Evidence for a projection from the lateral preoptic area and substantia innominata to the ‘mesencephalic locomotor region’ in the rat

Swanson, Larry W.; Mogenson, Gordon J.; Gerfen, Charles R.; Robinson, P.

doi:10.1016/0006-8993(84)90827-8

Cited by 318 publications

(102 citation statements)

References 57 publications

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“…Consistent with this latter possibility, electrical stimulation of the ventral pallidum modulates the amplitude of the acoustic startle reflex (Li et al, 1999). In addition, both the NAc shell and ventral pallidum project to the pedunculopontine tegmental nucleus, a structure that projects to the startle circuit and has been shown to play a role in spontaneous morphine withdrawal (Swanson et al, 1984;Koch et al, 1993;Usuda et al, 1998;Vargas-Perez et al, 2009). A role for the ventral pallidum seems particularly likely given that it is a target of the NAc shell neurons that co-express both D1-and D2-like receptors (Haber et al, 1985;Lu et al, 1997).…”

Section: Discussionmentioning

confidence: 77%

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Radke¹,

Gewirtz

2012

Neuropsychopharmacol

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A number of lines of evidence suggest that negative emotional symptoms of withdrawal involve reduced activity in the mesolimbic dopamine system. This study examined the contribution of dopaminergic signaling in structures downstream of the ventral tegmental area to withdrawal from acute morphine exposure, measured as potentiation of the acoustic startle reflex. Systemic administration of the general dopamine receptor agonist apomorphine or a cocktail of the D1-like receptor agonist SKF82958 and the D2-like receptor agonist quinpirole attenuated potentiated startle during morphine withdrawal. This effect was replicated by apomorphine infusion into the nucleus accumbens shell. Finally, apomorphine injection was shown to relieve startle potentiation during nicotine withdrawal and conditioned place aversion to morphine withdrawal. These results suggest that transient activation of the ventral tegmental area mesolimbic dopamine system triggers the expression of anxiety and aversion during withdrawal from multiple classes of abused drugs.

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Section: Discussionmentioning

confidence: 77%

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Radke¹,

Gewirtz

2012

Neuropsychopharmacol

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“…CG has in fact been described as a component of a "midbrain locomotor region" (Swanson et al, 1984). The midbrain locomotor area receives projections from various limbic forebrain areas, including the central amygdala, and projects to spinal motor neurons.…”

Section: Discussionmentioning

confidence: 99%

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

et al. 1988

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The purpose of the present study was to determine whether lesions of areas projected to by the central amygdaloid nucleus (ACE) would disrupt the classical conditioning of autonomic and/or behavioral emotional responses. The areas studied included 3 projection targets of the ACE: the lateral hypothalamic area (LH), midbrain central gray (CG) region, and bed nucleus of the stria terminalis (BNST). Lesions were made either electrolytically or by microinjection of ibotenic acid, which destroys local neurons without interrupting fibers of passage. Two weeks later, the animals were classically conditioned by pairing an acoustic stimulus with footshock. The next day, conditioned changes in autonomic activity (increases in arterial pressure) and emotional behavior (“freezing,” or the arrest of somatomotor activity) evoked by the acoustic conditioned stimulus (CS) were measured during extinction trials. Electrolytic and ibotenic acid lesions of the LH interfered with the conditioned arterial pressure response, but did not affect conditioned freezing. Electrolytic lesions of the rostral CG disrupted conditioned freezing but not conditioned changes in arterial pressure. Ibotenic acid injected into the rostral CG reduced neither the arterial pressure nor the freezing response. Injection of ibotenic acid in the caudal CG, like electrolytic lesions of the rostral CG, disrupted the freezing, but not the arterial pressure response. Injection of ibotenic acid into the BNST had no effect on either response. These data demonstrate that neurons in the LH are involved in the autonomic, but not the behavioral, conditioned response pathway, whereas neurons in the caudal CG are involved in the behavioral, but not the autonomic, pathway. Different efferent projections of the central amygdala thus appear to mediate the behavioral and autonomic concomitants of conditioned fear.

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“…These are part of an opioidergic projection arising in the nucleus accumbens (NAc) (Groenewegen and Russchen, 1984). The NAc to VP projection regulates VP outputs to motor control regions such as the pedunculopontine nucleus and mesencephalic locomotor regions (Swanson et al, 1984;Mogenson and Wu, 1986). Providing the first evidence for VP involvement in behavioral sensitization, we revealed that intra-VP injection of the μ-opioid receptor antagonist CTOP blocks the development of motor sensitization to systemic morphine (Johnson and Napier, 2000).…”

Section: Introductionmentioning

confidence: 88%

Changes in Accumbal and Pallidal pCREB and ΔFosB in Morphine-Sensitized Rats: Correlations with Receptor-Evoked Electrophysiological Measures in the Ventral Pallidum

McDaid

Dallimore

Mackie

et al. 2005

Neuropsychopharmacol

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Activation of μ-opioid receptors in the ventral pallidum (VP) is important for the induction of behavioral sensitization to morphine in rats. The present study was designed to ascertain if neurons within the VP demonstrate sensitization at a time when morphine-induced behavioral sensitization occurred (ie 3 or 14 days after five once-daily injections of 10 mg/kg i.p. morphine) in rats. Western blotting was used to evaluate transcription factors altered by opiates, CREB and ΔFosB. CREB levels did not change in the VP, but there was a significant decrease in levels of its active, phosphorylated form (pCREB) at both 3-and 14-days withdrawal. ΔFosB levels were elevated following a 3-day withdrawal, but returned to normal by 14 days. This profile also was obtained from nucleus accumbens tissue. In a separate group of similarly treated rats, in vivo electrophysiological recordings of VP neuronal responses to microiontophoretically applied ligands were carried out after 14-days withdrawal. The firing rate effects of local applications of morphine were diminished in rats withdrawn from i.p. morphine. Repeated i.p. morphine did not alter GABA-mediated suppression of firing, or the rate enhancing effects of the D1 dopamine receptor agonist SKF82958 or glutamate. However, VP neurons from rats withdrawn from repeated i.p. morphine showed a higher propensity to enter a state of depolarization inactivation to locally applied glutamate. Overall, these findings reveal that decreased pCREB in brain regions such as the VP accompanies persistent behavioral sensitization to morphine and that this biochemical alteration may influence the excitability of neurons in this brain region.

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Evidence for a projection from the lateral preoptic area and substantia innominata to the ‘mesencephalic locomotor region’ in the rat

Cited by 318 publications

References 57 publications

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

Changes in Accumbal and Pallidal pCREB and ΔFosB in Morphine-Sensitized Rats: Correlations with Receptor-Evoked Electrophysiological Measures in the Ventral Pallidum

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