Dopamine D4 Receptor Activation Inhibits Presynaptically Glutamatergic Neurotransmission in the Rat Supraoptic Nucleus

2001 ◽  
Vol 86 (3) ◽  
pp. 1149-1155 ◽  
Author(s):  
Christopher J. Price ◽  
Quentin J. Pittman
Keyword(s):  
Supraoptic Nucleus ◽  
Sch 23390 ◽  
Receptor Activation ◽  
Glutamatergic Neurotransmission ◽  
Magnocellular Neurons ◽  
Vasopressin Release ◽  
Paired Pulse ◽  
Postsynaptic Currents ◽  
Whole Cell Patch Clamp ◽  
D4 Receptor

Oxytocin and vasopressin release from magnocellular neurons of the supraoptic nucleus is under the control of glutamate-dependent excitation. The supraoptic nucleus also receives a generalized dopaminergic input from hypothalamic sources. To determine if dopamine can influence this excitatory drive onto the magnocellular neurons, we used whole-cell patch clamp to record the effect of dopamine on evoked and miniature excitatory postsynaptic currents in rat hypothalamic slices. Dopamine exposure (30 μM to 1 mM) induced a large and reversible reduction in the amplitude of evoked excitatory postsynaptic current in nearly all magnocellular cells tested. D4 receptors appeared to mediate dopamine's activity, based on inhibition of the response with 50 μM clozapine, but not by SCH 23390 or sulpiride, and mimicry of dopamine's action with the D4 specific agonist, PD 168077. Analysis of paired-pulse experiments and miniature postsynaptic currents indicated that dopamine's action involved a presynaptic mechanism, since the frequency of miniature postsynaptic currents was reduced with dopamine exposure without any change in current kinetics or amplitude, while the paired-pulse ratio increased. We therefore have demonstrated for the first time a role for dopamine D4 receptors in the supraoptic nucleus in the presynaptic inhibition of glutamatergic neurotransmission onto magnocellular neurons.

Activation of adenosine A2A receptors alters postsynaptic currents and depolarizes neurons of the supraoptic nucleus

2006 ◽  
Vol 291 (2) ◽  
pp. R359-R366 ◽  
Author(s):  
Todd A. Ponzio ◽  
Yu-Feng Wang ◽  
Glenn I. Hatton
Keyword(s):  
Supraoptic Nucleus ◽  
Cell Activity ◽  
Brain Slices ◽  
Cell Types ◽  
Receptor Activation ◽  
A2a Receptors ◽  
Postsynaptic Currents ◽  
Cgs 21680 ◽  
Whole Cell Patch Clamp ◽  
Sites Of Action

Supraoptic nucleus (SON) neurons secrete oxytocin or vasopressin in response to various physiological stimuli (e.g., lactation/suckling, dehydration). Released near fenestrated capillaries of the neurohypophysis, these peptides enter the blood and travel to peripheral target organs. The pervasive neuromodulator adenosine, acting at A1 receptors, is an important inhibitory regulator of magnocellular neuroendocrine cell activity. Another high-affinity adenosine receptor exists in this system, however. We examined the physiological effects of adenosine A2A receptor activation and determined its localization among various cell types within the SON. In whole cell patch-clamp recordings from rat brain slices, application of the selective adenosine A2A receptor agonist CGS-21680 caused membrane depolarizations in SON neurons, often leading to increased firing activity. Membrane potential changes were persistent (>10 min) and could be blocked by the selective A2A receptor antagonist ZM-241385, or GDP-β-S, the latter suggesting postsynaptic sites of action. However, ±-α-methyl-(4-carboxyphenyl)glycine or TTX also blocked CGS-21680 effects, indicating secondary actions on postsynaptic neurons. In voltage-clamp mode, application of CGS-21680 caused a slight increase (∼8%) in high-frequency clusters of excitatory postsynaptic currents. With the use of specific antibodies, adenosine A2A receptors were immunocytochemically localized to both the magnocellular neurons and astrocytes of the SON. Ecto-5′nucleotidase, an enzyme involved in the metabolism of ATP to adenosine, was also localized to astrocytes of the SON. These results demonstrate that adenosine acting at A2A receptors can enhance the excitability of SON neurons and modulate transmitter release from glutamatergic afferents projecting to the nucleus. We suggest that adenosine A2A receptors may function in neuroendocrine regulation through both direct neuronal mechanisms and via actions involving glia.

