Sat, 26 Jul 2008 05:49:57 BST CiteULike: awooga's immunology http://www.citeulike.org/user/awooga/tag/immunology CiteULike.org en-gb Copyright © 2004-2008 citeulike.org http://www.citeulike.org/user/awooga/article/2954891 <i>Cognition, Vol. 31, No. 1. (February 1989), pp. 1-44.</i><br /><br />Most biologists and some cognitive scientists have independently reached the conclusion that there is no such thing as learning in the traditional "instructive" sense. This is, admittedly, a somewhat extreme thesis, but I defend it here in the light of data and theories jointly extracted from biology, especially from evolutionary theory and immunology, and from modern generative grammar. I also point out that the general demise of learning is uncontroversial in the biological sciences, while a similar consensus has not yet been reached in psychology and in linguistics at large. Since many arguments presently offered in defense of learning and in defense of "general intelligence" are often based on a distorted picture of human biological evolution, I devote some sections of this paper to a critique of "adaptationism," providing also a sketch of a better evolutionary theory (one based on "exaptation"). Moreover, since certain standard arguments presented today as "knock-down" in psychology, in linguistics and in artificial intelligence are a perfect replica of those once voiced by biologists in favor of instruction and against selection, I capitalize on these errors of the past to draw some lessons for the present and for the future. Evolution, selection and cognition: from "learning" to parameter setting in biology and in the study of language. M Piattelli-Palmarini Cognition, Vol. 31, No. 1. (February 1989), pp. 1-44. 2008-07-03T03:29:34-00:00 1989 Cognition 0010-0277 31 1 1 44 cognitive-science evolution feedback immunology http://www.citeulike.org/user/awooga/article/2938727 <i>Behavioural Processes, Vol. 68, No. 3. (31 March 2005), pp. 283-287.</i> Manipulation: expansion of the paradigm Janice Moore Shelley Adamo Frédéric Thomas doi:10.1016/j.beproc.2004.10.005 Behavioural Processes, Vol. 68, No. 3. (31 March 2005), pp. 283-287. 2008-06-28T07:11:27-00:00 2005 Behavioural Processes 68 3 283 287 behaviour immunology neuromodulation parasitism http://www.citeulike.org/user/awooga/article/2820014 <i>Learn. Mem., Vol. 7, No. 6. (1 November 2000), pp. 400-412.</i><br /><br />Because exogenous application of a number of cytokines and growth factors can alter synaptic properties, we sought to determine if endogenous cytokine expression is affected by neuronal activity. In addition, we examined whether cytokine expression is altered by the techniques used to stimulate and record from hippocampal neurons. Using semi-quantitative RNase protection and RT-PCR assays, we studied the expression of 18 cytokine, growth factor, and receptor genes in the hippocampus following the induction of Schaffer collateral-CA1 long-term potentiation (LTP). We found that various cytokines are dramatically induced following preparation of slices for in vitro recording and as a result of injury following acute electrode placement in vivo. These increases can be overcome in vivo, however, using permanent electrodes implanted three weeks prior to testing. Using this chronic preparation, we found that interleukin-6 (IL-6) mRNA was upregulated nearly 20-fold by LTP induction in vivo, marking the first demonstration of endogenous regulation of this cytokine in response to LTP. In situ hybridization for IL-6 revealed that upregulation is tightly localized near the site of stimulation and is detected only in non-neuronal cells, identified as GFAP+ astrocytes and GFAP[-] cells within proximal blood vessels. Coupled with previous results showing that exogenously applied IL-6 can prevent the induction of LTP, this finding suggests a mechanism by which the local release of a cytokine could regulate LTP at nearby sites. 10.1101/lm.32600 Cytokine Responses to LTP Induction in the Rat Hippocampus: A Comparison of In Vitro and In Vivo Techniques Joanna Jankowsky Brian Derrick Paul Patterson doi:10.1101/lm.32600 Learn. Mem., Vol. 7, No. 6. (1 November 2000), pp. 400-412. 2008-05-21T13:22:43-00:00 2000 Learn. Mem. 7 6 400 412 cytokines electrophysiology hippocampus immunology ltp neuromodulation http://www.citeulike.org/user/awooga/article/2819825 <i>Proceedings of the National Academy of Sciences of the United States of America, Vol. 95, No. 13. (23 June 1998), pp. 7778-7783.