Regulation of anxiety by GABAA receptors in the rat amygdala

Sanders, Steven W.; Shekhar, Anantha

doi:10.1016/0091-3057(95)00153-n

Cited by 281 publications

(189 citation statements)

References 15 publications

Supporting

Mentioning

173

Contrasting

Unclassified

Order By: Relevance

“…We show that microinjection of the kainate agonist ATPA into the BLA can dosedependently increase anxiety-like behavior measured in a light/dark box, while having no effect on general locomotor activity. These observations are consistent with other microinjection studies showing that increased excitability within the BLA is associated with increased behavioral indices of anxiety-like behavior (Lack et al, 2007;Menard and Treit, 1999;Sanders and Shekhar, 1995). It has also been recently shown that i.p.…”

Section: Atpa-induced Synaptic Plasticity Is Inhibited By Acute Ethanolsupporting

confidence: 92%

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

et al. 2008

View full text Add to dashboard Cite

The neurobiological mechanisms governing alcohol-induced alterations in anxiety-like behaviors are not fully understood. Given that the amygdala is a major emotional center in the brain and regulates the expression of both learned-fear and anxiety, neurotransmitter systems within the basolateral amygdala represent likely mechanisms governing the anxiety-related effects of acute ethanol exposure. It is well established that, within the glutamatergic system, N-methyl-D-aspartate (NMDA)-type receptors, are particularly sensitive to intoxicating concentrations of ethanol. However, recent evidence suggests that kainate-type glutamate receptors are sensitive to ethanol as well. Therefore, we examined the effect of acute ethanol on kainate receptor (KA-R)-mediated synaptic transmission in the basolateral amygdala (BLA) of Sprague Dawley rats. Acute ethanol decreased KA-R-mediated excitatory postsynaptic currents (EPSCs) in the BLA in a concentrationdependent manner. Ethanol also inhibited currents evoked by focal application of the kainate receptor agonist (R, S)-2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl) propanoic acid (ATPA), and ethanol inhibition of kainate EPSCs was not associated with a change in paired-pulse ratio, suggesting a postsynaptic mechanism of ethanol action. The neurophysiological consequences of this acute sensitivity were tested by measuring ethanol's effects on KA-R-dependent modulation of synaptic plasticity. Acute ethanol, like the GluR5-specific antagonist (RS)-3-(2-carboxybenzyl)willardiine (UBP 296), robustly diminished ATPA-induced increases in synaptic efficacy. Lastly, to better understand the relationship between KA-R activity and anxiety-like behavior, we bilaterally microinjected ATPA directly into the BLA. We observed an increase in measures of anxiety-like behavior, assessed in the light/dark box, with no change in locomotor activity. This evidence suggests that kainate receptors in the BLA are inhibited by pharmacologically relevant concentrations of ethanol and may contribute to some of the acute anxiolytic effects of this drug.

show abstract

Section: Atpa-induced Synaptic Plasticity Is Inhibited By Acute Ethanolsupporting

confidence: 92%

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

et al. 2008

View full text Add to dashboard Cite

show abstract

“…In our previous studies utilizing Wistar rats, baseline SI duration ranged from 15 to 35 s, with a median duration of about 25 s (Sanders and Shekhar, 1995a;Sajdyk et al, 1999;Rainnie et al, 2004). In contrast, when we have utilized SpragueDawley rats, the baseline SI durations range from 40 to 70 s, with a median duration of about 50 s (Shekhar and Katner, 1995;Shekhar et al, 1996).…”

