BEHAVIOR ANALYSIS in NEUROSCIENCE - PART 8 docx

23 261 0
BEHAVIOR ANALYSIS in NEUROSCIENCE - PART 8 docx

Đang tải... (xem toàn văn)

Tài liệu hạn chế xem trước, để xem đầy đủ mời bạn chọn Tải xuống

Thông tin tài liệu

An Operant Analysis of Fronto-Striatal Function in the Rat 223 observational recording of behaviour, and also allows for a greater efficiency in collecting and processing data. In addition to allowing detailed functional studies, operant tests also allow a functional assessment of a wide variety of those surgical, cellular, or pharmacological interventions with potential clinical relevance. While hand testing and observational techniques may be more appropriate if the evaluation of a novel therapy is at an early stage, operant tasks allow for a fuller evaluation of the functional efficacy of treatments. Moreover, an understanding of how particular neural structures mediate function is crucial to the design of such interventions. 111 References 1. Wilson, S. A. K., An experimental research into the anatomy and physiology of the corpus striatum. Brain, 36, 492, 1914. 2. Jung, R. and Hassler, R., The extrapyramidal motor system, in The Handbook of Physiology. I. Neurophysiology, Volume 2. The American Physiological Society, Wash- ington, D.C., 1960, 863. 3. Huntington, G., On chorea. Adv. Neurol., 1, 33, 1872. 4. Huntington’s Disease Collaborative Research Group, A novel gene containing a trinu- cleotide repeat that is expanded and unstable on Huntington’s disease chromosomes. Cell, 72, 971, 1993. 5. Vonsattel, J P., Myers, R. H., and Stevens, T. J., Neuropathologic classification of Huntington’s disease. J. Neuropathol. Exp. Neurol., 44, 559, 1985. 6. Myers, R. H., Vonsattel, J P., Paskevich, P. A., Kiely, D. K., Stevens, T. J., Cupples, L. A., Richardson, E. P., and Bird, E. D., Decreased neuronal and increased oligoden- droglial densities in Huntington’s disease caudate nucleus. J. Neuropathol. Exp. Neu- rol., 50, 742, 1991. 7. Hedreen, J. C. and Folstein, S. E., Early loss of neostriatal striosome neurons in Huntington’s disease. J. Neuropathol. Exp. Neurol., 54, 105, 1995. 8. Fusco, F. R., Chen, Q., Lamoreaux, W. J., Figueredo-Cardenas, G., Jiao, Y., Coffman, J. A., Surmeier, D. J., Honig, M. G., Carlock, L. R., and Reiner, A., Cellular localization of huntingtin in striatal and cortical neurons in rats: Lack of correlation with neuronal vulnerability in Huntington’s disease. J. Neurosci., 19, 1189, 1999. 9. Davies, S. W., Turmaine, M., Cozens, B. A., DiFiglia, M., Sharp, A. H., Ross, C. A., Scherzinger, E., Wanker, E. E., Mangiarini, L., and Bates, G. P., Formation of neuronal intranuclear inclusions (NII) underlies the neurological dysfunction in mice transgenic for the HD mutation. Cell, 90, 537, 1997. 10. Ordway, J. M., Tallaksen-Greene, S., Gutekunst, C. A., Bernstein, E. M., Cearley, J. A., Wiener, H. W., Dure, L. S., Lindsey, R., Hersch, S. M., Jope, R. S., Albin, R. L., and Detloff, P. J., Ectopically expressed CAG repeats cause intranuclear inclusions and a progressive late onset neurological phenotype in the mouse. Cell, 91, 753, 1997. 11. Reddy, P. H., Charles, V., Williams, M., Miller, G., Whetsell, W. O., and Tagle, D. A., Transgenic mice expressing mutated full-length HD cDNA: a paradigm for locomotor changes and selective neuronal loss in Huntington’s disease. Phil. Trans. Roy. Soc. Lond. B, 354, 1035, 1999. 0704/C13/frame Page 223 Monday, July 17, 2000 5:33 PM © 2001 by CRC Press LLC 224 Methods of Behavior Analysis in Neuroscience 12. Hackam, A. S., Singaraja, R., Zhang, T. Q., Gan, L., and Hayden, M. R., In vitro evidence for both the nucleus and cytoplasm as subcellular sites of pathogenesis in Huntington’s disease. Hum. Mol. Genet., 8, 25, 1999. 13. DiFiglia, M., Sapp, E., Chase, K. O., Davies, S. W., Bates, G. P., Vonsattel, J P., and Aronin, N., Aggregation of huntingtin in neuronal intranuclear inclusions and dystro- phic neurites in brain. Science, 277, 1990, 1997. 14. Houk, J. C., Davis, J. L., and Beiser, D. G., Models of Information Processing in the Basal Ganglia, MIT Press, Cambridge MA, 1995. 15. Jahanshahi, M., Brown, R. G., and Marsden, C. D., A comparative study of simple and choice reaction time in Parkinson’s, Huntington’s and cerebellar disease. J. Neurol. Neurosurg. Psychiat., 56, 1169, 1993. 16. Girotti, F., Marano, R., Soliveri, P., Geminiani, G., and Scigliano, G., Relationship between motor and cognitive disorders in Huntington’s disease. J. Neurol., 235, 454, 1988. 