摘要

此篇研究在探討破壞大腦中膈區(septum) 對飲水行為的影響。在探討中膈對於抑制飲水現象，過去的相關研究中極少注意到下列數個問題(1) 中膈細胞在神經解剖上的異質性功能是否相似於對飲水行為的影響; (2) 中膈胞特定區域對於個體接受外來引發飲水刺激的反應;與(3) 相關的中樞神經作用藥物對中膈調節飲水的影響。因此，在本研究中設計了三個實驗來探討大白鼠中膈對於飲水行為的功能。實驗一中利用海人草酸(Kainic Acid) 之神經破壞法，來檢視中膈內不同次分區域被破壞後，對於飲水行為的影響。實驗二中則是探討內中膈後區破壞後，測試個體對於引發飲水刺激之專屬性與敏感度。實驗三則是直接對於中膈組織注射不同神經傳導物的相關藥物，探討中膈神經藥理之特性對於飲水行為的影響。實驗結果顯示，從比較破壞中膈之次分區域中，以內中膈後區(posterior medial septal) 對於飲水行為的促進作用高於內中膈前區及側中膈。而針對內中膈後區破壞後，發現個體對於NaCl注射後而產生飲水量增加的反應較敏感，但對於注射PEG(polyethylene glycol)的反應則端視濃度而定。另外，直接對於內中膈後區注射藥物所產生的反應以Acetylcholine 受體促進劑Carbachol 的效果最顯著，意即注射Carbachol 後顯著增加飲水行為。綜合上述實驗結果，本研究破壞內中膈後區所引發大白鼠飲水行為的增加，應具有專一之特性，此結果亦間接支持中膈的正常功能是扮演抑制飲水行為的角色。

Abstarct

The present study aimed to examine the effects of septal lesion on rat's drinking behavior. Regarding the septal hyperdipsia, following issues received little attention in the past: (1) Would the lesion of the subarea of the septum differentially affect drinking behavior? (2)Would the sensitivity for a speicific septal area to cellular and extracelluar thirst stimuli be different? (3)What type of neurotrasmitter system would be involved in the septal hyperdipsia as determined by the specific pharmacological agents? Three experiments were then designed in this study. Experiment 1 tested the water intake and locomotor activity of the rats which were

lesioned with kainic acid (O.5ug/O.5ul/site) on three septal subregions: anterio-medial(MSa), posterio-medial (MSp) , and lateral (LS) site. The drinking effects of cellular and extracellular thirst stimili injected in the MSp were investigated in Experiment 2. Effects of different centrally acting agents injected directly into

the MSp area were evaluted in Experiment 3.

The results showed that MSp lesion significantly increased water intake while the lesions of LS and MSa did not elicit such effects in Experiment 1. In Experiment 2, the rats were more sensitive to the injection of hypertonic NaCl on the drinking behavior after the lesions of the MSp in compare with the injection of PEG(20%). However, PEG(40%), significantly increased the water intake volume 8 hours after its administration. In Experiment 3, the injection of the carbachol produced the most significant effect on the rat's drinking response. Together, the lesion of the MSp plays important role in enhancing the rat's drinking volume. These effects were potentially

exerted via the activation -of cholinergic system. These results may imply that the MSp inhibits the drinking behavior in the normal rat.

