Interactions between p-tyramine, m-tyramine, or β-phenylethylamine and dopamine on single neurones in the cortex and caudate nucleus of the rat

1980 ◽  
Vol 58 (2) ◽  
pp. 222-227 ◽  
Author(s):  
R. S. G. Jones ◽  
A. A. Boulton

p-Tyramine, applied to cortical and caudate neurones with weak iontophoretic currents (0–10 nA), did not usually cause any alteration of base-line firing rate. However, neuronal responses to dopamine (DA) during such weak applications of p-tyramine were greatly enhanced. Cortical neurone responses to noradrenaline (NA) were similarly potentiated, but both cortical and caudate neurone responses to α-aminobutyric acid were unaffected by p-tyramine. In addition, weak background applications of DA which did not affect cell firing rate were also without effect on the neuronal responses to the standard application of DA. The responses of cortical neurones to DA were also potentiated by m-tyramine and β-phenylethylamine applied with weak cationic currents. The results may suggest that trace amines can enhance NA and DA transmission in the central nervous system.

2021 ◽  
Vol 22 (13) ◽  
pp. 6858
Author(s):  
Fanny Gaudel ◽  
Gaëlle Guiraudie-Capraz ◽  
François Féron

Animals strongly rely on chemical senses to uncover the outside world and adjust their behaviour. Chemical signals are perceived by facial sensitive chemosensors that can be clustered into three families, namely the gustatory (TASR), olfactory (OR, TAAR) and pheromonal (VNR, FPR) receptors. Over recent decades, chemoreceptors were identified in non-facial parts of the body, including the brain. In order to map chemoreceptors within the encephalon, we performed a study based on four brain atlases. The transcript expression of selected members of the three chemoreceptor families and their canonical partners was analysed in major areas of healthy and demented human brains. Genes encoding all studied chemoreceptors are transcribed in the central nervous system, particularly in the limbic system. RNA of their canonical transduction partners (G proteins, ion channels) are also observed in all studied brain areas, reinforcing the suggestion that cerebral chemoreceptors are functional. In addition, we noticed that: (i) bitterness-associated receptors display an enriched expression, (ii) the brain is equipped to sense trace amines and pheromonal cues and (iii) chemoreceptor RNA expression varies with age, but not dementia or brain trauma. Extensive studies are now required to further understand how the brain makes sense of endogenous chemicals.


1976 ◽  
Vol 231 (5) ◽  
pp. 1573-1578 ◽  
Author(s):  
T Hori ◽  
Y Harada

Water-perfused thermodes were implanted over the lumbothoracic spinal cord and unilaterally in the midbrain of urethan-anesthetized rabbits. Single-unit activities were recorded with steel microelectrodes from the thermosensitive neurons in the midbrain reticular formation (MRF), and the effects of heating and cooling of the spinal cord were studied. Of 38 cold-sensitive MRF neurons studied, 7 units decreased their firing rate upon elevation of spinal cord temperature (Tsc) and 3 units showed the opposite type of response to Tsc. The remaining 28 cold units were not affected by the changes in Tsc between 30 and 43 degrees C. Of 17 warm units, 3 units increased and one unit decreased the firing rate during spinal cord heating. These results suggest that the temperature signal arising from thermosensitive structures in the spinal cord may be transmitted to some of the locally thermosensitive neurons in the MRF.


1992 ◽  
Vol 263 (3) ◽  
pp. R679-R684
Author(s):  
J. B. Dean ◽  
J. A. Boulant

Thermoregulatory responses may be delayed in onset and offset by several minutes after changes in hypothalamic temperature. Our preceding study found neurons that displayed delayed firing rate responses during clamped thermal stimulation in remote regions of rat diencephalic tissue slices. The present study looked for similar delayed firing rate responses during clamped (1.5-10 min) changes in each neuron's local temperature. Of 26 neurons tested with clamped thermal stimulation, six (i.e., 23%) showed delayed responses, with on-latencies of 1.0-7.8 min. These neurons rarely showed off-latencies, and the delayed response was not eliminated by synaptic blockade. The on-latencies and ranges of local thermosensitivity were similar to delayed neuronal responses to remote temperature; however, remote-sensitive neurons displayed off-latencies, higher firing rates at 37 degrees C, and greater sensitivity to thermal stimulation. Our findings suggest that delayed thermosensitivity is an intrinsic property of certain neurons and may initiate more elaborate or prolonged delayed responses in synaptically connected diencephalic networks. These networks could explain the delayed thermoregulatory responses observed during hypothalamic thermal stimulation.


