Prenatal VPA exposure and changes in sensory processing by the superior colliculus

Frontiers in Integrative Neuroscience

Volumn 5, Issue , 2011, Pages

  Dendrinos, Georgia ^a   Hemelt, Marie ^a   Keller, Asaf ^a  

^a UNIVERSITY OF MARYLAND SCHOOL OF MEDICINE   (United States)

Author keywords

Rat; Sensory processing; Superior colliculus; Valproic acid

Indexed keywords

VALPROIC ACID;

ADULT ANIMAL; ANIMAL BEHAVIOR; ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; BRAIN NERVE CELL; CONTROLLED STUDY; FEMALE; IMMUNOHISTOCHEMISTRY; JUVENILE ANIMAL; NOCICEPTION; NONHUMAN; PRENATAL DRUG EXPOSURE; PREPULSE INHIBITION; RAT; SENSORY DYSFUNCTION; STARTLE REFLEX; STEREOLOGY; SUPERIOR COLLICULUS;

EID: 82255160720     PISSN: 16625145     EISSN: None     Source Type: Journal    
DOI: 10.3389/fnint.2011.00068     Document Type: Article

References (49)

1. Alsdorf, R., and Wyszynski, D. F. (2005). Teratogenicity of sodium valproate. Expert Opin. Drug. Saf. 4, 345-353.
2. Ardinger, H. H., Atkin, J. F., Blackston, R. D., Elsas, L. J., Clarren, S. K., Livingstone, S., Flannery, D. B., Pellock, J. M., Harrod, M. J., Lammer, E. J., Majewski, F., Schinzel, A., Toriello, H. V., Hanson, J. W., Optiz, J. M. and Reynolds, J. F. (1988). Verification of the fetal valproate syndrome phenotype. Am. J. Med. Genet. 29, 171-185.
3. Arndt, T. L., Stodgell, C. J., and Rodier, P. M. (2005). The teratologyofautism. Int. J. Dev. Neurosci. 23, 189-199.
4. Arpino, C., Brescianini, S., Robert, E., Castilla, E. E., Cocchi, G., Cornel, M. C., deVigan, C., Lancaster, P. A., Mer-lob, P., Sumiyoshi, Y., Zampino, G., Renzi, C., Rosano, A., and Mastroia-covo, P. (2000). Teratogeniceffectsof antiepileptic drugs: use of an International Database on Malforma-tionsand DrugExposure(MADRE). Epilepsia 41, 1436-1443.
5. Ayres, A. J. (1979). Sensory Integration and the Child. Los Angeles, CA: Western Psychological Services.
6. Baranek, G. T., Boyd, B. A., Poe, M. D., David, F. J., andWatson, L. R. (2007). Hyperresponsive sensory patterns in young children with autism, developmental delay, and typical development. Am. J. Ment. Retard. 112, 233-245.
7. Baranek, G. T., David, F. J., Poe, M. D., Stone, W. L., and Watson, L. R. (2006). Sensory experiences questionnaire: discriminating sensory features in young children with autism, developmental delays, and typical development. J. Child. Psy-chol. Psychiatry 47, 591-601.
8. Bar-Shalita, T., Vatine, J. J., Seltzer, Z., and Parush, S. (2009). Psychophysi-cal correlates in children with sensory modulation disorder (SMD). Physiol. Behav. 98, 631-639.
9. Ben-Ari, Y. (2002). Excitatory actions of gaba during development: the nature of the nurture. Nat. Rev. Neurosci. 3, 728-739.
10. Binkerd, P. E., Rowland, J. M., Nau, H., and Hendrickx, A. G. (1988). Evaluation of valproic acid (VPA) developmental toxicity and pharmacokinet-ics in Sprague-Dawleyrats. Fundam. Appl. Toxicol. 11, 485-493.
11. Crawley, J. N. (2004). Designing mouse behavioral tasks relevant to autistic-like behaviors. Ment. Retard Dev. Disabil. Res. Rev. 10, 248-258.
12. Fendt, M. (1999). Enhancement of pre-pulse inhibition after blockade of GABA activity within the superior colliculus. Brain Res. 833, 81-85.
13. Fendt, M., Li, L., and Yeomans, J. S. (2001). Brain stem circuits mediat-ing prepulse inhibition of the startle reflex. Psychopharmacology (Berl.) 156, 216-224.
14. Gruber, A. J., Calhoon, G. G., Shuster-man, I., Schoenbaum, G., Roesch, M. R., and O'Donnell, P. (2010). More is less: a disinhibited prefrontal cortex impairs cognitive flexibility. J. Neurosci. 30, 17102-17110.