</i><br /><br />It is widely accepted that interleukin-1beta (IL-1beta), a cytokine produced not only by immune cells but also by glial cells and certain neurons influences brain functions during infectious and inflammatory processes. It is still unclear, however, whether IL-1 production is triggered under nonpathological conditions during activation of a discrete neuronal population and whether this production has functional implications. Here, we show in vivo and in vitro that IL-1beta gene expression is substantially increased during long-term potentiation of synaptic transmission, a process considered to underlie certain forms of learning and memory. The increase in gene expression was long lasting, specific to potentiation, and could be prevented by blockade of potentiation with the N-methyl-D-aspartate (NMDA) receptor antagonist, (+/-)-2-amino-5-phosphonopentanoic acid (AP-5). Furthermore, blockade of IL-1 receptors by the specific interleukin-1 receptor antagonist (IL-1ra) resulted in a reversible impairment of long-term potentiation maintenance without affecting its induction. These results show for the first time that the production of biologically significant amounts of IL-1beta in the brain can be induced by a sustained increase in the activity of a discrete population of neurons and suggest a physiological involvement of this cytokine in synaptic plasticity. A neuromodulatory role of interleukin-1beta in the hippocampus. H Schneider F Pitossi D Balschun A Wagner A del Rey HO Besedovsky Proceedings of the National Academy of Sciences of the United States of America, Vol. 95, No. 13. (23 June 1998), pp. 7778-7783. 2008-05-21T13:04:22-00:00 1998 Proceedings of the National Academy of Sciences of the United States of America 0027-8424 95 13 7778 7783 cytokines electrophysiology hippocampus immunology ltp neuromodulation http://www.citeulike.org/user/awooga/article/2805355 <i>Endocrine reviews, Vol. 17, No. 1. (February 1996), pp. 64-102.</i> Immune-neuro-endocrine interactions: facts and hypotheses. HO Besedovsky A del Rey Endocrine reviews, Vol. 17, No. 1. (February 1996), pp. 64-102. 2008-05-16T14:23:56-00:00 1996 Endocrine reviews 0163-769X 17 1 64 102 cytokines immunology neuroendocrinology neuron-doctrine http://www.citeulike.org/user/awooga/article/2805289 <i>Brain Research Bulletin, Vol. 54, No. 4. (1 March 2001), pp. 329-338.</i><br /><br />cytokines and other products of the immune cells can modulate the action, differentiation, and survival of neuronal cells, while the neurotransmitter and neuropeptide release play a pivotal role in influencing the immune response. Cytokines and their receptors are constitutively expressed by and act on neurons in the central nervous system, in both its normal and its pathological state, but cytokine overexpression in the brain is an important factor in the pathogenesis of neurotoxic and neurodegenerative disorders. Accordingly, it can be accepted that the peripheral and central cytokine compartments appear to be integrated, and their effects might synergize or inhibit each other; however, it should always be taken into account that they are spatiotemporally differentially regulated. New concepts are reviewed in the regulation of relations between cytokine balance and neurodegeneration, including intracellular receptor-receptor, cell-cell, and systemic neuroimmune interactions that promote the further elucidation of the complexities and cascade of the possible interactions between cytokines and the central nervous system. Cytokines and the central nervous system Judith Szelényi doi:10.1016/S0361-9230(01)00428-2 Brain Research Bulletin, Vol. 54, No. 4. (1 March 2001), pp. 329-338. 2008-05-16T13:39:33-00:00 2001 Brain Research Bulletin 54 4 329 338 cytokine-balance cytokines immunology neuroendocrinology http://www.citeulike.org/user/awooga/article/2805288 <i>Brain, Behavior, and Immunity, Vol. 12, No. 4. (December 1998), pp. 249-271.</i><br /><br />Serotonin (5-HT) is one of the most extensively studied neurotransmitters of the central nervous system. 