17. Penney, J. B., Young, A. B., Shoulson, I., Starosta-Rubenstein, S., Snodgrass, S. R., Sanchez-Ramos, J., Ramos-Arrovo, M., Gomez, F., Penchas-Zadeh, G., Alvir, J., Esteves, J., Dequiroz, I., Marsol, N., Moreno, H., Conneally, P. M., Bonilla, E., and Wexler, N. S., Huntington’s disease in Venezuela — 7 years of follow-up on symp- tomatic and asymptomatic individuals. Mov. Dis., 5, 93, 1990. 18. Thompson, P. D., Berardelli, A., Rothwell, J. C., Day, B. L., Dick, J. P. R., Benecke, R., and Marsden, C. D., The coexistence of bradykinesia and chorea in Huntington’s disease and its implications for theories of basal ganglia control of movement. Brain, 111, 223, 1988. 19. Bradshaw, J. L., Phillips, J. G., Dennis, C., Mattingley, J. B., Andrewes, D., Chiu, E., Pierson, J. M., and Bradshaw, J. A., Initiation and execution of movement sequences in those suffering from and at risk of developing Huntington’s disease. J. Clin. Exp. Neuropsychol., 14, 179, 1992. 20. Brown, R. G. and Marsden, C. D., Subcortical dementia: the neuropsychological evidence. Neuroscience, 25, 363, 1988. 21. Butters, N., Sax, D., Montgomery, K., and Tarlow, S., Comparison of the neuropsy- chological deficits associated with early and advanced Huntington’s disease. Arch. Neurol., 35, 585, 1978. 22. Knopman, D. and Nissen, M. J., Procedural learning is impaired in Huntington’s disease — evidence from the serial reaction time task. Neuropsychologia, 29, 245, 1991. 23. Lange, K. W., Sahakian, B. J., Quinn, N. P., Marsden, C. D., and Robbins, T. W., Comparison of executive and visuospatial memory function in Huntington’s disease and dementia of Alzheimer-type matched for degree of dementia. J. Neurol. Neurosurg. Psychiat., 58, 598, 1995. 24. Lawrence, A. D., Sahakian, B. J., Hodges, J. R., Rosser, A. E., Lange, J. W., and Robbins, T. W., Executive and mnemonic functions in early Huntington’s disease. Brain, 119, 1633, 1996. 25. Harper, P. S., Huntington’s Disease, W.B. Saunders, London, 1996. 26. Laursen, A. M., Corpus striatum. Acta Physiol. Scand. suppl., 211, 1, 1963. 27. Coyle, J. T. and Schwarcz, R., Lesions of striatal neurones with kainic acid provides a model for Huntington’s chorea. Nature, 263, 244, 1976. 0704/C13/frame Page 224 Monday, July 17, 2000 5:33 PM © 2001 by CRC Press LLC An Operant Analysis of Fronto-Striatal Function in the Rat 225 28. Schwarcz, R. and Coyle, J. T., Striatal lesions with kainic acid: neurochemical char- acteristics. Brain Res., 127, 235, 1977. 29. McGeer, E. G. and McGeer, P. L., Duplication of the biochemical changes of Hunting- ton’s choreas by intrastriatal injection of glutamic and kainic acids. Nature, 263, 517, 1976. 30. Beal, M. F., Kowall, N. W., Ellison, D. W., Mazurek, M. F., Swartz, K. J., and Martin, J. B., Replication of the neurochemical characteristics of Huntington’s disease by quinolinic acid. Nature, 321, 168, 1986. 31. Beal, M. F., Ferrante, R. J., Swartz, K. J., and Kowall, N. W., Chronic quinolinic acid lesions in rats closely resemble Huntington’s disease. J. Neurosci., 11, 1649, 1991. 32. Schwarcz, R., Hökfelt, T., Fuxe, K., Jonsson, G., Goldstein, M., and Terenius, L., Ibotenic acid-induced neuronal degeneration: a morphological and neurochemical study. Exp. Brain Res., 37, 199, 1979. 33. Schwarcz, R., Whetsell, W. O., and Mangano, R. M., Quinolinic acid: an endogenous metabolite that produces axon-sparing lesions in rat brain. Science, 219, 316, 1983. 34. Beal, M. F., Brouillet, E. P., Jenkins, B. G., Ferrante, R. J., Kowall, N. W., Miller, J. M., Storey, E., Srivastava, R., Rosen, B. R., and Hyman, B. T., Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid. J. Neurosci., 13, 4181, 1993. 35. Borlongan, C. V., Koutouzis, T. K., and Sanberg, P. R., 3-Nitropropionic acid animal model and Huntington’s disease. Neurosci. Biobehav. Rev., 21, 289, 1997. 36. Meldrum, A., Page, K. J., Everitt, B. J., and Dunnett, S. B., Malonate: profile and mechanisms of striatal toxicity, in Mitochondrial Inhibitors as Tools for Neurobiology, P.R. Sanberg, H. Nishino, C.V. Borlongan, Eds., Humana, Totowa, NJ, 1999. 37. Mangiarini, L., Sathasivam, K., Seller, M., Cozens, B., Harper, A., Hetherington, C., Lawton, M., Trottier, Y., Lehrach, H., Davies, S. W., and Bates, G. P., Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell, 87, 493, 1996. 38. Hodgson, J. G., Agopyan, N., Gutekunst, C. A., Leavitt, B. R., LePiane, F., Singaraja, R., Smith, D. J., Bissada, N., McCutcheon, K., Nasir, J., Jamot, L., Li, X. J., Stevens, M. E., Rosemond, E., Roder, J. C., Phillips, A. G., Rubin, E. M., Hersch, S. M., and Hayden, M. R., A YAC mouse model for Huntington’s disease with full-length mutant huntingtin, cytoplasmic toxicity, and selective striatal neurodegeneration. Neuron, 23, 181, 1999. 