Regulation of Prepulse Inhibition by Ventral Pallidal Projections

Kodsi, M.; Swerdlow, Neal R.

doi:10.1016/s0361-9230(96)00440-6

Cited by 83 publications

(44 citation statements)

References 36 publications

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“…One might argue that the critical MPFC efferents responsible for reduced PPI project not to the ventral tegmental nucleus or NAC, but instead to the thalamus, via MPFC cells in layer 6. However, reduced PPI follows thalamic inhibition (Kodsi and Swerdlow, 1997;Swerdlow et al, 2002), which would be opposite to the effect predicted after activation of excitatory corticothalamic efferents.…”

Section: Discussionmentioning

confidence: 56%

Prefrontal D1 and ventral hippocampal N-methyl-d-aspartate regulation of startle gating in rats

et al. 2005

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Background-Sensorimotor gating, as measured by prepulse inhibition of the startle reflex, is deficient in schizophrenia patients, and in rats after specific manipulations of limbic cortico-striatopallido-thalamic circuitry. For example, prepulse inhibition in rats is disrupted after D1 blockade in the medial prefrontal cortex, and after N-methyl-D-aspartate infusion into the ventral hippocampus. In the present study, we examined whether these two substrates form part of an integrated circuit regulating sensorimotor gating, which might contribute to the loss of prepulse inhibition in patient populations.

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Section: Discussionmentioning

confidence: 56%

Prefrontal D1 and ventral hippocampal N-methyl-d-aspartate regulation of startle gating in rats

et al. 2005

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“…Thus, a reciprocally interacting thalamocortical network with a strong NE projection from LC to MD-thalamus could be recruited by LC stimulation, and produce profound deficits in PPI because of connections with other neocortical sites such as BLA and posterior mPFC. Interestingly, lesions or pharmacological inactivation of MD-thalamus disrupt PPI, but intra-MD-thalamus infusions of DA agonists do not, suggesting that this site regulates PPI independently of the DA system (Kodsi and Swerdlow, 1997;Swerdlow et al, 2002). The present results for the first time indicate a specific neurotransmitter system (NE) through which MD-thalamus regulation of PPI occurs, and raise the question of whether NE receptor stimulation in MDthalamus disrupts PPI by functionally inactivating this nucleus.…”

Section: Discussionmentioning

confidence: 58%

Discrete Forebrain Neuronal Networks Supporting Noradrenergic Regulation of Sensorimotor Gating

Alsene

Rajbhandari

Ramaker

et al. 2011

Neuropsychopharmacol

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Prepulse inhibition (PPI) refers to the reduction in the startle response when a startling stimulus is preceded by a weak prestimulus, and is an endophenotype of deficient sensorimotor gating in several neuropsychiatric disorders. Emerging evidence suggests that norepinephrine (NE) regulates PPI, however, the circuitry involved is unknown. We found recently that stimulation of the locus coeruleus (LC), the primary source of NE to the forebrain, induces a PPI deficit that is a result of downstream NE release. Hence, this study sought to identify LC-innervated forebrain regions that mediate this effect. Separate groups of male Sprague-Dawley rats received a cocktail solution of the a1-NE receptor agonist phenylephrine plus the b-receptor agonist isoproterenol (equal parts of each; 0, 3, 10, and 30 mg) into subregions of the medial prefrontal cortex (mPFC), nucleus accumbens (NAcc), extended amygdala, mediodorsal thalamus (MD-thalamus), or the dorsal hippocampus (DH) before PPI testing. NE agonist infusion into the posterior mPFC, NAcc shell, bed nucleus of the stria terminalis, basolateral amygdala, and the MD-thalamus disrupted PPI, with particularly strong effects in MD-thalamus. Sites in which NE receptor stimulation did not disrupt PPI (anterior mPFC, NAcc core, central amygdala, and DH) did support PPI disruptions with the dopamine D2 receptor agonist quinpirole (0, 10 mg). This pattern reveals new pathways in the regulation of PPI, and suggests that NE transmission within distinct thalamocortical and ventral forebrain networks may subserve the sensorimotor gating deficits that are seen in disorders such as schizophrenia, Tourette syndrome, and post-traumatic stress disorder.

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“…The apparent difference in the effects of systemic and prefrontal administration of baclofen on baseline PPI may result from the interference with GABA signaling at multiple brain regions following systemic injection. PPI is known to be modulated in a top-down manner by the PFC, and also by brain nuclei more proximal to the primary startle circuit such as the lateral globus pallidus (LGP) and the pedunculopontine nucleus (PPTg; Koch and Schnitzler, 1997;Kodsi and Swerdlow, 1997;Swerdlow et al, 2001). Interestingly, it was recently shown that PPTg-targeting GABAergic neurons in the LGP are activated at both prepulse and prepulse + pulse (PPI) conditions, and that transient inactivation of this region by lidocaine decreases PPI in mice.…”

Section: Regional Effects Of Baclofenmentioning

confidence: 99%

Prefrontal GABAB Receptor Activation Attenuates Phencyclidine-Induced Impairments of Prepulse Inhibition: Involvement of Nitric Oxide

Fejgin

Pålsson

Wass

et al. 2009

Neuropsychopharmacol

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Recent theories propose that both GABA and glutamate signaling are compromised in patients with schizophrenia. These deficits can be observed in several brain regions including the prefrontal cortex (PFC), an area extensively linked to the cognitive dysfunction in this disease and notably affected by NMDA receptor antagonists such as phencyclidine (PCP). We have previously demonstrated that inhibition of the nitric oxide (NO) pathways in the brain, particularly in the PFC, prevents a wide range of PCP-induced behavioral deficits including disruption of prepulse inhibition (PPI). This study investigated the role of GABA(B) receptor signaling and NO in the effects of PCP on PPI. Mice received systemic or prefrontal injections of the GABA(B) receptor agonist baclofen (2.5-5 mg/kg and 1 mM) before PCP treatment (5 mg/kg) and were thereafter tested for PPI. GABA/NO interactions were studied by combining baclofen and the NO synthase inhibitor L-NAME (20 mg/kg) in subthreshold doses. The role of GABA(B) receptors for NO production in vivo was assessed using NO-sensors implanted into the rat PFC. PCP-induced PPI deficits were attenuated in an additive manner by systemic baclofen treatment, whereas prefrontal microinjections of baclofen completely blocked the effects of PCP, without affecting PPI per se. The combination of baclofen and L-NAME was more effective in preventing the effects of PCP than any compound by itself. Additionally, baclofen decreased NO release in the PFC in a dose-related manner. This study proposes a role for GABA(B) receptor signaling in the effects of PCP, with altered NO levels as a downstream consequence. Thus, prefrontal NO signaling mirrors an altered level of cortical inhibition that may be of importance for information processing deficits in schizophrenia.

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Regulation of Prepulse Inhibition by Ventral Pallidal Projections

Cited by 83 publications

References 36 publications

Prefrontal D1 and ventral hippocampal N-methyl-d-aspartate regulation of startle gating in rats

Prefrontal D1 and ventral hippocampal N-methyl-d-aspartate regulation of startle gating in rats

Discrete Forebrain Neuronal Networks Supporting Noradrenergic Regulation of Sensorimotor Gating

Prefrontal GABAB Receptor Activation Attenuates Phencyclidine-Induced Impairments of Prepulse Inhibition: Involvement of Nitric Oxide

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