Dopamine D4 Receptor-Mediated Presynaptic Inhibition of GABAergic Transmission in the Rat Supraoptic Nucleus

2003 ◽  
Vol 90 (2) ◽  
pp. 559-565 ◽  
Author(s):  
Karima Azdad ◽  
Richard Piet ◽  
Dominique A. Poulain ◽  
Stéphane H. R. Oliet
Keyword(s):  
Supraoptic Nucleus ◽  
Sch 23390 ◽  
Hormone Release ◽  
D3 Receptor ◽  
Receptor Antagonists ◽  
Gabaergic Transmission ◽  
Inhibitory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
D4 Receptor ◽  
Supraoptic Neurons

The mechanism by which dopamine induces or facilitates neurohypophysial hormone release is not completely understood. Because oxytocin- and vasopressin-secreting supraoptic neurons are under the control of a prominent GABAergic inhibition, we investigated the possibility that dopamine exerts its action by modulating GABA-mediated transmission. Whole cell voltage-clamp recordings of supraoptic neurons were carried out in acute hypothalamic slices to determine the action of dopamine on inhibitory postsynaptic currents. Application of dopamine caused a consistent and reversible reduction in the frequency, but not the amplitude, of miniature synaptic events, indicating that dopamine was acting presynaptically to reduce GABAergic transmission. The subtype of dopamine receptor involved in this response was characterized pharmacologically. Dopamine inhibitory action was greatly reduced by two highly selective D4 receptor antagonists L745,870 and L750,667 and to a lower extent by the antipsychotic drug clozapine but was unaffected by SCH 23390 and sulpiride, D1/D5 and D2/D3 receptor antagonists, respectively. In agreement with these results, the action of dopamine was mimicked by the potent D4 receptor agonist PD168077 but not by SKF81297 and bromocriptine, D1/D5 and D2/D3 receptor agonists, respectively. Dopamine and PD168077 also reduced the amplitude of evoked inhibitory postsynaptic currents, an effect that was accompanied by an increase in paired-pulse facilitation. These data clearly indicate that D4 receptors are located on GABA terminals in the supraoptic nucleus and that their activation reduces GABA release in the supraoptic nucleus. Therefore dopaminergic facilitation of neurohypophysial hormone release appears to result, at least in part, from disinhibition of magnocellular neurons caused by the depression of GABAergic transmission.

Histamine Suppresses Non-NMDA Excitatory Synaptic Currents in Rat Supraoptic Nucleus Neurons

2000 ◽  
Vol 83 (5) ◽  
pp. 2616-2625 ◽  
Author(s):  
Zhenhui Li ◽  
Glenn I. Hatton
Keyword(s):  
Supraoptic Nucleus ◽  
Synaptic Currents ◽  
Excitatory Postsynaptic Currents ◽  
Paired Pulse ◽  
Paired Pulse Facilitation ◽  
Postsynaptic Currents ◽  
Whole Cell Patch Clamp ◽  
Bath Application ◽  
Intracellular Diffusion ◽  
Supraoptic Neurons

Whole cell patch-clamp recordings were obtained from supraoptic neurons to investigate the effects of histamine on excitatory postsynaptic currents evoked by electrical stimulation of areas around the posterior supraoptic nucleus. When cells were voltage-clamped at −70 mV, evoked excitatory postsynaptic currents had amplitudes of 88.4 ± 9.6 pA and durations of 41.1 ± 3.0 ms (mean ± SE; n = 43). With twin stimulus pulses (20 Hz) used, paired-pulse facilitation ratios were 1.93 ± 0.12. Bath application of 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX) abolished synaptic currents. Histamine at concentrations ∼0.1–10 μM reversibly suppressed excitatory postsynaptic currents in all supraoptic neurons tested. Within 2 min after application of (10 μM) histamine, current amplitudes and durations decreased by 61.5 and 31.0%, respectively, with little change in the paired-pulse facilitation ratio. Dimaprit or imetit (H2 or H3 receptor agonists) did not reduce synaptic currents, whereas pyrilamine (H1 receptor antagonist) blocked histamine-induced suppression of synaptic currents. When patch electrodes containing guanosine 5′- O-(2-thiodiphosphate) (GDP-β-S) were used to record cells, histamine still suppressed current amplitudes by 49.1% and durations by 41.9%. Similarly, intracellular diffusion of bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid (BAPTA) and H7 did not abolish histamine-induced suppression of synaptic currents, either. Bath perifusion of 8-bromo-quanosine 3′,5′-cyclic monophosphate reduced current amplitudes by 32.3% and durations by 27.9%. After bath perfusion of slices with Nω-nitro-l-arginine methyl ester (L-NAME), histamine injection decreased current amplitudes only by 31.9%, much less than the inhibition rate in control ( P < 0.01). In addition, histamine induced little change in current durations and paired-pulse facilitation ratios, representing a partial blockade of histamine effects on synaptic currents by L-NAME. In supraoptic neurons recorded using electrodes containing BAPTA and perifused with L-NAME, the effects of histamine on synaptic currents were completely abolished. Norepinephrine injection reversibly decreased current amplitudes by 39.1% and duration by 64.5%, with a drop in the paired-pulse facilitation ratio of 47.9%. Bath perifusion of L-NAME, as well as intracellular diffusion of GDP-β-S, , 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine , or BAPTA, failed to block norepinephrine-induced suppression of evoked synaptic currents. The present results suggest that histamine suppresses non- N-methyl-d-aspartate synaptic currents in supraoptic neurons through activation of H1receptors. It is possible that histamine first acts at supraoptic cells (perhaps both neuronal and nonneuronal) and induces the production of nitric oxide, which then diffuses to nearby neurons and modulates synaptic transmission by a postsynaptic mechanism.