1987 ◽  
Vol 57 (2) ◽  
pp. 381-413 ◽  
Author(s):  
D. N. Mastronarde

The retinal inputs to cells in the cat's lateral geniculate nucleus (LGN) were directly recorded to study the basis for the properties of two classes of LGN X-cells: Xs (single) and XL (lagged). The presence of excitatory or inhibitory input to an LGN cell from a particular simultaneously recorded ganglion cell was assessed with cross-correlograms during unstimulated activity. Because neighboring ganglion cells do not fire independently, features in a retinogeniculate correlogram can arise in two ways that must be distinguished by a direct effect of the ganglion cell on the LGN cell, or by correlated firing between that ganglion cell and some other ganglion cell that is an excitatory or inhibitory input to the LGN cell. It was possible to determine the origin of correlogram features because features indicating a retinogeniculate effect were distinctly different in timing and strength from features arising solely from correlated firing in the retina. The characteristic feature in a correlogram between an LGN cell and an excitatory retinal input was a sharp peak in LGN cell firing rate at the appropriate latency after the firing of the ganglion cell. The characteristic feature for an inhibitory input was a dip in LGN cell firing rate after the firing of the ganglion cell. Typically, this dip lasted 10-40 ms and was followed by a prolonged enhancement in LGN cell firing rate, which may reflect a postinhibitory rebound. XS-cells had a single retinal X input whose excitatory effect caused most of the LGN cell's spikes during stimulated and unstimulated activity. There was no conclusive evidence that any XS-cell received excitatory retinal input from either Y-cells or other X-cells of the same center sign. There was usually evidence for inhibition of XS-cells by retinal X-cells of opposite center sign with receptive fields highly overlapping that of the XS-cell, but rarely evidence for inhibition by Y-cells. XL-cells also had only a single excitatory input, but this X input had a relatively weak effect that caused only a minority of the LGN cell's spikes, typically 17% during maintained activity and 29% during visual stimulation. The input's excitatory effect was immediately followed by strong inhibition of the XL-cell. XL-cells were also inhibited by retinal X-cells of the same center sign that were adjacent (nearest neighbors) to the excitatory input. The strength and latency of both of these inhibitory effects indicate that the inhibition was disynaptic.(ABSTRACT TRUNCATED AT 400 WORDS)


2018 ◽  
Vol 315 (3) ◽  
pp. E327-E339 ◽  
Author(s):  
Alexandra Alvarsson ◽  
Sarah A. Stanley

The central nervous system relies on a continual supply of glucose, and must be able to detect glucose levels and regulate peripheral organ functions to ensure that its energy requirements are met. Specialized glucose-sensing neurons, first described half a century ago, use glucose as a signal and modulate their firing rates as glucose levels change. Glucose-excited neurons are activated by increasing glucose concentrations, while glucose-inhibited neurons increase their firing rate as glucose concentrations fall and decrease their firing rate as glucose concentrations rise. Glucose-sensing neurons are present in multiple brain regions and are highly expressed in hypothalamic regions, where they are involved in functions related to glucose homeostasis. However, the roles of glucose-sensing neurons in healthy and disease states remain poorly understood. Technologies that can rapidly and reversibly activate or inhibit defined neural populations provide invaluable tools to investigate how specific neural populations regulate metabolism and other physiological roles. Optogenetics has high temporal and spatial resolutions, requires implants for neural stimulation, and is suitable for modulating local neural populations. Chemogenetics, which requires injection of a synthetic ligand, can target both local and widespread populations. Radio- and magnetogenetics offer rapid neural activation in localized or widespread neural populations without the need for implants or injections. These tools will allow us to better understand glucose-sensing neurons and their metabolism-regulating circuits.


1980 ◽  
Vol 93 (2) ◽  
pp. 139-148 ◽  
Author(s):  
Andrea R. Genazzani ◽  
Franco Camanni ◽  
Ferdinando Massara ◽  
Enrico Picciolini ◽  
Daniela Cocchi ◽  
...  

