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 JBBS  Vol.1 No.3 , August 2011
Anxiety-Behavior Modulated by Ventral Medial Prefrontal Cortex of Rats Submitted to the Vogel Conflict Test Involves a Local NMDA Receptor and Nitric Oxide
Abstract: It was demonstrated in the Vogel conflict test (VCT) that the ventral portion of medial prefrontal cortex (vMPFC) of rats is involved with anxiety behavior. Moreover, the vMPFC local glutamatergic and nitrergic system interaction is involved in modulation of fear conditioning, a model of anxiety. To better understand the role of the MPFC-glutamatergic and nitrergic system on the VTC behavior response, male Wistar rats (250 g) were water deprived for 48 h before the VCT. After 24 h of water deprivation, they were subjected to an initial 3-min non-punished (pre-test) drinking session. Twenty-four hours later bilateral microinjections of NMDA-antagonist LY235959 (4 nmol/200 nL), the specific nNOS inhibitor N-Propyl-L-arginine (N-Propyl –0.08 nmol/200 nL), the NO scavenger Carboxi-PTIO (C-PTIO, 2 nmol/200 nL) or 200nL of vehicle were applied in the vMPFC. After 10 min, the animals were submitted to 3-min punished-licking session. LY235959 increased the number of punished licks. Similar to LY235959, both N-Propyl and C-PTIO also increased the number of punished licks. No changes were observed when LY235959, N-Propyl and C-PTIO were micro- injected into vMPFC surrounding structures such as the cingulate cortex area 1, the corpus callosum and the tenia tecta. In control experiments these drugs did not change neither the number of unpunished licks nor had any effect in the tail-flick test. The results show that NO signaling in the vMPFC can modulate anxiety-behavior in the VCT by control punished behavior. Moreover, this NO modulation could be associated with local glutamatergic activation through NMDA receptors.
Cite this paper: nullS. Lisboa, F. Guimarães and L. Resstel, "Anxiety-Behavior Modulated by Ventral Medial Prefrontal Cortex of Rats Submitted to the Vogel Conflict Test Involves a Local NMDA Receptor and Nitric Oxide," Journal of Behavioral and Brain Science, Vol. 1 No. 3, 2011, pp. 181-187. doi: 10.4236/jbbs.2011.13024.
References

[1]   M. Abbruzzese, L. Bellodi, S. Ferri and S. Scarone, “Frontal Lobe Dysfunction in Schizophrenia and Obsessive-Compulsive Disorder: A Neuropsychological Study,” Brain and Cognition, Vol. 27, No. 2, 1995, pp. 202-212. doi:10.1006/brcg.1995.1017

[2]   L. R. Baxter Jr., J. M. Schwartz, B. H. Guze, K. Bergman and M. P. Szuba, “PET Imaging in Obsessive Com- pulsive Disorder with and without Depression,” Journal of Clinical Psychiatry, Vol. 51, Suppl. 61-69; 1990, discussion 70.

[3]   A. L. Malizia, “What Do Brain Imaging Studies Tell Us About Anxiety Disorders? Journal of Psychopharmacology, Vol. 13, No. 4, 1999, pp. 372-378. doi:10.1177/026988119901300418

[4]   C. H. Beck and H. C. Fibiger, “Conditioned Fear-Induced Changes in Behavior and in the Expression of the Immediate Early Gene C-Fos: With and without Diazepam Pretreatment,” The Journal of Neuroscience, Vol. 15, No. 1, 1995, pp. 709-720.

[5]   L. Lacroix, S. Spinelli, C. A. Heidbreder and J. Feldon, “Differential Role of the Medial and Lateral Prefrontal Cortices in Fear and Anxiety,” Behavioral Neuroscience, Vol. 114, No. 6, 2000, pp. 1119-1130. doi:10.1037/0735-7044.114.6.1119

[6]   A. A. Shah and D. Treit, “Excitotoxic Lesions of the Medial Prefrontal Cortex Attenuate Fear Responses in the Elevated-Plus Maze, Social Interaction and Shock Probe Burying Tests,” Brain Research, Vol. 969, No. 1-2, 2003, pp. 183-194. doi:10.1016/S0006-8993(03)02299-6

[7]   A. A. Shah and D. Treit, “Infusions of Midazolam into the Medial Prefrontal Cortex Produce Anxiolytic Effects in the Elevated Plus-Maze and Shock-Probe Burying Tests,” Brain Research, Vol. 996, No. 1, 2004, pp. 31-40. doi:10.1016/j.brainres.2003.10.015

[8]   Sullivan RM, Gratton A. Behavioral Effects of Excitotoxic Lesions of Ventral Medial Prefrontal Cortex in the Rat Are Hemisphere-Dependent, Brain Research, Vol. 927, No. 1, 2002, pp. 69-79. doi:10.1016/S0006-8993(01)03328-5