39. Reddy, P. H., Williams, M., Charles, V., Garrett, L., Pike-Buchanan, L., Whetsell, W. O., Miller, G., and Tagle, D. A., Behavioural abnormalities and selective neuronal loss in HD transgenic mice expressing mutated full-length HD cDNA. Nature Genet., 20, 198, 1998. 40. Carter, R. J., Lione, L. A., Humby, T., Mangiarini, L., Mahal, A., Bates, G. P., Morton, A. J., and Dunnett, S. B., Characterisation of progressive motor deficits in mice transgenic for the human Huntington’s disease mutation. J. Neurosci., 19, 3248, 1999. 41. Lione, L. A., Carter, R. J., Bates, G. P., Morton, A. J., and Dunnett, S. B., Selective discrimination learning impairments in mice expressing the human Huntington’s dis- ease mutation. J. Neurosci., in press, 1999. 0704/C13/frame Page 225 Monday, July 17, 2000 5:33 PM © 2001 by CRC Press LLC 226 Methods of Behavior Analysis in Neuroscience 42. Dunnett, S. B., Isacson, O., Sirinathsinghji, D. J. S., Clarke, D. J., and Björklund, A., Striatal grafts in rats with unilateral neostriatal lesions. III. Recovery from dopamine- dependent motor asymmetry and deficits in skilled paw reaching. Neuroscience, 24 , 813, 1988. 43. Schwarcz, R., Fuxe, K., Agnati, L. F., Hökfelt, T., and Coyle, J. T., Rotational behavior in rats with unilateral striatal kainic acid lesions: a behavioural model for studies on intact dopamine receptors. Brain Res., 170, 485, 1979. 44. Fricker, R. A., Annett, L. E., Torres, E. M., and Dunnett, S. B., The locus of a striatal ibotenic acid lesion affects the direction of drug-induced rotation and skilled forelimb use. Brain Res. Bull., 41 , 409, 1996. 45. Borlongan, C. V., Randall, T. S., Cahill, D. W., and Sanberg, P. R., Asymmetrical motor behavior in rats with unilateral striatal excitotoxic lesions as revealed by the elevated body swing test. Brain Res., 676, 231, 1995. 46. Montoya, C. P., Astell, S., and Dunnett, S. B., Effects of nigral and striatal grafts on skilled forelimb use in the rat. Prog. Brain Res., 82, 459, 1990. 47. Kendall, A. L., Rayment, F. D., Torres, E. M., Baker, H. F., Ridley, R. M., and Dunnett, S. B., Functional integration of striatal allografts in a primate model of Huntington’s disease. Nature Med., 4, 727, 1998. 48. Skinner, B. F., The Behavior of Organisms, Appleton-Century-Crofts, New York, 1938. 49. Everitt, B. J., Fray, P., Kostarczyk, E., Taylor, S., and Stacey, P., Studies of instru- mental behavior with sexual reinforcement in male-rats (Rattus norvegicus). 1. Con- trol by brief visual stimuli paired with a receptive female. J. Comp. Psychol., 101, 395, 1987. 50. Sanberg, P. R., Pisa, M., and Fibiger, H. C., Avoidance, operant and locomotor behavior in rats with neostriatal injections of kainic acid. Pharmacol. Biochem. Behav., 10, 137, 1979. 51. Dunnett, S. B. and Iversen, S. D., Neurotoxic lesions of ventrolateral but not antero- medial neostriatum in rats impair differential reinforcement of low rates (DRL) per- formance. Behav. Brain Res., 6, 213, 1982. 52. Döbrössy, M. D., Svendsen, C. N., and Dunnett, S. B., The effects of bilateral striatal lesions on the acquisition of an operant test of short-term memory. NeuroReport, 6, 2059, 1995. 53. Reading, P. J., Dunnett, S. B., and Robbins, T. W., Dissociable roles of the ventral, medial and lateral striatum on the acquisition and performance of a complex visual stimulus-response habit. Behav. Brain Res., 45, 147, 1991. 54. Ungerstedt, U. and Arbuthnott, G. W., Quantitative recording of rotational behaviour in rats after 6-hydroxydopamine lesions of the nigrostriatal dopamine system. Brain Res., 24, 485, 1970. 55. Marshall, J. F., Richardson, J. S., and Teitelbaum, P., Nigrostriatal bundle damage and the lateral hypothalamic syndrome. J. Comp. Physiol. Psychol., 87, 808, 1974. 56. Evenden, J. L. and Robbins, T. W., Effects of unilateral 6-hydroxydopamine lesions of the caudate-putamen on skilled forepaw use in the rat. Behav. Brain Res., 14, 61, 1984. 57. Whishaw, I. Q., O’Connor, W. T., and Dunnett, S. B., The contributions of motor cortex, nigrostriatal dopamine and caudate-putamen to skilled forelimb use in the rat. Brain, 109, 805, 1986. 0704/C13/frame Page 226 Monday, July 17, 2000 5:33 PM © 2001 by CRC Press LLC An Operant Analysis of Fronto-Striatal Function in the Rat 227 58. Ljungberg, T. and Ungerstedt, U., Sensory inattention produced by 6-hydroxydopam- ine-induced degeneration of ascending dopamine neurons in the brain. Exp. Neurol., 53, 585, 1976. 