Abstract. The prolactin-(Prl) lowering effect of nomifensine (Nom), an antidepressant drug which activates dopamine (DA) neurotransmission mainly by inhibiting DA re-uptake in the central nervous system (CNS), was investigated in normoprolactinaemic subjects, in subjects with physiological puerperal hyperprolactinaemia or pathological hyperprolactinaemia. Nom (200 mg po) administered to 23 normoprolactinaemic women induced a significant decrease in baseline Prl, which was more marked (about 50% inhibition at 120 min) and prompt (30 min) in the subjects who had 'high' Prl levels (>12<20 ng/ml) (13 subjects) than in those with 'low' Prl levels (≤ 12 ng/ml). Also in 9 puerperal women (postpartum day 2) oral administration of 200 mg Nom was followed by a clear-cut decrease of base-line Prl, which started at 30 min and reached nadir values at 150–180 min (about 60% inhibition). Administration of Nom (200 mg po) to 47 subjects with pathological hyperprolactinaemia evidenced the presence of Nom non-responder (36 cases) or responder (11 cases) subjects. In 22 of the Nom non-responder subjects the existence of a Prl-se creting pituitary tumour was established at surgery by selective removal of an adenoma via the transsphenoidal route; of the 14 subjects who did not undergo surgery, 1 had evident and 5 had minor alterations of the sella turcica and, in addition, in 3 subjects the duration of amenorrhoea was longer than 5 years. Only 5 subjects of this group had no radiological alterations of the sella turcica, in presence of basal Prl levels ranging between 50–126 ng/ml. In contrast, 10 out of the 11 Nom-responder subjects had a radiologically normal sella turcica and basal Prl levels lower than 50 ng/ml. Administration of 2-Br-α-ergocriptine (2.5 mg po), a direct stimulant of pituitary DA receptors, to subjects with pathological hyperprolactinaemia (39 cases) induced a striking fall in plasma Prl levels (about 80% inhibition at 240 min), irrespective of the type of Prl responsiveness to Nom. These results indicate that Nom lowers plasma Prl levels in both normoprolactinaemic and hyperprolactinaemic subjects; in the latter, by virtue of its ability to affect selectively DA neurotransmission in the CNS, the drug appears capable of discriminating between individuals with and without pituitary adenoma.


1989 ◽  
Vol 62 (1) ◽  
pp. 220-230 ◽  
Author(s):  
T. J. Ness ◽  
G. F. Gebhart

1. The effect of morphine or clonidine administered systemically on visceral and cutaneous spinal nociceptive transmission was examined in 45 dorsal horn neurons in spinalized, decerebrate rats: 17 "cutaneous" dorsal horn neurons located in the L3-L5 spinal segments were excited by heating the glabrous skin of the hindpaw (48 degrees C, 15 s) and 28 "visceral" dorsal horn neurons located in the T13-L2 spinal segments were excited by colorectal distension (80 mmHg, 20 s). The 28 visceral dorsal horn neurons were subclassified as 18 short-latency abrupt neurons (SL-A), which were excited by colorectal distension at short latency (less than 1 s) and whose activity abruptly returned to base line following termination of the distending stimulus, and as 10 short-latency-sustained (SL-S) neurons, which also were excited at short latency (less than 1 s) by colorectal distension, but whose activity was sustained above base line for 4-31 s following termination of the distending stimulus. 2. Morphine produced a dose-dependent, naloxone-reversible inhibition of both spontaneous activity and/or neuronal responses during heating or colorectal distension of 8 SL-A, 7 SL-S, and 11 cutaneous dorsal horn neurons. Comparison of the effective doses of morphine to produce a 50% reduction in the response of the neurons (ED50s) during colorectal distension or heating demonstrated that, at the intensities of distension and heating employed, SL-S neurons were affected at the least dosage (ED50 = 0.46 mumol/kg), followed by SL-A neurons (ED50 = 1.95 mumol/kg) and cutaneous neurons (ED50 = 6.12 mumol/kg). Effects on spontaneous activity were variable: at low doses morphine produced an increase in the spontaneous activity of 2 SL-A and 5 cutaneous neurons; greater doses (up to 42 mumol/kg) inhibited in all of the SL-A and SL-S neurons, but not three cutaneous neurons studied. With the exclusion of these three neurons, the ED50s for inhibition of spontaneous activity were comparable to the ED50s for inhibition of neuronal responses during colorectal distension or heating of the hindpaw in all three neuronal groups. 3. Clonidine produced a dose-dependent, yohimbine- or phentolamine-reversible inhibition of both spontaneous activity and neuronal responses during heating or colorectal distension of 10 SL-A, 3 SL-S, and 6 cutaneous dorsal horn neurons.(ABSTRACT TRUNCATED AT 400 WORDS)


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