[9]   A. L. Jinks and I. S. McGregor, “Modulation of Anxiety- Related Behaviours Following Lesions of the Prelimbic or Infralimbic Cortex in the Rat,” Brain Research, Vol. 772, No. 1-2, 1997, pp. 181-190. doi:10.1016/S0006-8993(97)00810-X

[10]   L. B. Resstel and F. M. Correa, “Involvement of the Medial Prefrontal Cortex in Central Cardiovascular Modulation in the Rat,” Autonomic Neuroscience, Vol. 126-127, 2006, pp. 130-138. doi:10.1016/j.autneu.2006.02.022

[11]   L. B. Resstel, K. B. Fernandes and F. M. Correa, “Alpha- Adrenergic and Muscarinic Cholinergic Receptors Are Not Involved in the Modulation of the Parasympathetic Baroreflex by the Medial Prefrontal Cortex in Rats,” Life Sciences, Vol. 77, No. 13, 2005, pp. 1441-1451. doi:10.1016/j.lfs.2005.03.012

[12]   R. Dias, J. P. Aggleton, “Effects of Selective Excitotoxic Prefrontal Lesions on Acquisition of Nonmatching-and Matching-To-Place in the T-Maze in the Rat: Differential Involvement of the Prelimbic-Infralimbic and Anterior Cingulate Cortices in Providing Behavioural Flexibility,” Eur J Neurosci. Vol. 12, No. 12, 2000, pp. 4457-4466. doi:10.1046/j.0953-816X.2000.01323.x

[13]   L. B. Resstel, S. R. Joca, F. G. Guimaraes and F. M. Correa, “Involvement of Medial Prefrontal Cortex Neu- rons in Behavioral and Cardiovascular Responses to Contextual Fear Conditioning,” Neuroscience, Vol. 143, No. 2, 2006, pp. 377-385. doi:10.1016/j.neuroscience.2006.08.002

[14]   P. Flores and R. Pellon, “Antipunishment Effects of Diazepam on Two Levels of Suppression of Schedule-Induced Drinking in Rats,” Pharmacology Biochemistry and Behavior, Vol. 67, No. 2, 2000, pp. 207-214. doi:10.1016/S0091-3057(00)00313-0

[15]   M. J. Millan and M. Brocco, “The Vogel Conflict Test: Procedural Aspects, Gamma-Aminobutyric Acid, Glutamate and Monoamines,” European Journal of Pharmacology, Vol. 463, No. 1-3, 2003, pp. 67-96. doi:10.1016/S0014-2999(03)01275-5

[16]   J. R. Vogel, B. Beer and D. E. Clody, “A Simple and Reliable Conflict Procedure for Testing Anti-Anxiety Agents,” Psychopharmacologia, Vol. 21, 1971, pp. 1-7. doi:10.1016/S0014-2999(03)01275-5

[17]   L. B. Resstel, R. F. Souza, F. S. Guimaraes, “Anxiolytic- Like Effects Induced by Medial Prefrontal Cortex Inhibition in Rats Submitted to the Vogel Conflict Test,” Physiology & Behavior, Vol. 93, No. 1-2, 2008, pp. 200- 205. doi:10.1016/j.physbeh.2007.08.009

[18]   B. Moghaddam, “Stress Preferentially Increases Extra- neuronal Levels of Excitatory Amino Acids in the Prefrontal Cortex: Comparison to Hippocampus and Basal Ganglia,” Journal of Neurochemistry, Vol. 60, No. 5, 1993, pp. 1650-1657. doi:10.1111/j.1471-4159.1993.tb13387.x

[19]   L. B. Resstel, F. M. Correa and F. S. Guimaraes, “The Expression of Contextual Fear Conditioning Involves Activation of an NMDA Receptor-Nitric Oxide Pathway in the Medial Prefrontal Cortex,” Cerebral Cortex, Vol. 18, No. 9, 2008, pp. 2027-2035. doi:10.1093/cercor/bhm232

[20]   S. F. Lisboa, L. B. Resstel, D. C. Aguiar and F. S. Guimaraes, Activation of cannabinoid CB1 Receptors in the Dorsolateral Periaqueductal Gray Induces Anxiolytic Effects in Rats Submitted to the Vogel Conflict Test,” European Journal of Pharmacology, Vol. 593, No. 1-3, 2008, pp. 73-78. doi:10.1016/j.ejphar.2008.07.032

[21]   L. B. Resstel and F. M. Correa, “Injection of l-Glutamate into Medial Prefrontal Cortex Induces Cardiovascular Responses through NMDA Receptor—Nitric Oxide in Rat,” Neuropharmacology, Vol. 51, No. 1, 2006, pp. 160-167. doi:10.1016/j.neuropharm.2006.03.010

[22]   L. B. Resstel and F. M. Correa, “Medial Prefrontal Cortex NMDA Receptors and Nitric Oxide Modulate the Parasympathetic Component of the Baroreflex,” Euro- pean Journal of Neuroscience, Vol. 23, No. 2, 2006, pp. 481-488.doi:10.1111/j.1460-9568.2005.04566.x

