Nicotine-induced anxiogenic-like behaviours of rats in the elevated plus-maze: possible role of NMDA receptors of the central amygdala

2011 ◽  
Vol 26 (4) ◽  
pp. 555-563 ◽  
Author(s):  
Mohammad Reza Zarrindast ◽  
Arash Aghamohammadi-Sereshki ◽  
Ameneh Rezayof ◽  
Parvin Rostami

The objective of the present study was to investigate the possible role of the N-methyl-D-aspartate (NMDA) receptor system of the central amygdala (CeA) in the anxiogenic-like effect of nicotine. Male Wistar rats with cannulas aimed to the CeA were submitted to the elevated plus-maze (EPM). Intraperitoneal (i.p.) injections of nicotine (0.6 and 0.8 mg/kg) decreased percentage open arm time spent (%OAT) and percentage open arm entries (%OAE), but not locomotor activity, indicating an anxiogenic-like response. Bilateral intra-CeA microinjection of NMDA (0.005–0.1 μ g/rat) decreased %OAT, but not %OAE and locomotor activity. Moreover, intra-CeA microinjection of NMDA (0.05 μ g) with an ineffective dose of nicotine (0.4 mg/kg, i.p.) reduced %OAT and %OAE without effect on locomotor activity. On the other hand, intra-CeA microinjection of the NMDA receptor antagonist D-AP5 (0.05–0.5 μ g/rat) increased both %OAT and %OAE, showing an anxiolytic-like effect of the drug. Co-administration of the same doses of D-AP5 with nicotine (0.6 mg/kg, i.p.) increased %OAT and %OAE, but not locomotor activity. Intra-CeA microinjection of D-AP5 reversed the response induced by NMDA (0.1 μ g/rat) in the EPM. The results may support the possible involvement of glutamate transmission, through NMDA receptors of central amygdala in the anxiogenic-like effect of nicotine in the EPM task.

2004 ◽  
Vol 286 (3) ◽  
pp. R451-R464 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Shaun W. Phillips ◽  
Susan M. Barman

We tested the hypothesis that blockade of N-methyl-d-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 ± 8 and 24 ± 6% of control ( n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 ± 22 to 129 ± 13% of control; n = 4) and vertebral nerves (from 253 ± 41 to 154 ± 20% of control; n = 7) and mean arterial pressure (from 39 ± 7 to 21 ± 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.


2011 ◽  
Vol 26 (S2) ◽  
pp. 436-436
Author(s):  
M.R. Zarrindast ◽  
M. Nasehi ◽  
N. Heidari ◽  
A. Torkaman Boutorabi

IntroductionSome investigations showed that the glutamate receptors have critical role for cognition such as learning and anxiety in the brain.ObjectivesThe possible involvement of cholinergic system of dorsal hippocampus in the anxiolytic-like response induced by NMDA receptor antagonist, MK801 has been investigated in the present study.MethodsThe male wistar rats were used and the elevated plus maze apparatus has been used to test parameters (%OAT, %OAE, locomotor activity, grooming, rereading and defection) of anxiety-like behaviors.ResultsThe data indicated that intra-CA1 administration of MK801 (2 μg/rat) increased %OAT and %OAE but did not other exploratory behaviors, indicating an anxiolytic-like response. Moreover, intra-hippocampal injection of cholinergic receptor antagonists, mecamylamine (2 μg/rat) and scopolamine (4 μg/rat) by itselves, 5 min before testing increased %OAT and %OAE, but did not alter locomotor activity and other exploratory behaviors, suggesting anxiolytic-like behavior. On the other hand, intra-CA1 co-administration of ineffective doses of scopolamine (3 μg/rat), but not mecamylamine (1 μg/rat) with ineffective dose of MK801 (1 μg/rat) increased %OAT and %OAE.ConclusionThe data may indicate that the possible involvement of cholinergic system of CA1 on anxiolytic-like response induced by MK801.