5-HT is, however, also present in a variety of peripheral tissues including in constituents of the immune system. The function of 5-HT in the immune system has received increasing attention since about 1984, but has been reviewed only once, in 1985. In recent years, modern techniques of molecular biology such as reverse-transcriptase polymerase chain reaction and targeted gene disruption have made it possible to study new important aspects of 5-HT in the immune system. In the first part of the review, we explore whether 5-HT is involved in interactions between the central nervous and immune systems. It emerges that 5-HT may mediate interactions of these two systems by four different pathways. In the second part, we dissect the functional roles of 5-HT in the immune system. We describe the distribution of 5-HT receptors and the 5-HT transporter on immune cells and estimate which levels 5-HT may attain in the extracellular space in physiological conditions and under pathological circumstances such as inflammation, thrombosis, and ischemia. At these 5-HT concentrations, four major functions for 5-HT emerge. These include T cell and natural killer cell activation, delayed-type hypersensitivity responses, production of chemotactic factors, and natural immunity delivered by macrophages. Finally, we discuss promising future avenues to further advance knowledge of the role of 5-HT in the immune system and in neuroimmune interactions. Role of Serotonin in the Immune System and in Neuroimmune Interactions Rainald Mössner Klaus-Peter Lesch doi:10.1006/brbi.1998.0532 Brain, Behavior, and Immunity, Vol. 12, No. 4. (December 1998), pp. 249-271. 2008-05-16T13:38:57-00:00 1998 Brain, Behavior, and Immunity 12 4 249 271 immunology neuroendocrinology serotonin http://www.citeulike.org/user/awooga/article/2805287 <i>Physiol. Rev., Vol. 79, No. 1. (1 January 1999), pp. 1-71.</i> Regulation of the Hypothalamic-Pituitary-Adrenal Axis by Cytokines: Actions and Mechanisms of Action Andrew Turnbull Catherine Rivier Physiol. Rev., Vol. 79, No. 1. (1 January 1999), pp. 1-71. 2008-05-16T13:37:55-00:00 1999 Physiol. Rev. 79 1 1 71 cytokines hypothalamus immunology http://www.citeulike.org/user/awooga/article/2795598 <i>Brief Bioinform, Vol. 2, No. 3. (1 January 2001), pp. 245-257.</i><br /><br />Like most other fields in biology, immunology has been revolutionised by the techniques of molecular biology and the resulting explosion in available experimental data. It is argued that efforts to integrate the data to gain insight into how various subsystems in the immune system interact and function require mathematical modelling and computer simulation in close collaboration with experimentalists. This paper illustrates some of the techniques available for modelling immune systems, and highlights the issues that should be borne in mind by anyone starting down the modelling path. 10.1093/bib/2.3.245 An approach to modelling in immunology Andrew Yates Cliburn Chan Robin Callard Andrew George Jaroslav Stark doi:10.1093/bib/2.3.245 Brief Bioinform, Vol. 2, No. 3. (1 January 2001), pp. 245-257. 2008-05-13T16:32:48-00:00 2001 Brief Bioinform 2 3 245 257 immunology modelling review http://www.citeulike.org/user/awooga/article/2794640 <i>Science, Vol. 180, No. 4088. (1973), pp. 871-872.</i><br /><br />Injection of rabbits with acetylcholine receptor highly purified from the electric organ of Electrophorus electricus emulsified in complete Freund's adjuvant resulted in the production of precipitating antibody to acetylcholine receptor. After the second injection of antigen, the animals developed the flaccid paralysis and abnormal electromyographs characteristic of neuromuscular blockade. Treatment with the anticholinesterases edrophonium or neostigmine dramatically alleviated the paralysis and the fatigue seen in electromyography. Autoimmune Response to Acetylcholine Receptor Jim Patrick Jon Lindstrom doi:10.2307/1736585 Science, Vol. 180, No. 4088. (1973), pp. 871-872. 2008-05-13T11:30:25-00:00 1973 Science 180 4088 871 872 American Association for the Advancement of Science acetylcholine immunology http://www.citeulike.org/user/awooga/article/2761137 <i>Brain, Behavior, and Immunity, Vol. In Press, Corrected Proof</i> Brief Commentary: Autistic children: A neuroimmune perspective Robert Dantzer Keith Kelley doi:10.1016/j.bbi.2008.03.001 Brain, Behavior, and Immunity, Vol. In Press, Corrected Proof 2008-05-06T13:26:59-00:00 Brain, Behavior, and Immunity In Press, Corrected Proof autism immunology http://www.citeulike.org/user/awooga/article/329647 <i>Nature Immunology, Vol. 6, No. 10. (21 September 2005), pp. 973-979.</i> Are innate immune signaling pathways in plants and animals conserved? Frederick Ausubel doi:10.1038/ni1253 Nature Immunology, Vol. 6, No. 10. (21 September 2005), pp. 973-979. 