scholarly journals Catecholamine-stimulated cyclic GMP accumulation in the rat pineal: apparent presynaptic site of action.

1976 ◽  
Vol 73 (10) ◽  
pp. 3398-3402 ◽  
Author(s):  
R. F. O'Dea ◽  
M. Zatz
Keyword(s):  
Cyclic Gmp ◽  
Presynaptic Site ◽  
Site Of Action

scholarly journals Cyclic GMP Inhibits a Pharmacologically Distinct Na+/H+ Exchanger Variant in Cultured Rat Astrocytes via an Extracellular Site of Action

2002 ◽  
Vol 68 (4) ◽  
pp. 1451-1461 ◽  
Author(s):  
Rhian M. Touyz ◽  
Sylvie Picard ◽  
Ernesto L. Schiffrin ◽  
Christian F. Deschepper
Keyword(s):  
Cyclic Gmp ◽  
Site Of Action ◽  
Rat Astrocytes

Control of the Subthalamic Innervation of the Rat Globus Pallidus by D2/3 and D4 Dopamine Receptors

2006 ◽  
Vol 96 (6) ◽  
pp. 2877-2888 ◽  
Author(s):  
Adán Hernández ◽  
Osvaldo Ibáñez-Sandoval ◽  
Arturo Sierra ◽  
René Valdiosera ◽  
Dagoberto Tapia ◽  
...  
Keyword(s):  
Globus Pallidus ◽  
Receptor Agonist ◽  
Brain Slices ◽  
Mean Amplitude ◽  
Patch Clamp Technique ◽  
Antidromic Activation ◽  
Whole Cell Patch Clamp ◽  
Presynaptic Site ◽  
Site Of Action

The effects of activating dopaminergic D2/3 and D4 receptors during activation of the subthalamic projection to the globus pallidus (GP) were explored in rat brain slices using the whole cell patch-clamp technique. Byocitin labeling and both orthodromic and antidromic activation demonstrated the integrity of some subthalamopallidal connections in in vitro parasagittal brain slices. Excitatory postsynaptic currents (EPSCs) that could be blocked by CNQX and AP5 were evoked onto pallidal neurons by local field stimulation of the subthalamopallidal pathway in the presence of bicuculline. Bath application of dopamine and quinpirole, a dopaminergic D2-class receptor agonist, reduced evoked EPSCs by about 35%. This effect was only partially blocked by sulpiride, a D2/3 receptor antagonist. The sulpiride-sensitive reduction of the subthalamopallidal EPSC was associated with an increase in the paired-pulse ratio (PPR) and a reduction in the frequency but not the mean amplitude of spontaneous EPSCs (sEPSCs), indicative of a presynaptic site of action, which was confirmed by variance–mean analysis. The sulpiride-resistant EPSC reduction was mimicked by PD 168,077 and blocked by L-745,870, selective D4 receptor agonist and antagonist, respectively, suggesting the involvement of D4 receptors. The reduction of EPSCs produced by PD 168,077 was not accompanied by changes in PPR or the frequency of sEPSCs; however, it was accompanied by a reduction in mean sEPSC amplitude, indicative of a postsynaptic site of action. These results show that dopamine modulates subthalamopallidal excitation by presynaptic D2/3 and postsynaptic D4 receptors. The importance of this modulation is discussed.

Evidence for angiotensin II receptors in the urinary bladder of the rabbit

1984 ◽  
Vol 62 (4) ◽  
pp. 390-395 ◽  
Author(s):  
Gordon F. Anderson ◽  
Robin A. Barraco ◽  
Howard J. Normile ◽  
Todd N. Rosen
Keyword(s):  
Angiotensin Ii ◽  
Gradual Increase ◽  
Specific Binding ◽  
Intrinsic Activity ◽  
Detrusor Muscle ◽  
Angiotensin I ◽  
Onset Of Action ◽  
Presynaptic Site ◽  
Angiotensin Iii ◽  
Site Of Action

Dose–response (DR) curves for several angiotensin analogs were examined on isolated rabbit detrusor strips with washout and rest between each addition. The order of potency was [Val5]-angiotensin II > [IIe5]-angiotensin II > [IIe5]-angiotensin I > [Val4]-angiotensin III. Repeated cumulative DR to [Val5]-AII resulted in a gradual increase in potency and intrinsic activity for four DR. However, the maximum force generated occurred at lower agonist concentrations and was less than that of the single methods, suggesting tachyphylaxis. Atropine (1.0 μM) shifted the cumulative DR curve downward, suggesting some cholinergic component possibly involving a presynaptic site of action. The magnitude of field-stimulated atropine-resistant contractions was reduced by both 1.0 and 10 μM saralasin as well as 10 μM naloxone. Tissue binding with 125I-labelled angiotensin II on isolated detrusor smooth muscle membranes indicated specific binding saturation occurred at 14.3 fmol/mg with a KD of 0.72 nM in EDTA–Tris buffered saline. Thus our results show that angiotensin II (AII) receptors can be demonstrated in detrusor muscle by ligand binding experiments on ceil membranes and that saralasin and naloxone partially block atropine-resistant contractions. However, it seems unlikely that AII serves as a neurotransmitter because of the delay in onset of action of exogenous AII in isolated bath experiments and the apparent inability of saralasin to totally abolish the atropine-resistant field-stimulated preparation. If AII serves a role in neurotransmission it most probably is as a neuromodulator.