59. Marshall, J. F. and Teitelbaum, P., Further analysis of sensory inattention following lateral hypothalamic damage in the rat. J. Comp. Physiol. Psychol., 86, 375, 1974. 60. Marshall, J. F., Turner, B. H., and Teitelbaum, P., Sensory neglect produced by lateral hypothalamic damage. Science, 174, 423, 1971. 61. Turner, B. H., Sensorimotor syndrome produced by lesions of the amygdala and lateral hypothalamus. J. Comp. Physiol. Psychol., 82, 37, 1973. 62. Carli, M., Evenden, J. L., and Robbins, T. W., Depletion of unilateral striatal dopamine impairs initiation of contralateral actions and not sensory attention. Nature, 313, 679, 1985. 63. Robbins, T. W., Muir, J. L., Killcross, A. S., and Pretsell, D., Methods of assessing attention and stimulus control in the rat, in Behavioural Neuroscience, Volume I, A. Sahgal, Ed., IRL Press, Oxford, 1993, 13. 64. Carli, M., Jones, G. H., and Robbins, T. W., Effects of unilateral dorsal and ventral striatal dopamine depletion on visual neglect in the rat: a neural and behavioural analysis. Neuroscience, 29, 309, 1989. 65. Mittleman, G., Brown, V. J., and Robbins, T. W., Intentional neglect following unilateral ibotenic acid lesions of the striatum. Neurosci. Res. Comm., 2, 1, 1988. 66. Brown, V. J. and Robbins, T. W., Deficits in response space following unilateral striatal dopamine depletion in the rat. J. Neurosci., 9, 983, 1989. 67. Brasted, P., Humby, T., Dunnett, S. B., and Robbins, T. W., Response space deficits following unilateral excitotoxic lesions of the dorsal striatum in the rat. J. Neurosci., 17, 8919, 1997. 68. Bisiarch, E. and Luzzatti, C., Unilateral neglect of representational space. Cortex, 14, 129, 1978. 69. Heilman, K. M., Neglect and related disorders, in Clinical Neuropsychology, K.M. Heilman, E.S. Valenstein, Eds., Oxford University Press, Oxford, 1979. 70. Divac, I., Rosvold, H. E., and Szwarcbart, M. K., Behavioral effects of selective ablation of the caudate nucleus. J. Comp. Physiol. Psychol., 63, 184, 1967. 71. Rosvold, H. E. and Delgado, J. M. R., The effect on delayed alternation test performance of stimulating or destroying electrically structures within the frontal lobes of the monkey’s brain. J. Comp. Physiol. Psychol., 49, 365, 1956. 72. Rosvold, H. E., The frontal lobe system: cortical-subcortical interrelationships. Acta Neurobiol. Exp., 32, 439, 1972. 73. Rosvold, H. E. and Szwarcbart, M. K., Neural structures involved in delayed response performance, in The Frontal Granular Cortex and Behavior, J.M. Warren, K. Akert, Eds., McGraw-Hill, New York, 1964, 1. 74. Leonard, C. M., The prefrontal cortex of the rat. I cortical projection of the mediodorsal neucleus. II Efferent connections. Brain Res., 12, 321, 1969. 75. Krettek, J. E. and Price, J. L., The cortical projections of the mediodorsal nucleus and adjacent thalamic nuclei in the rat. J. Comp. Neurol., 171, 157, 1977. 76. Divac, I., Markowitsch, H. J., and Pritzel, M., Behavioural and anatomical conse- quences of small intrastriatal injections of kainic acid in the rat. Brain Res., 151, 523, 1978. 0704/C13/frame Page 227 Monday, July 17, 2000 5:33 PM © 2001 by CRC Press LLC 228 Methods of Behavior Analysis in Neuroscience 77. Dunnett, S. B. and Iversen, S. D., Learning impairments following selective kainic acid-induced lesions within the neostriatum of rats. Behav. Brain Res., 2, 189, 1981. 78. Sanberg, P. R., Lehmann, J., and Fibiger, H. C., Impaired learning and memory after kainic acid lesions of the striatum: a behavioral model of Huntington’s disease. Brain Res., 149, 1204, 1978. 79. D’Amato, M. R., Delayed matching and short-term memory in monkeys. Psychol. Learn. Motiv., 7, 227, 1973. 80. Aggleton, J. P., One-trial object recognition by rats. Quart. J. Exp. Psychol. B., 37B, 279, 1985. 81. Dunnett, S. B., Comparative effects of cholinergic drugs and lesions of nucleus basalis or fimbria-fornix on delayed matching in rats. Psychopharmacology, 87, 357, 1985. 82. Dunnett, S. B., Operant delayed matching and non-matching to position in rats, in Behavioural Neuroscience: A Technical Approach, A. Sahgal, Ed., IRL Press, Oxford, 1993, 123. 83. Mishkin, M. and Manning, F. J., Non-spatial memory after selective prefrontal lesions in monkeys. Brain Res., 143, 313, 1978. 84. Kowalska, D. M., Bachevalier, J., and Mishkin, M., The role of the inferior prefrontal convexity in performance of delayed nonmatching-to-sample. Neuropsychologia, 29, 583, 1991. 