Section: Discussionmentioning

confidence: 79%

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

Lee

Fitz

Johnson

et al. 2008

Neuropsychopharmacol

View full text Add to dashboard Cite

Increased extra-hypothalamic corticotrophin-releasing factor (CRF) neurotransmission has been suggested as one putative factor in the pathophysiology of anxiety disorders. We have previously reported that administering repeated subanxiogenic doses (termed 'priming') of the CRF receptor agonist urocortin 1 (Ucn1) into the basolateral amygdala (BLA) of rats elicited long-lasting behavioral changes in social interaction (SI) and elevated plus maze (EPM) tests of anxiety. Although substantial similarity exists, the bed nucleus of the stria terminals (BNST) and the amygdala are thought to play distinct roles in anxiety responses. Rats primed with Ucn1 in the BLA not only demonstrated increased anxiety-like behaviors, but also physiological sensitivity to intravenous sodium lactate infusions, which is seen in subjects with panic or posttraumatic stress disorders, but not social or generalized anxiety disorders. In the present study, we tested if similar priming with subanxiogenic doses of Ucn1 in the BNST of rats will induce either chronic anxiety or sensitivity to sodium lactate. After determining the dose of Ucn1 that is subanxiogenic when injected into the BNST, repeated intra-BNST injections of this subanxiogenic dose of Ucn1 (6 fmol/100 nl) elicited persistent (present even after 4 weeks) anxiety-like responses in the SI but not EPM test. Prior local injection of a CRF receptor antagonist, astressin, into the BNST blocked this effect. Unlike Ucn1 priming in the BLA, rats primed in the BNST showed no cardiovascular changes following lactate infusion. Thus, BNST priming appears to selectively model the pathophysiology of subjects with anxiety syndromes like social anxiety, which are not lactate sensitive.

show abstract

“…Pharmacological studies showed that GABA A receptor activation increases chloride conductance and inhibits neuronal activity by hyperpolarisation or depolarisation block and attenuates anxietyand stress-related behavioural aberrations, whereas antagonists of this receptor usually enhance the behavioural sequelae generated by stressors and administration of these agents could induce behavioural disturbances and physiological changes comparable to those observed in stressed and anxious animals (21,23). Although some studies have reported that bicuculline generally has no specific effects on animal models of anxiety (24,25) and it has been suggested that anxiogenesis observed after bicuculline administration may be attributed to behavioural suppression rather than to any effect on anxiety (24), several studies have shown the anxiogenic effects of bicuculline when injected into different brain areas (9,26,27).…”

Section: Discussionmentioning

confidence: 99%

Activation of GABA_A receptors in the medial prefrontal cortex produces an anxiolytic-like response

Solati

Hajikhani

Golub

2013

Acta Neuropsychiatr.

View full text Add to dashboard Cite

Solati J, Hajikhani R, Golub Y. Activation of GABA A receptors in the medial prefrontal cortex produces an anxiolytic-like response.Objectives: There has been increasing evidence that the g-aminobutyric acid (GABA)ergic system is involved in the neurobiology of anxiety. The present study aimed to investigate the role of GABAergic systems in the modulation of anxiety in the medial prefrontal cortex (mPFC) of rats using the elevated plus maze test. Methods: Rats were anaesthetised with a mixture of ketamine and xylazine, and then special cannulae were inserted stereotaxically into the mPFC. After 5-7 days of recovery, the effects of intra-mPFC administration of GABAergic agents were studied. Results: Bilateral injection of the GABA A receptor agonist muscimol (0.25, 0.5 and 1 mg/rat) produces an anxiolytic-like effect, shown by significant increases in the percentage of open-arm time (%OAT) and percentage of open-arm entries (%OAE). Intra-mPFC administration of the GABA A receptor antagonist bicuculline (0.25, 0.5 and 1 mg/rat) produces significant anxiogenic-like behaviour. However, intra-mPFC injection of the GABA B receptor agonist baclofen (0.05, 0.1 and 0.2 mg/rat) and the GABA B receptor antagonist CGP35348 (5, 10 and 15 mg/rat) did not alter %OAT and %OAE significantly. Conclusion:The results of the present study demonstrate that the GABAergic system of the mPFC modulates anxiety-related behaviours of rats through GABA A receptors. Significant outcomes> Anxiety behaviours of animals are controlled by the g-aminobutyric acid (GABA)ergic system of the medial prefrontal cortex (mPFC).

show abstract

Regulation of anxiety by GABAA receptors in the rat amygdala

Cited by 281 publications

References 15 publications

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

Activation of GABA_A receptors in the medial prefrontal cortex produces an anxiolytic-like response

Contact Info

Product

Resources

About

Regulation of anxiety by GABAA receptors in the rat amygdala

Cited by 281 publications

References 15 publications

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

Repeated Stimulation of CRF Receptors in the BNST of Rats Selectively Induces Social but not Panic-Like Anxiety

Activation of GABAA receptors in the medial prefrontal cortex produces an anxiolytic-like response

Contact Info

Product

Resources

About

Activation of GABA_A receptors in the medial prefrontal cortex produces an anxiolytic-like response