[23]   H. Q. Zhang, W. Fast, M. A. Marletta, P. Martasek and R. B. Silverman, “Potent and Selective Inhibition of Neuronal Nitric Oxide Synthase by N omega-propyl- L-arginine,” Journal of Medicinal Chemistry, Vol. 40, No. 24, 1997, pp. 3869-3870. doi:10.1021/jm970550g

[24]   R. F. Tavares, L. B. Resstel and F. M. Correa, “Interaction between Glutamatergic and Nitrergic Mechanisms Mediating Cardiovascular Responses to L-Glutamate Injection in the Diagonal Band of Broca in Anesthetized Rats,” Life Science, Vol. 81, No. 10, 2007, pp. 855-862. doi:10.1016/j.lfs.2007.07.028

[25]   F. S. Guimaraes, V. Beijamini, F. A. Moreira, D. C Aguiar and A. C. de Lucca, “Role of Nitric Oxide in Brain Regions Related to Defensive Reactions,” Neuroscience & Biobehavioral Reviews, Vol. 29, No. 8, 2005, pp. 1313-1322. doi:10.1016/j.neubiorev.2005.03.026

[26]   J. Gigg, A. M. Tan and D. M. Finch, “Glutamatergic Hippocampal Formation Projections to Prefrontal Cortex in the Rat are Regulated by Gabaergic Inhibition And Show Convergence with Glutamatergic Projections From the Limbic Thalamus,” Hippocampus, Vol. 4, No. 2, 1994, pp. 189-198. doi:10.1002/hipo.450040209

[27]   M. M. Nicolle and M. G. Baxter, “Glutamate Receptor Binding in the Frontal Cortex and Dorsal Striatum of Aged Rats with Impaired Attentional Set-Shifting,” European Journal of Neuroscience, Vol. 18, No. 12, 2003, pp. 3335-3342. doi:10.1111/j.1460-9568.2003.03077.x

[28]   H. Y. Yun, V. L. Dawson and T. M. Dawson, “Nitric Oxide in Health and Disease of the Nervous System,” Molecular Psychiatry, Vol. 2, No. 4, 1997, pp. 300-310. doi:10.1038/sj.mp.4000272

[29]   A. Plaznik, W. Palejko, M. Nazar and M. Jessa, “Effects of Antagonists at the NMDA Receptor Complex in Two Models of Anxiety,” European Neuropsychopharmacology, Vol. 4, No. 4, 1994, pp. 503-512. doi:10.1016/0924-977X(94)90299-2

[30]   R. E. Adamec, P. Burton, T. Shallow and J. Budgell, “NMDA Receptors Mediate Lasting Increases in Anxiety-Like Behavior Produced by the Stress of Predator Exposure-Implications for Anxiety Associated with Posttraumatic Stress Disorder,” Physiology & Behavior, Vol. 65, No. 4-5, 1999, pp. 723-737. doi:10.1016/S0031-9384(98)00226-1

[31]   M. Jessa, M. Nazar, A. Bidzinski and A. Plaznik, “The Effects of Repeated Administration of Diazepam, MK- 801 and CGP 37849 on Rat Behavior in Two Models of Anxiety,” European Neuropsychopharmacology, Vol. 6, No. 1, 1996, pp. 55-61. doi:10.1016/0924-977X(95)00068-Z

[32]   S. F. Lisboa, M. F. Stecchini, F. M. Correa, F. S. Guimaraes and L. B. Resstel, “Different Role of the Ventral Medial Prefrontal Cortex on Modulation of Innate and Associative Learned Fear,” Neuroscience, Vol. 171, No. 3, pp. 760-768. doi:10.1016/j.neuroscience.2010.09.048

[33]   G. D. Fisk and J. M. Wyss, “Descending Projections of Infralimbic Cortex That Mediate Stimulation-Evoked Changes in Arterial Pressure,” Brain Research, Vol. 859, No. 1, 2000, pp. 83-95. doi:10.1016/S0006-8993(00)01935-1

[34]   R. P. Vertes, “Differential Projections of the Infralimbic and Prelimbic Cortex in the Rat,” Synapse, Vol. 51, No. 1, 2004, pp. 32-58. doi:10.1002/syn.10279

[35]   M. J. Millan, “The Neurobiology and Control of Anxious States,” Progress in Neurobiology, Vol. 70, No. 2, 2003, pp. 83-244. doi:10.1016/S0301-0082(03)00087-X

[36]   K. A, Corcoran and G. J. Quirk, “Activity in Prelimbic Cortex Is Necessary for the Expression of Learned, But Not Innate, Fears,” The Journal of Neuroscience, Vol. 27, No. 4, 2007, pp. 840-844. doi:10.1523/JNEUROSCI.5327-06.2007

 
 
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