85. Goldman-Rakic, P. S., Circuitry of primate prefrontal cortex and regulation of behavior by representational memory, in Handbook of Physiology — The Nervous System V, American Physiological Association, Baltimore, 1989, 373. 86. Dunnett, S. B., Role of prefrontal cortex and striatal output systems in short-term memory deficits associated with ageing, basal forebrain lesions, and cholinergic-rich grafts. Can. J. Psychol., 44, 210, 1990. 87. Döbrössy, M. D., Svendsen, C. N., and Dunnett, S. B., Bilateral striatal lesions impair retention of an operant test of short-term memory. Brain Res. Bull., 41, 159, 1996. 88. Dunnett, S. B., Is it possible to repair the damaged prefrontal cortex by neural tissue transplantation? Prog. Brain Res., 85, 285, 1990. 89. Jacobsen, C. F. and Nissen, H. W., Studies of cerebral function in primates. IV. The effect of frontal lobe lesions on the delayed alternation habit in monkeys. J. Comp. Psychol., 23, 101, 1937. 90. Jacobsen, C. F., Studies of cerebral function in primates. I. The functions of the frontal association areas in monkeys. Comp. Psychol. Monogr., 13, 3, 1936. 91. Campbell, P., Therapeutic horizons. Nature suppl., 392, 1, 1998. 92. Brown, R. G. and Marsden, C. D., Subcortical dementia — the neuropsychological evidence. Neuroscience, 25, 363, 1998. 93. Larsen, J. K. and Divac, I., Selective ablations within the prefrontal cortex of the rat and performance of delayed alternation. Physiol. Psychol., 6, 15, 1978. 94. Georgiou, N., Bradshaw, J. L., Phillips, J. G., and Chiu, E., Effect of directed attention in Huntington’s disease. J. Clin. Exp. Neuropsychol., 19, 367, 1997. 95. Brandt, J., Strauss, M. E., Larus, J., Jensen, B., Folstein, S. E., and Folstein, M. F., Clinical correlates of dementia and disability in Huntington’s disease. J. Cogn. Neu- ropsychol., 6, 401, 1984. 0704/C13/frame Page 228 Monday, July 17, 2000 5:33 PM © 2001 by CRC Press LLC An Operant Analysis of Fronto-Striatal Function in the Rat 229 96. Mogensen, J., Iversen, I. H., and Divac, I., Neostriatal lesions impaired rats delayed alternation performance in a T-maze but not in a two-key operant chamber. Acta Neurobiol. Exp., 47, 45, 1987. 97. Heise, G. A., Conner, R., and Martin, R. A., Effects of scopolamine on variable intertrial interval spatial alternation and memory in the rat. Psychopharmacology, 49, 131, 1978. 98. Numan, R. and Quaranta, J. R., Effects of medial septal lesions on operant delayed alternation in rats. Brain Res., 531, 232, 1990. 99. van Haaren, F., de Bruin, J. P. C., Heinsbroek, R. P. W., and van de Poll, N. E., Delayed spatial response alternation: effects of delay-interval duration and lesions of the medial prefrontal cortex on response accuracy of male and female Wistar rats. Behav. Brain Res., 18, 41, 1985. 100. Dunnett, S. B., Nathwani, F., and Brasted, P. J., Medial prefrontal and neostriatal lesions disrupt performance in an operant delayed alternation task in rats. Behav. Brain Res., in press, 1999. 101. Jacobsen, C. F. and Haslerud, G. M., Studies of cerebral function in primates. III. A note on the effect of motor and premotor lesions on delayed response in monkeys. Comp. Psychol. Monogr., 13, 66, 1936. 102. Isacson, O., Dunnett, S. B., and Björklund, A., Graft-induced behavioral recovery in an animal model of Huntington disease. Proc. Natl. Acad. Sci. U.S.A., 83, 2728, 1986. 103. Sanberg, P. R. and Coyle, J. T., Scientific approaches to Huntington’s disease. CRC Crit. Rev. Clin. Neurobiol., 1, 1, 1984. 104. Mogenson, G. J., Jones, D. L., and Yim, C. Y., From motivation to action: functional interface between the limbic system and the motor system. Prog. Neurobiol., 14, 69, 1980. 105. Berridge, K. C., Food reward: Brain substrates of wanting and liking. Neurosci. Biobe- hav. Rev., 20, 1, 1996. 106. Salamone, J. D., Kurth, P., McCullough, L. D., and Sokolowski, J. D., The effects of nucleus accumbens dopamine depletions on continuously reinforced operant respond- ing: Contrasts with the effects of extinction. Pharmacol. Biochem. Behav., 50, 437, 1995. 107. Salamone, J. D., Cousins, M. S., and Snyder, B. J., Behavioral functions of nucleus accumbens dopamine: Empirical and conceptual problems with the anhedonia hypoth- esis. Neurosci. Biobehav. Rev., 21, 341, 1997. 108. Hodos, W. and Kalman, G., Effects of increment size and reinforcer volume on pro- gressive ratio performance. J. Exp. Anal. Behav., 6, 387, 1963. 