2009 ◽  
Vol 202 (2) ◽  
pp. 171-178 ◽  
Author(s):  
Ameneh Rezayof ◽  
Sedighe-sadat Hosseini ◽  
Mohammad-Reza Zarrindast

1998 ◽  
Vol 275 (4) ◽  
pp. H1236-H1246 ◽  
Author(s):  
Maria Luz Aylwin ◽  
John M. Horowitz ◽  
Ann C. Bonham

Area postrema (AP) modulates cardiovascular function through excitatory projections to neurons in nucleus tractus solitarius (NTS), which also process primary sensory (including cardiovascular-related) input via the solitary tract (TS). The neurotransmitter(s) and their receptors in the AP-NTS pathway have not been fully characterized. We used whole cell recordings in voltage- and current-clamp modes in the rat brain stem slice to examine the role of ionotropic glutamatergic receptors and α2-adrenergic receptors in the pathway from AP to NTS neurons receiving visceral afferent information via the TS. In neurons voltage clamped at potentials from −100 to +80 mV, AP stimulation (0.2 Hz) evoked excitatory postsynaptic currents having a fast component blocked by the non- N-methyl-d-aspartate (NMDA) receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzoquinoxaline-7-sulfonamide (NBQX; 3 μM, n = 7) and a slow component blocked by the NMDA receptor antagonistdl-2-amino-5-phosphonovaleric acid (APV; 50 μM, n = 8). Although NBQX (3 μM, n = 14) abolished AP-evoked action potentials, APV (50 μM, n = 9 or 500 μM, n = 6) or yohimbine, (200 nM, n = 5 or 2 μM, n = 10) did not. Thus, although AP stimulation activates both non-NMDA and NMDA receptors on NTS neurons receiving TS input, only non-NMDA receptors are required for synaptic transmission.


2018 ◽  
Vol 150 ◽  
pp. 59-65 ◽  
Author(s):  
Rocio Donaire ◽  
Shannon E. Conrad ◽  
Joanna B. Thompson ◽  
Mauricio R. Papini ◽  
Carmen Torres

2011 ◽  
Vol 301 (2) ◽  
pp. R448-R455 ◽  
Author(s):  
Jason Wright ◽  
Carlos Campos ◽  
Thiebaut Herzog ◽  
Mihai Covasa ◽  
Krzysztof Czaja ◽  
...  

Intraperitoneal injection of CCK reduces food intake and triggers a behavioral pattern similar to natural satiation. Reduction of food intake by CCK is mediated by vagal afferents that innervate the stomach and small intestine. These afferents synapse in the hindbrain nucleus of the solitary tract (NTS) where gastrointestinal satiation signals are processed. Previously, we demonstrated that intraperitoneal (IP) administration of either competitive or noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonists attenuates reduction of food intake by CCK. However, because vagal afferents themselves express NMDA receptors at both central and peripheral endings, our results did not speak to the question of whether NMDA receptors in the brain play an essential role in reduction of feeding by CCK. We hypothesized that activation of NMDA receptors in the NTS is necessary for reduction of food intake by CCK. To test this hypothesis, we measured food intake following IP CCK, subsequent to NMDA receptor antagonist injections into the fourth ventricle, directly into the NTS or subcutaneously. We found that either fourth-ventricle or NTS injection of the noncompetitive NMDA receptor antagonist MK-801 was sufficient to inhibit CCK-induced reduction of feeding, while the same antagonist doses injected subcutaneously did not. Similarly fourth ventricle injection of d-3-(2-carboxypiperazin-4-yl)-1-propenyl-1-phosphoric acid (d-CPPene), a competitive NMDA receptor antagonist, also blocked reduction of food intake following IP CCK. Finally, d-CPPene injected into the fourth ventricle attenuated CCK-induced expression of nuclear c-Fos immunoreactivity in the dorsal vagal complex. We conclude that activation of NMDA receptors in the hindbrain is necessary for the reduction of food intake by CCK. Hindbrain NMDA receptors could comprise a critical avenue for control and modulation of satiation signals to influence food intake and energy balance.


2002 ◽  
Vol 60 (1) ◽  
pp. 15-26 ◽  
Author(s):  
Juan Carlos Martı́nez ◽  
Fernando Cardenas ◽  
Marisol Lamprea ◽  
Silvio Morato
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