The effect of kindling of different nuclei in the left and right amygdala on anxiety in the rat

Adamec, Robert E.; Morgan, Hywel

doi:10.1016/0031-9384(94)90002-7

Cited by 118 publications

(60 citation statements)

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“…Additionally, lesions of the right BLA induced 6-h post-training induced greater retention impairment for contextual fear conditioning than did lesions of the left BLA (Baker and Kim 2004). Other previous findings indicated that kindling of the right BLA in rats is anxiogenic, whereas kindling of the left BLA is anxiolytic (Adamec and Morgan 1994) and that higher serotonin levels in the right amygdala correlate with greater anxiety in an elevated plus maze (Andersen and Teicher 1999). Recent studies indicate that activity of the right amygdala in human males and the left amygdala in human females during encoding of emotionally arousing material correlates with long-term retention for the material (Cahill et al 2001(Cahill et al , 2004Canli et al 2002).…”

Section: Lateralization Of Memory Enhancement To the Rightblamentioning

confidence: 71%

Memory enhancement induced by post-training intrabasolateral amygdala infusions of β-adrenergic or muscarinic agonists requires activation of dopamine receptors: Involvement of right, but not left, basolateral amygdala

LaLumiere

McGaugh²

2005

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Previous findings indicate that the noradrenergic, dopaminergic, and cholinergic innervations of the basolateral amygdala (BLA) modulate memory consolidation. The current study investigated whether memory enhancement induced by post-training intra-BLA infusions of a ␤-adrenergic or muscarinic cholinergic agonist requires concurrent activation of dopamine (DA) receptors in the BLA. Rats with implanted BLA cannulae were trained on an inhibitory avoidance (IA) task and, 48 h later, tested for retention. Infusions of the ␤-adrenergic agonist clenbuterol into the right BLA, but not the left, enhanced retention, and concurrent infusions of the nonspecific DA receptor antagonist cis-Flupenthixol (Flu) blocked the enhancement. Post-training infusions of the muscarinic agonist oxotremorine into the right BLA also enhanced retention, and concurrent infusions of Flu blocked this effect. Additional experiments investigated whether memory modulation was lateralized to the right BLA. Post-training DA infusions into the right BLA, but not the left, enhanced retention. Post-training infusions of lidocaine or muscimol, which impair retention when infused bilaterally, had no effect when infused unilaterally into either the right or left BLA. These findings, together with earlier work, suggest that the dopaminergic system in the BLA is critically involved in memory modulation induced by noradrenergic and cholinergic influences. Additionally, these findings indicate that the enhancement, but not impairment, of memory consolidation is lateralized to the right BLA.Considerable evidence indicates that the dopaminergic, noradrenergic, and muscarinic cholinergic systems in the basolateral amygdala (BLA) play important roles modulating memory consolidation. Post-training intra-BLA infusions of noradrenergic agonists, norepinephrine, dopamine (DA), or muscarinic cholinergic agonists enhance retention of training in a variety of tasks (Introini-Collison et al. 1996;Hatfield and McGaugh 1999;LaLumiere et al. 2003LaLumiere et al. , 2004Power et al. 2003a;McGaugh 2004). Moreover, these systems are critical for memory modulation induced by other neurotransmitters or hormones. Post-training intra-BLA infusions of ␤-adrenoceptor antagonists block the memory-enhancing effects of opioid-peptidergic antagonists, glucocorticoid agonists, and DA (McGaugh et al. 1988;Quirarte et al. 1997;LaLumiere et al. 2004). Similarly, post-training intra-BLA infusions of muscarinic cholinergic antagonists block the memory-enhancing effects of glucocorticoid agonists, ␤-adrenergic agonists, and DA (Introini-Collison et al. 1996;Power et al. 2000;LaLumiere et al. 2004).Studies of the effects of DA receptor antagonists provide additional evidence suggesting that the dopaminergic system in the BLA is also critically involved in memory modulation. Post-training intra-BLA infusions of a D1 or D2 receptor antagonist impair retention for inhibitory avoidance (IA) training (LaLumiere et al. 2004), and post-training intra-BLA infusions of the nonspecific DA receptor antagon...

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Section: Lateralization Of Memory Enhancement To the Rightblamentioning

confidence: 71%

Memory enhancement induced by post-training intrabasolateral amygdala infusions of β-adrenergic or muscarinic agonists requires activation of dopamine receptors: Involvement of right, but not left, basolateral amygdala

LaLumiere

McGaugh²

2005

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“…Partial amygdala kindling also renders aggressive cats less aggressive but more defensively fearful [37]. Full kindling is anxiogenic as measured with the elevated plus maze [38,39]. The results of these experiments suggest that the kindling process alters the brain's response to fear provoking stimuli.…”

Section: Discussionmentioning

confidence: 85%

Phenytoin normalizes exaggerated fear behavior in p-chlorophenylalanine (PCPA)-treated rats