109. Eagle, D. M., Humby, T., Dunnett, S. B., and Robbins, T. W., Effects of regional striatal lesions on motor, motivational and executive aspects of progressive ratio performance in rats. Behav. Neurosci., in press, 1999. 110. Skjoldager, P., Pierre, P. J., and Mittleman, G., Reinforcer magnitude and progressive ratio responding in the rat: effects of increased effort, prefeeding and extinction. Learn. Motiv., 24, 303, 1993. 111. Dunnett, S. B. and Everitt, B. J., Topographic factors affecting the functional viability of dopamine-rich grafts in the neostriatum, in Cell Transplantation for Neurological Disorders, T.B. Freeman, J.H. Kordower, Eds., Humana Press, Totowa, NJ, 1998, 135. 0704/C13/frame Page 229 Monday, July 17, 2000 5:33 PM © 2001 by CRC Press LLC © 2001 by CRC Press LLC 14 Chapter Use of Autoshaping with Non-Delayed and Delayed Reinforcement for Studying Effects upon Acquisition and Consolidation of Information Sheldon B. Sparber Contents I. Introduction and Overview A. Choice of Autoshaping as a Behavioral Assay B. Wrongful Expectations of Simple, Linear Dose-Response Relationships C. Vasopressin and Enhanced Cognition or Arousal? D. Trimethyltin Neurobehavioral Toxicity and the Learning-Performance Distinction E. Effects of Pharmacological Manipulations Upon Performance: Problems of Interpretation F. Physostigmine and Autoshaping: Examples of Hypotheses Testing, Complex Experimental Design, and Data Analyses II. Materials and Methods 0704/C14/frame Page 231 Monday, July 17, 2000 5:36 PM Use of Autoshaping with Non-Delayed and Delayed Reinforcement 233 autoshaped behavior is primarily a classically conditioned behavior, an instrumen- tally conditioned behavior, a bridge between the two (S-R vs. R-S contingencies) or a new class of behavior with components of each, can be gleaned from the many chapters in the book edited by Locurto, Terrace and Gibbon 3 entitled Autoshaping and Conditioning Theory . Although the majority of studies dealing with the phenomenon of autoshaping have used a procedure whereby delivery of reinforcers was not contingent upon a specified response, my own laboratory has taken advantage of the automaticity and lack of experimenter-induced bias conveyed by autoshaping and we too have utilized a response-contingent component whereby the subject (normally a rat but we, as others 4 have, used autoshaping with chickens as well) is given the opportunity to manipulate its environment (e.g., touching the extended lever, initiating its retraction earlier than programmed to do so noncontingently) leading to the delivery of a reinforcing stimulus (e.g., food) slightly sooner than its delivery in the absence of an operant (lever touch) response. For protocols we generally use, the subject cannot earn more reinforcers during a daily session in which 12 to 30 or more trials are presented and their session lengths cannot be shortened by more than a fraction, thereby most likely obviating a shortened session length as a reinforcing outcome (i.e., trials without an autoshaped response typically are comprised of the presenta- tion of a retractable lever for 15 s, followed by retraction and either immediate delivery of a reinforcing stimulus or delaying the reinforcer for up to 8 or 9 s) followed by a random or fixed time ITI, typically averaging 45 s. By introducing a delay of reinforcement we believe we have introduced a so-called working memory component as a variation of the task and this has enabled us to demonstrate selective and specific effects of neurotoxic insults to the hippocampus and associated struc- tures ( vide infra ). As is often the case, behavioral toxicologists, behavioral pharmacologists and psychopharmacologists borrow procedures and protocols from the experimental and cognitive psychologists and because of their training and reliance upon concepts like dose-response relationships, often discover a need to systematically manipulate antecedent and consequential variables which had not previously been carried out adequately by others. Likewise, it may be necessary to modify the typical physical environment used by others so that drug-behavior studies can be carried out in such a manner that ancillary measures of unconditioned behaviors can also be recorded concurrently, either automatically or via closed circuit television monitors and video recorders for later off-line analyses. Because this contribution is for a book recommending and describing methods, I have chosen to discuss the advantages and disadvantages of the variations of autoshaping procedures we have used over the past 25 years. I have also included comments on