15. Hargreaves, K., Dubner, R., Brown, F., Flores, C., and Joris, J. (1988). Anew and sensitive method for measuring thermal nociception in cutaneous hyperalgesia. Pain 32, 77-88.
16. Ingram, J. L., Peckham, S. M., Tisdale, B., and Rodier, P. M. (2000). Prenatal exposure of rats to valproic acid reproduces the cerebellar anomalies associatedwithautism. Neurotoxicol. Teratol. 22, 319-324.
17. Leret, M. L., Lecumberri, M., Garcia-Montojo, M., and Gonzalez, J. C. (2007). Role of maternal corticos-terone in the development and maturation of the aminoacidergic systems of the rat brain. Int. J. Dev. Neurosci. 25, 465-471.
18. Levav-Rabkin, T., Melamed, O., Clarke, G., Farber, M., Cryan, J. F., Dinan, T. G., Grossman, Y., and Golan, H. M. (2010). A sensitive period of mice inhibitory system to neonatal GABAenhancement byvigabatrin is brain region dependent. Neuropsy-chopharmacology 35, 1138-1154.
19. Lipton, J. W., Robie, H. C., Ling, Z., Weese-Mayer, D. E., and Carvey, P. M. (1998). The magnitude of brain dopamine depletion from prenatal cocaine exposure is a function of uterine position. Neurotoxicol. Tera-tol. 20, 373-382.
20. Lombardo, S. A., Leanza, G., Meli, C., Lombardo, M. E., Mazzone, L., Vincenti, I., and Cioni, M. (2005). Maternal exposure to the antiepilep-tic drug vigabatrin affects postnatal development in the rat. Neurol. Sci. 26, 89-94.
21. Loscher, W. (1982). Anticonvulsant and biochemical effects of inhibitors of GABA amino trans ferase and val-proic acid during subchronic treatment in mice. Biochem. Pharmacol. 31, 837-842.
22. Manent, J. B., Jorquera, I., Mazzuc-chelli, I., Depaulis, A., Perucca, E., Ben-Ari, Y., and Represa, A. (2007). Fetal exposure to GABA-acting antiepileptic drugs generates hippocampal and cortical dysplasias. Epilepsia 48, 684-693.
23. Mangeot, S. D., Miller, L. J., McIn-tosh, D. N., McGrath-Clarke, J., Simon, J., Hagerman, R. J., and Gold-son, E. (2001). Sensory modulation dysfunction in children with attention-deficit-hyperactivity disorder. Dev. Med. Child Neurol. 43, 399-406.
24. Markram, H., Rinaldi, T., and Mark, K. (2007). The intense world syndrome - an alternative hypothesis for autism. Front. Nerusosci. 1:77-96. doi:10. 3389/neuro.01.1.1.006.2007
25. Markram, K., and Markram, H. (2010). The intense world theory - a unifying theory of the neurobiology of autism. Front. Hum. Neurosci. 4:224. doi:10.3389/fnhum.2010.00224
26. Markram, K., Rinaldi, T., La Mendola, D., Sandi, C., and Markram, H. (2008). Abnormal fear conditioning and amygdala processing in an animal model of autism. Neuropsy-chopharmacology 33, 901-912.
27. Monyer, H., and Markram, H. (2004). Interneuron diversity series: molecular and genetic tools to study GABAergic interneuron diversity and function. Trends Neurosci. 27, 90-97.
28. Moore, S. J., Turnpenny, P., Quinn, A., Glover, S., Lloyd, D. J., Montgomery, T., and Dean, J. C. (2000). A clinical study of 57 children with fetal anticonvulsant syndromes. J. Med. Genet. 37, 489-497.
29. Owens, D. F., and Kriegstein, A. R. (2002). Is there more to GABA than synaptic inhibition? Nat. Rev. Neu-rosci. 3, 715-727.
30. Paxinos, G., and Watson, C. (1998). The Rat Brain in Stereotaxic Coordinates. San Diego: Academic Press.
31. Phiel, C. J., Zhang, F., Huang, E. Y., Guenther, M. G., Lazar, M. A., and Klein, P. S. (2001). Histone deacety-lase is adirect targetofvalproic acid, a potent anticonvulsant, mood stabilizer, and teratogen. J. Biol. Chem. 276, 36734-36741.
32. Redgrave, P., Simkins, M., McHaffie, J. G., and Stein, B. E. (1996). Nocicep-tive neurones in rat superior colliculus. II. Effects of lesions to the con-tralateral descending output pathway on nocifensive behaviours. Exp. Brain Res. 109, 197-208.
