Amygdaloid neurons respond to clozapine rather than haloperidol in behaving rats pretreated with intra-amygdaloid amphetamine

Wang, Zhongrui; Rebec, George V.

doi:10.1016/0006-8993(95)01401-2

Cited by 10 publications

(8 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In fact, intra-CeA infusions of amphetamine produced locomotion at a dose that was ineffective following ICV infusions. The dose-response curve for locomotion following intra-CeA infusions of amphetamine is consistent with previous research demonstrating that intra-CeA infusions of a high dose of amphetamine (10 g) do not alter stimulant behaviors, whereas infusions of a lower dose of amphetamine (5 g) produce an increase in locomotion and rearing irrespective of the amygdaloid nuclei (Carr and White 1987;Wang and Rebec 1996). The lack of locomotion at higher intra-CeA doses of amphetamine may be related to arousal processes, as stimulation of the CeA produces an arrest of ongoing behavior and an orienting response (see Kapp et al 1992).…”

Section: Discussionsupporting

confidence: 89%

See 1 more Smart Citation

Behavioral Effects of Psychomotor Stimulant Infusions into Amygdaloid Nuclei

O’Dell

Sussman

Meyer

et al. 1999

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 89%

“…Furthermore, it is possible that other amygdaloid nuclei may play a role in initiating these behaviors. Indeed, Wang and Rebec (1996) demonstrated that unilateral infusions of amphetamine into the amygdala, but not directed at a specific nucleus, elicit rotational behavior, rearing, and sniffing.…”

mentioning

confidence: 99%

Behavioral Effects of Psychomotor Stimulant Infusions into Amygdaloid Nuclei

O’Dell

Sussman

Meyer

et al. 1999

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

“…Previous studies (Wang and Rebec 1996) have shown that clozapine blocked the electrical and behavioral excitatory effects of intra-amygdala infusion of amphetamine, whereas, haloperidol failed to reverse the increase in neuronal activity and only partially blocked the behavioral activation. Moreover, FLI studies (Sebens et al 1995) have shown that clozapine induced a higher increase of FLI in the central amygdaloid nucleus, as compared to haloperidol.…”

Section: Fos-like-immunoreactivity After Haloperidolmentioning

confidence: 76%

“…Induction of the early gene c-fos by antipsychotics in the central amygdaloid nucleus (Sebens et al 1995) and antagonism of the excitatory effects induced by a local infusion of amphetamine in the amygdaloid complex by clozapine (Wang and Rebec 1996) have been reported. Moreover, it was recently shown (Beck 1994;Duncan et al 1996;Morelli et al 1999) that antidepressant drugs inhibiting either noradrenaline or serotonin re-uptake, induced the expression of the early gene c-fos in areas belonging to the rat extended amygdala, suggesting a role of the extended amygdala in disorders characterized by affective disturbance.…”

mentioning

confidence: 99%

Differential Induction of Fos-Like-Immunoreactivity in the Extended Amygdala after Haloperidol and Clozapine

