Research reportAdenylyl cyclase activity and G-protein subunit levels in postmortem frontal cortex of suicide victims
References (39)
- et al.
Regionally selective increases in β-adrenergic receptor density in the brains of suicide victims
Brain Res.
(1988) - et al.
Brain 5-HT2 receptor binding sites in depressed suicide victims
Brain Res.
(1988) - et al.
Differential expression of low molecular weight form of Gs-α in neostriatum and cerebellum: correlation with expression of calmodulin-independent adenylyl cyclase
Brain Res.
(1990) - et al.
Brain β-adrenoceptor binding sites in antidepressant-free depressed suicide victims
Brain Res.
(1990) - et al.
Antibodies directed against synthetic peptides distinguish between GTP-binding proteins in neutrophil and brain
J. Biol. Chem.
(1987) - et al.
Differential effects of electroconvulsive shock and antidepressant drugs on serotonin-2 receptors in rat brain
Eur. J. Pharmacol.
(1981) - et al.
A modification of the standard Lowry procedure to simplify protein determination in membranes and lipoprotein samples
Anal. Biochem.
(1978) - et al.
Post-receptor-mediated increases in adenylate cyclase activity after chronic antidepressant treatment: relationship to receptor desensitisation
Eur. J. Pharmacol.
(1989) - et al.
Differential effects of chronic administration of desipramine on the cyclic AMP response in cortical slices and membranes in the rat
Neuropharmacology
(1987) - et al.
Reduced basal and stimulated (isoprenaline, Gpp(NH)p, forskolin) adenylate cyclase activity in Alzheimer's disease correlated with histopathological changes
Brain Res.
(1991)
Serotonergic mechanisms in brains of suicide victims
Brain Res.
Increased serotonin-2-binding sites in frontal cortex of suicide victims
Lancet
Antidepressant-anxiolytic interaction: decreased density of benzodiazepine receptors in rat brain following chronic administration of antidepressants
Eur. J. Pharmacol
Enhancement of responsiveness of the central serotonergic system and serotonin-2 receptor density in rat frontal cortex by electroconvulsive treatment
Eur. J. Pharmacol.
5HT2 receptor changes in major depression
Biol. Psychiatry
Development of β-adrenergic receptor subsensitivity by antidepressants
Nature
Effect of electroconvulsive shock on monoaminergic receptor binding sites in rat brain
Nature
Receptor sensitivity and the mechanism of action of antidepressant treatment
Arch. Gen. Psychiatry
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Phosphodiesterase-4 enzyme as a therapeutic target in neurological disorders
2020, Pharmacological ResearchPDE11A regulates social behaviors and is a key mechanism by which social experience sculpts the brain
2016, NeuroscienceCitation Excerpt :Cyclic nucleotide signaling specifically within the ventral hippocampal formation (VHIPP) may be particularly important because VHIPP lesions and knockdown of CREB in the rodent VHIPP impair social behaviors (Kogan et al., 2000; Brightwell et al., 2005; Tseng et al., 2009). This is consistent with the fact that both cyclic nucleotide signaling deficits (Ebstein et al., 1976; Belmaker et al., 1978; Bowers and Study, 1979; Kafka et al., 1979, 1986; Hoshino et al., 1980; Garver et al., 1982; Gattaz et al., 1983; Kafka and van Kammen, 1983; Memo et al., 1983; Goldberg et al., 1984; Kanof et al., 1986, 1987, 1989; Lerer et al., 1987; Ofuji et al., 1989; Kaiya et al., 1990; Kang, 1990; Young et al., 1991, 1993, 1994; Kaiya, 1992; Cowburn et al., 1994; Avissar et al., 1997; Gurguis et al., 1997, 1999a,b; Rahman et al., 1997; Avissar et al., 2001a,b; Bacchelli et al., 2003; Edmunds et al., 2008; Kelley et al., 2008; Turetsky and Moberg, 2009; Woolfrey et al., 2009; Ji et al., 2011) and abnormalities in the VHIPP (Suddath et al., 1990; Shenton et al., 1992; Rajarethinam et al., 2001; Jessen et al., 2003; Pegues et al., 2003; Lee et al., 2004; Rametti et al., 2007; Rusch et al., 2008; Zhou et al., 2008; Ghose et al., 2009; Nesvaderani et al., 2009; Schobel et al., 2009a,b; Hall et al., 2010; Goldman et al., 2011; Zhang et al., 2011) (referred to as the anterior hippocampus in primates) are observed in patients with neuropsychiatric disorders in which social deficits are known to occur. Phosphodiesterase 11A (PDE11A, specifically isoform PDE11A4) is the only PDE with expression in brain restricted to the hippocampal formation, with a 3–10-fold enrichment in the VHIPP versus dorsal HIPP (Fig. 1A) (Kelly et al., 2010, 2014; Kelly, 2014, 2015; Hegde et al., 2016; Pathak et al., in press) and little to no expression in peripheral organs (c.f., (Kelly, 2015)).
Do certain signal transduction mechanisms explain the comorbidity of epilepsy and mood disorders?
2014, Epilepsy and Behavior