theoretical and philosophical issues, where apparently appropriate, and discussions or comments about the technology used and choice of data collec- tion, reduction, and statistical analyses. The last points are not especially restricted to autoshaping as a behavioral paradigm, or to behavioral neuroscience in particular, but are important enough for a few comments at the outset because it has been my experience, in common with some colleagues, that as technological advances have enabled us to collect more 0704/C14/frame Page 233 Monday, July 17, 2000 5:36 PM © 2001 by CRC Press LLC © 2001 by CRC Press LLC 234 Methods of Behavior Analysis in Neuroscience and more data, at faster rates, not enough attention has been paid to the importance of experimental design, how the voluminous data will be handled once they are collected and the validity or appropriateness of whichever statistical analytical pro- cedures are used. In my laboratory this is a continuing, evolutionary process and we continue attempting to devise/design experiments which enable us to rely upon pre- planned statistical contrasts. To the credit of most psychologists and behavioral neuroscientists, at least reasonable attempts at dealing with these issues are more commonplace than has been my experience when attempting to interact or collab- orate with colleagues of a more reductionist persuasion. I have, on more than a few occasions, asked a colleague who points to the obviously more intense band or spot on a gel or chromatogram, derived from a single experiment (single subject’s or pooled tissue) that it is also obvious (at least living in the midwestern plains of the U.S.) that the world is flat. All one has to do is to look out of the window to confirm it. Of equally great concern (frustration?) is trying to convince a colleague that 5 to 10 experiment(s) carried out with xenopus oocytes expressing one or another recep- tor, but upon oocytes derived from a single female frog, is nothing more than one experiment with 5 to 10 replications and that standard parametric or nonparametric statistical analytical procedures designed for independent observations from indi- viduals (or parts thereof), randomly assigned to one or another treatment condition, are not appropriate, even if he/she is willing to consider using such statistical contrasts. Over the years we have used variations of autoshaped behavior acquisition and/or maintenance to study the actions of drugs or toxins upon this class of behavior(s) in mature experimental subjects, either exposed to a drug or toxin insult during development (e.g., in ovo [chick] or in utero [rat] ) or after exposure to drugs, withdrawal from them or exposure to toxins postnatally, at a more mature age. Other laboratories have followed our lead and have used identical or similar protocols to study the autoshaped acquisition of intravenous cocaine self-admin- istration, 5 to study the effects of experimenter-administered cocaine upon autoshaped behavior acquisition, 6 and to study effects of pyrogens/cytokines, which reportedly specifically disrupt or interfere with acquisition of food-rein- forced autoshaped behavior based upon the fact that the same behavior, once established, was not affected by the same treatment. 7 It has been the policy of my laboratory to attempt to give something back to the discipline from which we have borrowed theoretical and/or methodological underpinnings. I believe our contributions in this regard can be gleaned to some extent from the publication list appended to this chapter. Thus, I have chosen to emphasize some of the ways we have devised to maximize the use of autoshaped behavior in order to control for as many potential confounding variables which can interfere with design, implementation, and, most importantly, the interpretation of data derived from such studies. Almost of necessity, it is a quasi-chronology of the evolution of protocols currently in use in my laboratory (and those of colleagues who have asked for advice or patterned their work from one or more of our publications in which autoshaped behavior was one of the protocols we utilized). 0704/C14/frame Page 234 Monday, July 17, 2000 5:36 PM © 2001 by CRC Press LLC © 2001 by CRC Press LLC [...]