that under stressful conditions the increased glucocorticoid levels may modulate the activity of the stimulated hippocampal cholinergic terminals. Together the findings support the notion that the stress-induced response of the septo-hippocampal cholinergic system represents an integrated output of converging neuronal and hormonal stimuli which convey signals of stress to this limbic brain region.