Pinna

Morelli

1999

Neuropsychopharmacology

View full text Add to dashboard Cite

The extended amygdala is composed of the central and medial amygdaloid nucleus which through the sublenticular extended amygdala (SLEA) and the interstitial nucleus of the posterior limb of the anterior commissure (IPAC) merge into the bed nucleus of stria terminals (BST). Based on anatomical connections with limbic areas, the extended amygdala has been proposed to play an important role in cognitive and affective processes. This study examines the effect of the atypical antipsychotic clozapine and the classical antipsychotic haloperidol on Fos-like-immunoreactivity (FLI) induction in areas belonging to the extended amygdala.Acute administration of clozapine (10-20 mg/kg) The amygdaloid complex is an ensemble of nuclei that play a central role in emotional processes, particularly in the assignment of affective significance to specific stimuli (Aggleton 1993;Aggleton and Mishkin 1985;Gallagher and Chiba 1996;Le Doux 1995). Information elaborated in the basolateral amygdaloid nuclei enter into the central amygdaloid nucleus, which conveys the stimuli together to elicit appropriate behavioral responses (Pitkänen et al. 1997).Neuronal cell groups composing the central and medial amygdaloid nucleus form a continuum of cells that extend through the sublenticular extended amygdala (SLEA) and the interstitial nucleus of the posterior limb of the anterior commissure (IPAC) to merge with the bed nucleus of stria terminalis (BST) and form the socalled extended amygdala (Alheid and Heimer 1988;Alheid et al. 1995;Heimer et al. 1997b).The central division of the extended amygdala, which is formed by the central amygdaloid nucleus, BST lateral division, IPAC, and SLEA central division, establishes reciprocal neuronal connections with the caudal aspect of the nucleus accumbens shell (Acb shell) and is also connected with the prefrontal cortex (de Olmos et al. 1985;Heimer et al. 1997a;Heimer et al. 1997b;Zahm and Brog 1992 Based on anatomical connections, the extended amygdala seems to be an important site involved in neuropsychiatric disorders (Heimer et al. 1997b); however, specific data showing the effect of drugs used in the therapy of these disorders in the extended amygdala are scarce. Induction of the early gene c-fos by antipsychotics in the central amygdaloid nucleus (Sebens et al. 1995) and antagonism of the excitatory effects induced by a local infusion of amphetamine in the amygdaloid complex by clozapine (Wang and Rebec 1996) have been reported. Moreover, it was recently shown (Beck 1994;Duncan et al. 1996;Morelli et al. 1999) that antidepressant drugs inhibiting either noradrenaline or serotonin re-uptake, induced the expression of the early gene c-fos in areas belonging to the rat extended amygdala, suggesting a role of the extended amygdala in disorders characterized by affective disturbance.Induction of the early gene c-fos is secondary to neuronal activation and is correlated to an increased function of specific areas in the CNS (Sagar et al. 1988). Moreover, detection of the c-fos-encoded protein Fos, throug...

show abstract

“…In the current study, inactivation of the BLA also prevented the decrease in VTA activity following acute withdrawal. Amphetamine administration alone does not induce changes in synaptic strength in the BLA (Rademacher et al, 2010), although changes in neuronal activity have been described (Wang and Rebec, 1996). This suggests that the drug alone does not induce changes in synaptic plasticity in the BLA.…”

Section: Discussionmentioning

confidence: 97%

Withdrawal from Acute Amphetamine Induces an Amygdala-Driven Attenuation of Dopamine Neuron Activity: Reversal by Ketamine

Belujon

Jakobowski

Dollish

et al. 2015

Neuropsychopharmacol

View full text Add to dashboard Cite

Drug addiction is a chronic disorder characterized by a cycle composed of drug seeking, intoxication with drug taking and withdrawal associated with negative affect. Numerous studies have examined withdrawal/negative affect after chronic use; however, very few have examined the effect of acute administration on the negative affective state after acute drug withdrawal. One dose of amphetamine was injected into Sprague-Dawley rats. Despair behavior using the modified forced swim test (FST) and dopamine (DA) activity in the ventral tegmental area using in vivo electrophysiological recordings were studied 18, 48 and 72 h after injection of amphetamine. The effects of inactivation of the basolateral amygdala (BLA) and ketamine administration on VTA DA neuron activity and passivity in the modified FST were examined. Eighteen hours following amphetamine withdrawal, there was a substantial decrease in the number of active DA neurons, as well as an increase in time spent immobile in the modified FST, which returned to baseline after 72 h. Inactivation of the BLA after acute amphetamine prevented the decrease in DA neuron tonic activity. Injection of ketamine also prevented the decrease in DA population activity but had no effect on immobility measured in the modified FST. The data support a model in which the negative affective state following acute amphetamine withdrawal is associated with a decrease in DA neuron population activity, driven by hyperactivity of the BLA. Although ketamine reversed the hypodopaminergic state following withdrawal, the failure to reduce immobility in the modified FST indicates that different processes underlying negative emotional state may exist between depression and drug withdrawal.

show abstract

Amygdaloid neurons respond to clozapine rather than haloperidol in behaving rats pretreated with intra-amygdaloid amphetamine

Cited by 10 publications

References 66 publications

Behavioral Effects of Psychomotor Stimulant Infusions into Amygdaloid Nuclei

Behavioral Effects of Psychomotor Stimulant Infusions into Amygdaloid Nuclei

Differential Induction of Fos-Like-Immunoreactivity in the Extended Amygdala after Haloperidol and Clozapine

Withdrawal from Acute Amphetamine Induces an Amygdala-Driven Attenuation of Dopamine Neuron Activity: Reversal by Ketamine

Contact Info

Product

Resources

About