2005-09-22T05:54:07-00:00 2005 Nature Immunology 1529-2908 6 10 973 979 Nature Publishing Group immunology http://www.citeulike.org/user/awooga/article/945537 <i>Nature, Vol. 444, No. 7117., pp. 323-329.</i> The plant immune system Jonathan Jones Jeffery Dangl doi:10.1038/nature05286 Nature, Vol. 444, No. 7117., pp. 323-329. 2006-11-16T03:45:43-00:00 Nature 0028-0836 444 7117 323 329 Nature Publishing Group immunology http://www.citeulike.org/user/awooga/article/2483849 <i>Brain Research, Vol. 731, No. 1-2. (26 August 1996), pp. 1-11.</i><br /><br />Systemic administration of interleukin-2 (IL-2) provoked marked alterations of responding for rewarding brain stimulation from the medial forebrain bundle (MFB). In particular, when animals were tested for ICSS immediately following IL-2 treatment only a modest disturbance of responding was evident. However, if animals were subsequently exposed to repeated daily ICSS sessions (24-168 h) in the drug-free state, rightward shifts in the rate intensity functions and significant increases in reward thresholds were apparent. These results were dependent upon the presence of IL-2 during the initial ICSS session. If animals were tested for ICSS 24 h after IL-2 administration, without an intervening test, performance was unaffected. Evaluation of nonreinforced behavior after IL-2 treatment revealed that ICSS remained under stimulus control and the cytokine did not provoke reward-unrelated performance deficits. Dopamine (DA) activity in the nucleus accumbens has been implicated in goal-directed responding to positively reinforcing stimuli and in the present investigation, using in vivo microdialysis, it was observed that IL-2 markedly reduced DA release from this region. It was suggested that the protracted consequences of IL-2 on ICSS likely do not involve motoric, soporific, attentional or cognitive changes, but may be attributable to its specific actions on motivational arousal, possibly engendered by the cytokine-induced diminution of accumbal DA efflux. Interleukin-2 decreases accumbal dopamine efflux and responding for rewarding lateral hypothalamic stimulation Hymie Anisman L Kokkinidis Z Merali doi:10.1016/0006-8993(96)00460-X Brain Research, Vol. 731, No. 1-2. (26 August 1996), pp. 1-11. 2008-03-07T12:28:16-00:00 1996 Brain Research 731 1-2 1 11 cytokines dopamine hypothalamus immunology neuromodulation http://www.citeulike.org/user/awooga/article/2483856 <i>J. Neurosci., Vol. 13, No. 8. (1 August 1993), pp. 3574-3581.</i> Interleukin-1 beta augments release of norepinephrine, dopamine, and serotonin in the rat anterior hypothalamus F Shintani S Kanba T Nakaki M Nibuya N Kinoshita E Suzuki G Yagi R Kato M Asai J. Neurosci., Vol. 13, No. 8. (1 August 1993), pp. 3574-3581. 2008-03-07T12:29:37-00:00 1993 J. Neurosci. 13 8 3574 3581 cytokines dopamine hypothalamus immunology neuromodulation noradrenaline serotonin http://www.citeulike.org/user/awooga/article/2483809 <i>Glia, Vol. 40, No. 2. (2002), pp. 140-155.</i><br /><br />Cytokines constitute a significant portion of the immuno- and neuromodulatory messengers that can be released by activated microglia. By virtue of potent effects on resident and invading cells, microglial cyto- and chemokines regulate innate defense mechanisms, help the initiation and influence the type of immune responses, participate in the recruitment of leukocytes to the CNS, and support attempts of tissue repair and recovery. Microglia can also receive cyto- and chemokine signals as part of auto- and paracrine communications with astrocytes, neurons, the endothelium, and leukocyte infiltrates. Strong responses and modulatory influences can be demonstrated, adding to the emerging view that microglial behavior is highly dependent on the (cytokine) environment and that reactions to a challenge may vary with the stimulation context. In principle, microglial activation aims at CNS protection. However, failed microglial engagement due to excessive or sustained activation could significantly contribute to acute and chronic neuropathologies. Dysregulation of microglial cytokine production could thereby promote harmful actions of the defense mechanisms, result in direct neurotoxicity, as well as disturb neural cell functions as they are sensitive to cytokine signaling. GLIA 40:140-155, 2002. © 2002 Wiley-Liss, Inc. Microglia as a source and target of cytokines Uwe-Karsten Hanisch doi:10.1002/glia.10161 Glia, Vol. 40, No. 2. (2002), pp. 140-155. 2008-03-07T12:17:49-00:00 2002 Glia 40 2 140 155 cytokines glia immunology