Ba-mah niṿasheaʻ : kolelet arbaʻa maʾamarim bi-sheʾalot haṭavat matsav ha-ḥomri yehude Rusiʾa /

BSLW YIVOL Clean-up ProjectDigital imag

Control of serotonergic neurons in rat brain by dopaminergic receptors outside the dorsal raphe nucleus

We studied the control of dorsal raphe (DR) serotonergic neurons by dopaminergic transmission in rat brain using microdialysis and single unit extracellular recordings. Apomorphine (0.5–3.0 mg/kg s.c.) and quinpirole (0.5 mg/kg s.c.) increased serotonin (5-HT) output in the DR and (only apomorphine) in striatum. These effects were antagonized by 0.3 mg/kg s.c. SCH 23390 (in DR and striatum) and 1 mg/kg s.c. raclopride (in DR). 5-HT1A receptor blockade potentiated the 5-HT increase produced by apomorphine in the DR. Apomorphine (50–400 µg/kg i.v.) increased the firing rate of most 5-HT neurons, an effect prevented by SCH 23390 and raclopride. Quinpirole (40–160 µg/kg i.v.) also enhanced the firing rate of 5-HT neurons. When applied in the DR, neither drug increased the 5-HT output in the DR or striatum. Likewise, micropressure injection of quinpirole (0.2–8 pmol) failed to increase the firing rate of 5-HT neurons. In situ hybridization showed that the dopamine (DA) D2 receptor transcript was almost absent in the DR and abundant in the substantia nigra (SN) and the periaqueductal grey matter (PAG). Using dual probe microdialysis, the application of tetrodotoxin or apomorphine in SN significantly increased the DR 5-HT output. Thus, the discrepancy between local and systemic effects of dopaminergic agonists and the absence of DA D2 receptor transcript in 5-HT neurons suggest that DA D2 receptors outside the DR control serotonergic activity.Peer reviewe

Role of catecholaminergic inputs to the medial prefrontal cortex in local and subcortical expression of Fos after psychological stress

A wide variety of stressors elicit Fos expression in the medial prefrontal cortex (mPFC). No direct attempts, however, have been made to determine the role of the inputs that drive this response. We examined the effects of lesions of mPFC catecholamine terminals on local expression of Fos after exposure to air puff, a stimulus that in the rat acts as an acute psychological stressor. We also examined the effects of these lesions on Fos expression in a variety of subcortical neuronal populations implicated in the control of adrenocortical activation, one classic hallmark of the stress response. Lesions of the mPFC that were restricted to dopaminergic terminals significantly reduced numbers of Fos-immunoreactive (Fos-IR) cells seen in the mPFC after air puff, but had no significant effect on stress-induced Fos expression in the subcortical structures examined. Lesions of the mPFC that affected both dopaminergic and noradrenergic terminals also reduced numbers of Fos-IR cells observed in the mPFC after air puff. Additionally, these lesions resulted in a significant reduction in stress-induced Fos-IR in the ventral bed nucleus of the stria terminalis. These results demonstrate a role for catecholaminergic inputs to the mPFC, in the generation of both local and subcortical responses to psychological stress. (C) 2004 Wiley-Liss, Inc