33. Rinaldi, T., Kulangara, K., Antoniello, K., and Markram, H. (2007). Elevated NMDAreceptor levels and enhanced postsynaptic long-term potentiation induced byprenatal exposure to val-proic acid. Proc. Natl. Acad. Sci. U. S. A. 104, 13501-13506.
34. Rinaldi, T., Perrodin, C., and Markram, H. (2008a). Hyper-connectivity and hyper-plasticity in the medial prefrontal cortex in the val-proic acid animal model of autism. Front. Neural Circuits 2:4. doi:10. 3389/neuro.04.004.2008
35. Rinaldi, T., Silberberg, G., and Markram, H. (2008b). Hyper-connectivity of local neocortical microcircuitry induced by prenatal exposure to valproic acid. Cereb. Cortex 18, 763-770.
36. Rodier, P. M., Ingram, J. L., Tisdale, B., and Croog, V. J. (1997). Linking etiologies in humans and animal models: studies of autism. Reprod. Toxicol. 11, 417-422.
37. Rodier, P. M., Ingram, J. L., Tisdale, B., Nelson, S., and Romano, J. (1996). Embryological origin for autism: develop mental anomalies of the cranial nerve motor nuclei. J. Comp. Neurol. 370, 247-261.
38. Rogers, S. J., and Ozonoff, S. (2005). Annotation: what do we know a bout sensory dysfunction in autism? A critical review of the empirical evidence. J. Child. Psychol. Psychiatry 46, 1255-1268.
39. Schneider, T., Labuz, D., and Przewlocki, R. (2001). Nociceptive changes in rats after prenatal exposure to val-proic acid. Pol. J. Pharmacol. 53, 531-534.
40. Schneider, T., and Przewlocki, R. (2005). Behavioral alterations in rats prena-tallyexposed to valproic acid: animal model of autism. Neuro psycho pharmacology 30, 80-89.
41. Schneider, T., Turczak, J., and Przewlocki, R. (2006). Environmental enrichment reverses behavioral alterations in rats pre-natally exposed to valproic acid: issues for a therapeutic approach in autism. Neuro psychopharmacology 31, 36-46.
42. Stein, B. E., and Meredith, M. A. (1993). The Merging of the Senses. Cambridge: MIT Press.
43. Stodgell, C. J., Ingram, J. L., O'Bara, M., Tisdale, B. K., Nau, H., and Rodier, P. M. (2006). Induction of the homeotic gene Hoxa1 through valproic acid's teratogenic mechanism ofaction. Neurotoxicol. Teratol. 28, 617-624.
44. Truitt, W. A., Sajdyk, T. J., Dietrich, A. D., Oberlin, B., McDougle, C. J., and Shekhar, A. (2007). From anxiety to autism: spectrum of abnormal social behaviors modeled by progressive disruption of inhibitory neuronal function in the basolateral amygdala in Wistar rats. Psychopharmacology (Berl.) 191, 107-118.
45. Vorhees, C. V. (1987). Behavioral ter-atogenicity of valproic acid: selective effects on behavior after prenatal exposure to rats. Psychopharmacology(Berl.) 92, 173-179.
46. Wagner, G. C., Reuhl, K. R., Cheh, M., McRae, P., and Halladay, A. K. (2006). A new neurobehavioral model of autism in mice: pre- and postnatal exposure to sodium val-proate. J. Autism Dev. Disord. 36, 779-793.
47. Won, H., Mah, W., Kim, E., Kim, J. W., Hahm, E. K., Kim, M. H., Cho, S., Kim, J., Jang, H., Cho, S. C., Kim, B. N., Shin, M. S., Seo, J., Jeong, J., Choi, S. Y., Kim, D., Kang, C., and Kim, E. (2011). GIT1 is associated with ADHD in humans and ADHD like behaviors in mice. Nat. Med. 17, 566-572.
48. Wyszynski, D. F., Nambisan, M., Surve, T., Alsdorf, R. M., Smith, C. R., and Holmes, L. B. (2005). Increased rate of major malformations in offspring exposed to valproate during pregnancy. Neurology 64, 961-965.
49. Yeomans, J. S., Lee, J., Yeomans, M. H., Steidl, S., and Li, L. (2006). Midbrain pathways for prepulse inhibition and startle activation in rat. Neuroscience 142, 921-929.