Hughes

Keele

2006

Epilepsy & Behavior

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Temporal lobe epilepsy may be associated with emotional difficulties such as depression or anxiety. Since the amygdala is involved in both epilepsy and emotion, common neural mechanisms in this temporal lobe structure may underlie the emotional disturbances observed in people with epilepsy. The neurotransmitter serotonin (5-hydroxytryptamine, or 5-HT) is implicated in many psychopathologies, and 5-HT also modulates amygdala excitability. Therefore, the present study used the fear potentiated startle (FPS) paradigm to investigate the effect of neuronal excitability on fear behavior in rats treated with p-chlorophenylalanine (PCPA) to chronically inhibit 5-HT synthesis. PCPA treatment selectively enhanced FPS in individually-housed rats. The exaggerated FPS response was reduced to control level by the anticonvulsant phenytoin (10mg/kg) and phenytoin (30 mg/kg) further decreased FPS behavior. These data suggest that a sub-seizure state of neuronal excitability mediated by low 5-HT in brain fear circuits may be associated with pathological fear behavior.

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“…For instance, it has been shown that short-term kindling of the right BLA has anxiogenic effects, whereas short-term kindling of the left BLA has anxiolytic effects (Adamec and Morgan 1994). It is also known that an asymmetrical seizureinduced breakdown of the blood-brain barrier can be obtained in rats (Kutlu et al 2002).…”

Section: Hemispheric Differencesmentioning

confidence: 99%

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

Schubert¹,

Siegmund²,

Pape³

et al. 2005

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Temporal lobe epilepsy (TLE) is often accompanied by interictal behavioral abnormalities, such as fear and memory impairment. To identify possible underlying substrates, we analyzed long-term synaptic plasticity in two relevant brain regions, the lateral amygdala (LA) and the CA1 region of the hippocampus, in the kindling model of epilepsy. Wistar rats were kindled through daily administration of brief electrical stimulations to the left basolateral nucleus of the amygdala. Field potential recordings were performed in slices obtained from kindled rats 48 h after the last induced seizure, and in slices from sham-implanted and nonimplanted controls. Kindling resulted in a significant impairment of long-term potentiation (LTP) in both the LA and the CA1, the magnitude of which was dependent on the number of prior stage V seizures. Saturation of CA1-LTP, assessed through repeated spaced delivery of high-frequency stimulation, occurred at lower levels in kindled compared to sham-implanted animals, consistent with the hypothesis of reduced capacity of further synaptic strengthening. Furthermore, theta pulse stimulation elicited long-term depression in the amygdala in nonimplanted and sham-implanted controls, whereas the same stimulation protocol stimulation caused LTP in kindled rats. In conclusion, kindling differentially affects the magnitude, saturation, and polarity of LTP in the CA1 and LA, respectively, most likely indicating an activity-dependent mechanism in the context of synaptic metaplasticity.Convulsive diseases in humans such as temporal lobe epilepsy (TLE) are often accompanied by impairments of learning and memory. In addition, TLE patients typically display emotional disturbances, in particular negative emotions such as fear, anxiety, and depression (Kalynchuk 2000). A wealth of data has established that the amygdala plays a critical role in neuronal activity and synaptic plasticity related to both emotionally modulated signal processing and epilepsy (Gloor 1990;Maren 1999;LeDoux 2000). Synapses in the amygdala display long-term potentiation (LTP) (Chapman and Chattarji 2000; LeDoux 2000; Maren 2001), a long-lasting increase of synaptic strength that is widely believed to be a cellular basis of learning and memory (Bliss and Collingridge 1993). The amygdala possesses the lowest threshold for the induction of kindling (Löscher 1997), an established experimental model of TLE in which daily electrical stimulation results in a gradual progression and intensification of limbic motor seizures (Goddard et al. 1969). Although kindling has been extensively investigated in the context of its clinical relevance to epilepsy and seizure-induced synaptic potentiation, only a few studies that relate to plastic synaptic changes after kindling are available. Therefore, the present study was undertaken to systematically analyze the influence of kindling 48 h after the last seizure on long-term synaptic plasticity, LTP, and long-term depression (LTD) in the lateral nucleus of the amygdala (LA) in rats. The LA was chosen ...

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The effect of kindling of different nuclei in the left and right amygdala on anxiety in the rat

Cited by 118 publications

References 56 publications

Memory enhancement induced by post-training intrabasolateral amygdala infusions of β-adrenergic or muscarinic agonists requires activation of dopamine receptors: Involvement of right, but not left, basolateral amygdala

Memory enhancement induced by post-training intrabasolateral amygdala infusions of β-adrenergic or muscarinic agonists requires activation of dopamine receptors: Involvement of right, but not left, basolateral amygdala

Phenytoin normalizes exaggerated fear behavior in p-chlorophenylalanine (PCPA)-treated rats

Kindling-induced changes in plasticity of the rat amygdala and hippocampus

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