scholarly journals Regulation of Inhibitory Synapses by Presynaptic D4 Dopamine Receptors in Thalamus

2010 ◽  
Vol 104 (5) ◽  
pp. 2757-2765 ◽  
Author(s):  
Gubbi Govindaiah ◽  
Tongfei Wang ◽  
Martha U. Gillette ◽  
Shane R. Crandall ◽  
Charles L. Cox
Keyword(s):  
Substantia Nigra ◽  
Globus Pallidus ◽  
Receptor Agonist ◽  
Receptor Activation ◽  
Substantia Nigra Pars Compacta ◽  
Inhibitory Synapses ◽  
Reticular Nucleus ◽  
Postsynaptic Currents ◽  
Presynaptic Site ◽  
Site Of Action

Dopamine (DA) receptors are the principal targets of drugs used in the treatment of schizophrenia. Among the five DA receptor subtypes, the D4 subtype is of particular interest because of the relatively high affinity of the atypical neuropleptic clozapine for D4 compared with D2 receptors. GABA-containing neurons in the thalamic reticular nucleus (TRN) and globus pallidus (GP) express D4 receptors. TRN neurons receive GABAergic afferents from globus pallidus (GP), substantia nigra pars reticulata (SNr), and basal forebrain as well as neighboring TRN neuron collaterals. In addition, TRN receives dopaminergic innervations from substantia nigra pars compacta (SNc); however, the role of D4 receptors in neuronal signaling at inhibitory synapses is unknown. Using whole cell recordings from in vitro pallido-thalamic slices, we demonstrate that DA selectively suppresses GABAA receptor-mediated inhibitory postsynaptic currents (IPSCs) evoked by GP stimulation. The D2-like receptor (D2,3,4) agonist, quinpirole, and selective D4 receptor agonist, PD168077, mimicked the actions of DA. The suppressive actions of DA and its agonists were associated with alterations in paired pulse ratio and a decrease in the frequency of miniature IPSCs, suggesting a presynaptic site of action. GABAA receptor agonist, muscimol, induced postsynaptic currents in TRN neurons were unaltered by DA or quinpirole, consistent with the presynaptic site of action. Finally, DA agonists did not alter intra-TRN inhibitory signaling. Our data demonstrate that the activation of presynaptic D4 receptors regulates GABA release from GP efferents but not TRN collaterals. This novel and selective action of D4 receptor activation on GP-mediated inhibition may provide insight to potential functional significance of atypical antipsychotic agents. These findings suggest a potential heightened TRN neuron activity in certain neurological conditions, such as schizophrenia and attention deficit hyperactive disorders.

scholarly journals Kainate Acts at Presynaptic Receptors to Increase GABA Release From Hypothalamic Neurons

1999 ◽  
Vol 82 (2) ◽  
pp. 1059-1062 ◽  
Author(s):  
Qing-Song Liu ◽  
Peter R. Patrylo ◽  
Xiao-Bing Gao ◽  
Anthony N. van den Pol
Keyword(s):  
Transmitter Release ◽  
Hippocampal Neurons ◽  
Gaba Release ◽  
Presynaptic Receptors ◽  
Inhibitory Neurons ◽  
Kainate Receptors ◽  
Nmda Receptor Antagonists ◽  
Presynaptic Site ◽  
Site Of Action ◽  
Inhibitory Transmitter

Recent reports suggest that kainate acting at presynaptic receptors reduces the release of the inhibitory transmitter GABA from hippocampal neurons. In contrast, in the hypothalamus in the presence of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) receptor antagonists [1-(4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466) and d,l-2-amino-5-phosphonopentanoic acid (AP5)], kainate increased GABA release. In the presence of tetrodotoxin, the frequency, but not the amplitude, of GABA-mediated miniature inhibitory postsynaptic currents (IPSCs) was enhanced by kainate, consistent with a presynaptic site of action. Postsynaptic activation of kainate receptors on cell bodies/dendrites was also found. In contrast to the hippocampus where kainate increases excitability by reducing GABA release, in the hypothalamus where a much higher number of GABAergic cells exist, kainate-mediated activation of transmitter release from inhibitory neurons may reduce the level of neuronal activity in the postsynaptic cell.

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