The Amygdala Modulates Memory Consolidation of Fear-Motivated Inhibitory Avoidance Learning But Not Classical Fear Conditioning

Wilensky, Ann E.; Schafe, Glenn E.; LeDoux, Joseph E.

doi:10.1523/jneurosci.20-18-07059.2000

Cited by 246 publications

(175 citation statements)

References 45 publications

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“…The results of Experiment 2 also indicate that unilateral intra-BLA infusions of Musc or lidocaine did not affect retention when infused into either the right or left BLA. The lack of effect on retention by Musc and lidocaine is not due to a dosage issue, as previous findings indicate that bilateral intra-amygdala/BLA infusions of the doses used in the current study impair retention (ColemanMesches and McGaugh 1995;Wilensky et al 2000). These findings suggest that the right BLA, but not the left, is involved in the enhancing modulation of memory consolidation induced by intra-BLA infusions and that either BLA alone, intact, and unmanipulated, is sufficient for normal retention.…”

Section: Lateralization Of Memory Enhancement To the Rightblasupporting

confidence: 66%

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

Learn. Mem.

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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 Rightblasupporting

confidence: 66%

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

Learn. Mem.

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“…Consonant with such view, a number of studies have shown a high density of BDZ sites in the BLA (Niehoff and Kuhar, 1983) and a clear anticonflict effect after the local infusion of BDZ in the BLA (see review by Davis, 1997). Moreover, the pharmacological stimulation of GABA A sites or the stimulation of GABAergic neurotransmission in the BLA induced a robust decrease of fear learning (Wilensky et al, 2000). In fact, inactivation of BLA neurons with a GABA A receptor agonist reduces both the acquisition and expression of fear conditioning (Helmstetter and Bellgowan, 1994;Muller et al, 1997;Wilensky et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Increased Fear Learning Coincides with Neuronal Dysinhibition and Facilitated LTP in the Basolateral Amygdala following Benzodiazepine Withdrawal in Rats

Isoardi

Martijena

Carrer

et al. 2004

Neuropsychopharmacol

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Animals chronically administered with diazepam (DZM -2 mg/kg/day i.p.) or vehicle (VEH) for 21 days were tested in a fear-conditioning paradigm 4 days after the last administration. Increased freezing was observed in DZM withdrawn rats as compared to VEH injected control rats in both associative and nonassociative context and this increase was greatest for the DZM withdrawal group in the paired context. In animals anesthetized with urethane, single pulses in the medial prefrontal cortex evoked a field potential including a population spike (PS) in the basolateral complex of the amygdala (BLA) of control animals, whereas in DZM withdrawn animals multiple PSs were evoked. In brain slices from control rats, stimulation of the external capsule evoked a field potential including a PS in the BLA, whereas in DZM withdrawn rats multiple PSs were evoked. The amplitude of the PS was smaller in slices obtained from DZM withdrawn rats than from control rats, and paired pulse inhibition was significantly less in the former. Perfusion with DZM 2 mM of slices obtained from DZM withdrawn rats eliminated repetitive spiking. GABAergic blockade with 50 mM picrotoxin in control rats resulted in the appearance of multiple secondary PSs. In slices from DZM withdrawn rats high-frequency stimulation induced a highly significant potentiation that lasted at least 2 h (LTP), whereas in control rats the same stimulation did not induce LTP. Neuronal hyperexcitability leading to facilitated LTP observed in BLA of DZM withdrawn rats could be due to depressed GABAergic activity (dysinhibition). The increased synaptic plasticity may be at the root of the increased fear learning observed in withdrawn animals.

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“…NE agonists infused directly into the amygdala immediately after training enhanced retention (Liang et al 1986(Liang et al , 1990. GABA agonists infused directly into the amygdala immediately after training impaired retention (Castellano et al 1989;Willensky et al 2000). Amygdala is reported to play a crucial role, preferentially in avoidance learning than spatial learning (Takashina et al 1995) and is also involved with the formation of enhanced declarative memory for emotionally arousing events (Adolphs et al 1997;Cahill and McGaugh 1998;Hamann et al 1997).…”

Section: Memory Retention and Cognitionmentioning

confidence: 99%

Psychomotor functions at various weeks of chronic renal failure in rats

Chandanathil¹,

Upadhya

Bhat³

2014

Cogn Neurodyn

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In chronic renal failure there is a gradual retention of substances in the tissues and body fluids, called as uremic retention toxins, which can bring about a number of biochemical activities in the body. Chronic renal insufficiency also leads to progressive behavioural conflict. Uremic toxins can affect both the central and the peripheral nervous system. Uremic encephalopathy is also associated with problems in cognition and memory. To study the psychomotor functional disorders in rats with progressive chronic renal failure surgical nephrectomy was done by resection method. The animals were grouped into two control groups, Sham control (SC) and normal control (NC) and two uremic groups, moderate uremia (G M ) and severe uremia (G S ). Psychomotor analysis was done by passive avoidance and open field in these animals at 4, 8, 12, and 16 weeks. After the incubation period, the nephrectomised groups (G M and G S ) showed significant changes in exploratory, locomotor and emotional behaviour when compared to the controls (NC and SC). Psychomotor changes involve poor cognition, reduced memory, reduced locomotor activity and decreased exploratory drive and emotional disturbance like increased fear during the initial stages. During the later stages a restless behaviour was noticed, associated with diminished fear.

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The Amygdala Modulates Memory Consolidation of Fear-Motivated Inhibitory Avoidance Learning But Not Classical Fear Conditioning

Cited by 246 publications

References 45 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

Increased Fear Learning Coincides with Neuronal Dysinhibition and Facilitated LTP in the Basolateral Amygdala following Benzodiazepine Withdrawal in Rats

Psychomotor functions at various weeks of chronic renal failure in rats

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