Opioids intrinsically inhibit the genesis of mouse cerebellar granule neuron precursors in vitro: differential impact of mu and delta receptor activation on proliferation and neurite elongation.

Although opioids are known to affect neurogenesis in vivo, it is uncertain the extent to which opioids directly or indirectly affect the proliferation, differentiation or death of neuronal precursors. To address these questions, the intrinsic role of the opioid system in neurogenesis was systematically explored in cerebellar external granular layer (EGL) neuronal precursors isolated from postnatal mice and maintained in vitro. Isolated neuronal precursors expressed proenkephalin-derived peptides, as well as specific mu and delta, but negligible kappa, opioid receptors.

High performance liquid chromatographic analysis of the pharmacologically active quinones and related compounds in the oil of the black seed (Nigella sativa L.).

An HPLC method for quantifying the putative pharmacologically active constituents: thymoquinone (TQ), dithymoquinone (DTQ), thymohydroquinone (THQ), and thymol (THY), in the oil of Nigella sativa seed is described. Extraction of the constituents from the oil was carried out using C18 PrepSep mini columns followed by quantification of the recovered constituents by HPLC on a reversed-phase muBondapak C18 analytical column, using an isocratic mobile phase of water:methanol:2-propanol (50:45:5% v/v) at a flow rate of 2 ml min(-1). UV detection was at 254 nm for TQ, DTQ, and THY, and at 294 nm for THQ.

Effect of nicotine use and withdrawal on brain preproenkephalin A mRNA.

Although the effect of nicotine on brain neurotransmitters and behavior has been studied, the mechanism(s) by which nicotine contributes to tobacco use remains unclear. One transmitter that may relate to long-term nicotine use and its withdrawal is enkephalin, a five-amino acid opioid peptide derived from the proenkephalin A family. In the present study we determined the effect of acute and chronic nicotine treatment and its withdrawal on preproenkephalin A mRNA levels (PPE mRNA) in specific rat brain regions using Northern blot analysis.

Aortic peak flow velocity as an index of myocardial contractility in the conscious rat.

The present studies were conducted in conscious, instrumented rats to evaluate measurements of aortic peak flow velocity (PFV) as an index of myocardial contractility. Because our previous studies had characterized/verified procedures to determine pressure-derived indices of contractile function in the anesthetized, ventilated, open-chest rat, we first correlated PFV with (a) maximum rate of left ventricular pressure development (max +dP/dt) and (b) a contractility index derived by dividing max +dP/dt by left ventricular pressure at max +dP/dt [(dP/dt)/P] in anesthetized rats (n = 5). The positive inotropic agent, isoproterenol, given by bolus intravenous injection (0.

Effects of beta-FNA on sympathoadrenal, cardiovascular, and analgesic responses to DAMPGO at rest and during stress.

To elucidate further the role of mu-opioid receptors in mediating analgesia and cardiovascular function at rest and during stress, rats were pretreated ICV with either saline (5 microliters) or beta-funaltrexamine (beta-FNA, 5 nmol/5 microliters), a noncompetitive opioid receptor antagonist that inactivates irreversibly mu receptors, 2 days prior to [D-Ala2, N MePhe4, Gly5-ol]enkephalin (DAMPGO, 1 nmol, ICV) administration. Pretreatment with beta-FNA blocked DAMPGO-induced analgesia as measured by the tail-flick test. DAMPGO also produced an increase in blood pressure (BP), sympathoadrenal outflow, and a bradycardia.