GABAB presynaptically modulates suprachiasmatic input to hypothalamic paraventricular magnocellular neurons

2000 ◽  
Vol 278 (5) ◽  
pp. R1210-R1216 ◽  
Author(s):  
Lu-Ning Cui ◽  
Elaine Coderre ◽  
Leo P. Renaud
Keyword(s):  
G Proteins ◽  
Receptor Activation ◽  
Magnocellular Neurons ◽  
Membrane Conductances ◽  
Whole Cell Patch Clamp ◽  
Neurosecretory Neurons ◽  
Hypothalamic Slice ◽  
Dose Dependent ◽  
Paired Pulse Depression ◽  
Reversible Reduction

This study used whole cell patch clamp recordings in rat hypothalamic slice preparations to evaluate the effects of GABAB receptor activation on GABAA-mediated inhibitory postsynaptic currents (IPSCs) in paraventricular nucleus magnocellular neurons evoked by electrical stimulation in the suprachiasmatic nucleus (SCN). Baclofen induced a dose-dependent (1–10 μM) and reversible reduction in SCN-evoked IPSC amplitude (11/11 cells), blockable with 2-hydroxysaclofen (300 μM; 3/3 cells). IPSCs displayed paired-pulse depression (PPD), attenuated by both baclofen and 2-hydroxysaclofen, but neither altered resting membrane conductances or IPSC time constants of decay. Baclofen induced a significant dose-dependent (1–100 μM) reduction in frequency, but not amplitude, of spontaneous IPSCs and miniature IPSCs, reversible with 2-hydroxysaclofen pretreatment. Baclofen effects and PPD persisted in slices pretreated with pertussis toxin (PTX) and N-ethylmaleimide, implying that these GABABreceptors are coupled to PTX-insensitive G proteins. Responses were unaltered by barium (2 mM) or nimodipine, ruling out involvement of K+ channels and L-type Ca2+ channels. Thus pre- and postsynaptic GABAB and GABAA receptors participate in SCN entrainment of paraventricular neurosecretory neurons.

Opioidergic Modulation of Voltage-Activated K+Currents in Magnocellular Neurons of the Supraoptic Nucleus in Rat

1999 ◽  
Vol 81 (4) ◽  
pp. 1617-1625 ◽  
Author(s):  
Wolfgang Müller ◽  
Stephan Hallermann ◽  
Dieter Swandulla
Keyword(s):  
Supraoptic Nucleus ◽  
Opioid Antagonist ◽  
Delayed Rectifier ◽  
Patch Clamp Recording ◽  
Opioid Agonist ◽  
Magnocellular Neurons ◽  
Vasopressin Release ◽  
Axon Terminals ◽  
Delayed Rectifier Current ◽  
Voltage Dependent

Opioidergic modulation of voltage-activated K+ currents in magnocellular neurons of the supraoptic nucleus in rat. Opioidergic modulation plays an important role in the control of oxytocin and vasopressin release by magnocellular neurons (MCNs) in the supraoptic and paraventricular nuclei of the hypothalamus. We have used whole cell patch-clamp recording in acute slices of the supraoptic nucleus (SON) of the hypothalamus to study opioidergic modulation of voltage-dependent K+ currents in MCNs that are involved in release activity. The μ-receptor agonistd-Ala2, N-Me-Phe4, Gly5-ol-enkephalin (DAMGO, 2 μM) affected K+currents in 55% of magnocellular neurons recorded from. In these putative oxytocinergic cells, DAMGO increased the delayed rectifier current ( I K(V)) amplitude by ∼50% without significant effects on its activation kinetics. The transient A current ( I A) was enhanced by DAMGO by ