Tourette syndrome: A case for noradrenergic and opiatergic mechanisms

Sandyk, Reuven

doi:10.3109/00207458608985682

Cited by 2 publications

(1 citation statement)

References 43 publications

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“…Schizophrenia is often considered the prime example of these diseases; however, Tourette syndrome and post-traumatic stress disorder (PTSD) are also reliably associated with disrupted PPI Castellanos et al, 1996;Grillon et al, 1996;Swerdlow, 2001). These disorders are well known to be responsive to NE-based drugs and potentially involve dysregulation of the NE system (Bhidayasiri, 2005;Breier et al, 1990;Gay et al, 1989;Gomes et al, 1980;Leckman et al, 1995;Sandyk, 1986). Therefore, it is possible that increased NE signaling at a1-and b-receptors in regions such as posterior mPFC, NAccSh, BNST, BLA, and MD-thalamus could contribute to the pathophysiology of these psychiatric disorders.…”

Section: Discussionmentioning

confidence: 99%

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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