參考文獻
Blass, E. M. & Epstein, A. N. (1971). A Lateral preoptic ososmosensitive zone for thirst in the rat. Journal of Comparative and Phtsiological Psychology, 76, 378-394.
Blass, E. M. & Hanson, D. G. (1970). Primary hyperdipsia in the rat following septal lesions. Journal of Comparatlve and Physiological Psychology, 70, 87-93.
Blass, E. M., Nussbaum, A. I. & Hanson, D. G. (1974). Septal Hyperdipsia: specific enhancement of drinking to angiotensin in rats. Journal of Comparative and
Physiological Psychology, 87, 422-439.
Bridges, J. G. & Halton, G. I., (1973). Septal unit activity in response to alterations in blood volume and osmotic pressure. Physioloqy & Behavior, 10, 769-774.
Carlson, N. R. (1991). Physiology of Behavior (4th Ed.),421-472. Boston: Allyn and Bacon.
De Castro, J. M. & Taggart, D. (1979). Medical septal lesions: Body weight loss and its relationship to polyuria in rats. Physiology & Behavior, 22, 855-859.
Epstein, A. N. (1983). The neuropsychology of drinking behavior. In Satinoff, E. & Teitelbaum, P. (Eds.). Motivation: Handbook of Behavioral Neurobiology, 6, 367-
423. New York: Plenum Press.
Fitzsimons, J. T. (1970). Interactions of intracranially administrated renin and angiotensin and other thirst stimuli on drinking. Journal of Physiology, 210, 152-153.
Fitzsimons, J. T. (1987). Some mathods for inverstigating thirst and sodium appetite. In Toates, F. M. & Rowland , N. E. (Eds.). Techniques in the Behavioral and Neural
Sciences: Feeding and drinking, 1, 393-427. New York : Elsevier Press.
Fregly, M. J. & Rowland, N. E. (1986). Do peripheral and cerebroventricular injections of angiotensin 2 act at the same site? studies an addituity of drinking. Brain Research Bulletin; 16, 249-257.
Harrell, L. E., Parsons, D. E., Peagler, A. & Barlow, T. S. (1987). Alternations in regulatory behavior induced by medial septal lesions and superior cervical ganglionectomy. Brain Research, 408, 131-140.
Harvey, J. A. & Hunt, H. F. (1965). Effect of septal lesions on thirst in the rat as indicated by water consumption and operant responding for water reward. Journal of
Comparative and Physiological Psychology, 59, 49-56.
Haibara, A. S., Saad, W. A., Camargo, L. A. A., Me-ani, J. V., Renzi, A., L. A. DE LUCA, JR. & J. Antunes-rodrigues. (1992). opiate activation suppresses the drinking, pressor and natriuretic responses induced by cholinergic stimulation of the medial septal area. Brain Research Bulletin, 28, 155-160.
Iovino, M., Monteleone, P. & Annuziato, L. (1985). Effect of nicotine on drinking and diuresis in septal lesioned rats. Physiology & Behavior, 34, 307-309.
Iovino, M., Poenaru, S. & Annuziato, L. (1983). Basal and Thirst-evoked vasopressin secretion in rats with electrolytic lesion of the medioventral septal area. Brain
Research Bulletin; 17, 823-828.
Isaacson, R. L. (1982). The Limbic System, 137-168. New York: Binghamton.
Johnson, A. K. & Edwards, G. L. (1990). The neuroendocrinology of thirst: afferent signaling and mechanisms of central integration. In Ganten, D. & Pfaff, D. (Eds.)
Current Topics in Neuroendocrinology, 10, 149-190. Springer-Verlag Berlin Heidelberg.
Lee, H. Y., Lin, Y. P. & Yin, T. H. (1987). Effects of lateral and medial septal lesions on various activity and reactivity measures in rats. Physiology & Behavior, 42
97-102.
Lind, R. W., Van Hoesen, G. W. & Johnson, A. K. (1982). An HRP study of connectons of the subfornical organ of the rat. Journal of Comparative Neurology, 210, 265-277.
Mason, S. T., Sanberg, P. R. & Fibiger, H. C. (1978). Kainic acid lesions of the striatum dissociate amphetamine and apomorphine stereotype: stimalarities to Huntington's
chorea: Science, 201, 352-355.
McCleary, R. A. (1966). Response-modulation functions of the limbic system: initation and suppression. In Stellar, I . E. & Sprague, J. M. (Eds.). Progress in Physiological Psychology, 1, 209-272. New York: Raven Press.
McGeer, E. G., Olney, J. W. & McGeer, P. L. (1978). Kainic acid as a tool in Neurobiology, New York: Raven Press.
McGowan, M. K., Brown, B. & Grossman, S. P. (1988). Depletion of neurons from preoptic area impairs drinking to various dipsogens. Physiology & Behavior, 43, 815-822.
Montes, R., Garcia del Rio, C., Bolanos, J. & Mora, F.(1986) Adipsia-polydipsia induced by simultaneous lesion of the medioventral septum and anteroventral third ventricle
area in the rat. Brain Research Bulletin, 17, 823-828.
Moran, J. S. & Blass, E. M. (1976). Inhibition of drinking by septal stimulation in rats. Physiology & Behavior, 17, 23-27.
Myhrer, T. (1989). Exploratory behavior and reaction to novelty in rats: effects of medial and lateral septal lesions. Behavioral Neuroscience, 103,1226-1233.
Nicoll, R. A. (1985). The Septo-hippocampal projection: a model cholinergic pathway. Trends in Neuroscience, 12, 533-536.
Paxinos, G. & Waston, C. (1986). The Rat Brain in stereotaxic Coordinates. Sydney: Academic Press.
Peck, J. W. & Novin, D. (1971). Evidence that osmoreceptors mediating drinking in rabbits are in the lateral preoptic area. Journal of Comparative and Physiological Psychology, 74, 134-147.
Pepeu, G., Mulas, A., Ruffi, A., & Sotgiu, P. (1971). Brain acetylcholine levels in rats with septal lesions. Life Science, 10, 181-184.
Rowland, N. (1976). Circadian rhythms and partial recovery of regulatory drinking after lateral hypothalamic lesions. Journal of Comparative and Physiological Psychology, 90, 382-393.
Sagvolden, T. (1982). Continuous reinforcement of responding for water in rats with medial or dorsolateral septal lesions: effect of deprivation level. Behavioral and Neural Biology, 34, 372-383.
Simpson, J. B., Epstein, A. N. & Camardo, J. S., Jr. (1978). The localization of dipsogenic receptors for angiotensin 2 in the subfornical organ. Journal of Comparative and Physiological Psychology, 92, 581-608.
Sorensen, J. P. Jr. & Harvey, J. A. (1971). Brain acetylcholine after septal lesions in rats: Correlation with thirst. Physiology & Behavior, 6, 723-725.
Stricker, E. M. (1978). Excessive drinking by rats with septal lesions during hypovolemia induced by subcutaneous colloid treatment. Physiology & Behavior, 21, 905-907.
stricker, E. M. (1984). Thirst and sodium appetite after colloid treatment in rats with septal lesions. Behavioral Neuroscience, 98, 356-360.
stricker, E. M., Gannon, K. S. & Smith, J. C. (1991). Thirst and salt appetite induced by hypovolemia in rats: analysis of drinking behavior. Physiology & Behavior, 51, 27-37.
Swanson, L. W. & Cowan, W. M. (1976). Autoradiographic studies of the development and connections of the septal area in the rat. In DeFrance, J. F. (Ed.). The Septal Nuclie: Advances ln Behavioral Bio l ogy, 20,37-64. New York: Plenum Press.
Tagzouti, K., simon, H., Tazi, A. Dantzer, R. & Moal, M. L. (1985). The effect of 6-0HDA lesions of the lateral septum on schedule-induced polydipsia. Behavioral Brain Research, 15, 1-8.
Thorne, B. M., Lin, K. & Weaver, M. L. (1983). water intake after septal damage in long-evans hooded rats and muricide, irritability .to handling and open-field activity
. Physiological Psychology, 11, 73-77.
Winn, P. (1990). Cholinergic stimulation of substantia nigra: effects on feeding, drinking and sexual behavior in the male rat. Psychopharmacology, 104, 208-214.