... lever touches during the intertrial and delay of reinforcement intervals are typically recorded for each session Lever touches, when the lever is retracted (intertrial and reinforcement delay intervals) consist mainly of © 2001 by CRC Press LLC © 2001 by CRC Press LLC 0704/C14/frame Page 2 48 Monday, July 17, 2000 5:36 PM 2 48 Methods of Behavior Analysis in Neuroscience nose-poking behavior, although... Autoshaping Sessions 1 to 13 Treatment Session 1 Sessions 2–3 Sessions 4–7 Sessions 8 12 Session 13 Cg/D13ga Saline Saline Saline Saline 0.2 mg/kg D1G 0.2 mg/kg 0.2 mg/kg 0.2 mg/kg 0.067 mg/kg Saline HCG 0.2 mg/kg 0.2 mg/kg 0.2 mg/kg 0.067 mg/kg Saline PSGb 0.2 mg/kg 0.2 mg/kg 0.2 mg/kg 0.067 mg/kg Saline D4G Saline Saline 0.2 mg/kg 0.067 mg/kg Saline D8G Saline Saline Saline 0.2 mg/kg Saline a Control... experimental tool continues to this day A National Library of Medicine-Medline search, using trimethlytin and toxicity as index terms, brought up 229 citations, with about half appearing between 1990–1999 The learning-performance distinction or conundrum is all too often casually dispensed with, being considered less and less these days as investigators unschooled in behavioral neuroscience attempt... by refraining from engaging in lever-directed behaviors, having learned about the irrelevance of the lever.34 The rats treated with the high doses of TMT continue to engage in lever-directed exploratory behaviors, indicative of a reduced ability to learn to suppress behaviors toward stimuli which ordinarily should have lost their saliency or novelty.20 The divergent autoshaped lever touch behavioral... nontoxic doses of CH3Hg without the potential for introducing an experimenter bias by hand-shaping operant behavior during the learning phase Secondly, we were interested in determining if there were critical or sensitive periods during development when such exposure caused behavioral dysfunctional effects Lastly, we wanted to determine if autoshaping acquisition or performance, alone or upon a psychopharmacological... discussed in detail elsewhere,20,31,32 the dose-effect relationship between TMT and neurochemical or learning-performance variables is anything but linear or quasi-linear What we had concluded by the end of the 1 980 s was that doses of TMT that had the greatest effect upon binding of 3H-corticosterone to hippocampal cytosolic receptors interfered most with acquisition of autoshaping with a working memory... to sessions 1 and 2, the control group (CG/D13G) and the D4G and D8G were injected with saline The rats in the group injected with physostigmine while in their home cages (HCG) were injected with saline after their autoshaping sessions and the group injected with physostigmine after (post) autoshaping sessions (PSG) was injected with saline before the sessions For a more complete description of the experimental... Methods of Behavior Analysis in Neuroscience 254 50 D Session 8 Strip Touches 40 30 20 10 † 0 CG/D13G D8G D4G D1G HCG PSG Treatment Group FIGURE 14.1 (Continued) compared to the CG/D13G’s 9.11 ELT during Session 8, the D8G’s performance was significantly depressed only during Session 8 Thereafter, the D8G level of performance (ELTs) was not different from that of the CG/D13G As stated above, the group injected... Autoshaping with Non-Delayed and Delayed Reinforcement 255 Extended Lever Touches/12 Trials A CG/D13G 12 D1G 10 D4G D8G 8 6 4 ** * ** ** * * ** ** ** ** ** ** ** ** ** ** 2 * 0 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 Autoshaping Session FIGURE 14.2 Extended lever touches (ELT) during autoshaping sessions All groups were injected with 2 doses of saline or saline and 0.2 mg physostigmine/kg until Session 8, after... taken into account is the inverted U-shaped function often associated with drug studies on learning or memory, and the possible reason for the descending arm of the dose-effect curves, even if there is some evidence of learning enhancement If “high” doses of a drug like physostigmine are toxic (i.e., would fall on the descending arm of an inverted dose-effect curve) and, by definition, punishing in relation . Function in the Rat 227 58. Ljungberg, T. and Ungerstedt, U., Sensory inattention produced by 6-hydroxydopam- ine-induced degeneration of ascending dopamine neurons in the brain. Exp. Neurol., 53, 585 ,. mg/kg Saline D4G Saline Saline 0.2 mg/kg 0.067 mg/kg Saline D8G Saline Saline Saline 0.2 mg/kg Saline a Control Group injected once, prior to the 13th session. b Physostigmine injected post-sessions. 0704/C14/frame. of Behavior Analysis in Neuroscience 77. Dunnett, S. B. and Iversen, S. D., Learning impairments following selective kainic acid-induced lesions within the neostriatum of rats. Behav. Brain Res.,

Ngày đăng: 09/08/2014, 20:22

Tài liệu cùng người dùng

Tài liệu liên quan