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This hypothesis is supported by the findings that activation of presynaptic a2-ARs can inhibit glutamate transmission in other brainstem neurons, for example in the spinal trigeminal nucleus and dorsal motor nucleus of the vagus.
Tyramine is an endogenous compound which exists in the brain as a trace amine (Durden and Davis, 1993), but it is also an exogenous compound which is found in foods such as cheese and wine. Although the level is very low, evidence obtained from animal studies has indicated that this trace amine has a very rapid turnover rate. Its presence in a brain synaptosomal fraction suggests a possible involvement in the process of neurotransmission (Philips et al., 1978).
There is a general agreement that the hypertensive action of the indirectly acting sympathomimetic tyramine is due to the release of norepinephrine from peripheral noradrenergic nerves. However, the mechanism of action of tyramine in brain regions that are involved in cardiovascular regulation is largely unknown. Tyramine microinjected into the rostral ventrolateral medulla (RVL, C1 area) elicits a dose-dependent decrease in arterial pressure, heart rate and sympathetic renal nerve activity and this effect was blocked by previous microinjection desmethylimipramine, reserpine, 6-hydroxydopamine (6-OHDA), or phentolamine (Granata et al., 1985, 1986; Granata and Reis, 1987).
Norepinephrine is probably not the only amine released by tyramine since tyramine causes a release of several granular amines (5-HT, NA, DA) in synaptosomes from guinea-pig brain (Peyer et al., 1982). In this study, we tested this hypothesis by examining the effects of tyramine and other indirectly acting sympathomimetics in the C1 area, the locus coeruleus, and the caudal raphe nuclei, which contain adrenergic, noradrenergic, and serotoninergic neurons, respectively.
To investigate the glomerular circuitry, visually guided single and paired recordings were obtained from glomerular neurons in rat olfactory bulb slices.
Based on classical morphological studies there are 3 classes of glomerular neurons: external tufted (ET) cells, periglomerular (PG) cells and short axon (SA) cells, collectively referred to as “juxtaglomerular (JG) neurons”.
In order to identify the neurons, physiologically characterized cells were filled with Lucifer Yellow and reconstructed.
The first type of cell I will show is the ET cell.
External tufted cells have intrinsic burst firing and they are contacted directly by olfactory nerve (ON) terminals. They also fire in synchrony and contact inhibitory interneurons, namely periglomerular (PG) and short axon cells (SA), which in turn exhibit bursts of EPSPs. The PG cell dendrites ramify in one single glomerulus and thus might serve for intraglomerular inhibition via dendrodendritic interactions with ET tufted dendrites. In contrast, SA cell have neurites extending throughout several glomeruli and thus might serve for interglomerular inhibition.
Whole-cell current clamp paired recording from 2 External Tufted cells filled with biocytin and reconstructed using NeuroLucida software (middle right panel). First panel shows a sample of 5 sec recording of membrane potentials: the blue and red superimposed traces correspond to recording from the 2 neurons drawn in red and blue, respectively. Note that the 2 neurons fire bursts of action potential either together or alone. The 2 neurons exhibited highly synchronous membrane potential oscillations and bursting as also indicated by the cross-correlogram. The coefficient of correlation at zero time lag was C = 0.56
Dual recording from an EPSC-bursting cell in whole-cell voltage clamp mode (red traces) and a spike-bursting cell in cell-attached mode (blue traces). Pane A shows 10 superimposed spontaneous burst-triggered traces. The thick line is the average of 135 similar traces. Panel B shows an example of a burst of EPSCs evoked by a burst of spikes that was itself produced by an extracellular injection of a positive current pulse (700 pA). Panel C shows superimposed 5 traces of similarly evoked bursts of EPSCs in control, CNQX (10 µM) and after washout. Note that CNQX reversibly abolished both the spontaneous and evoked EPSCs.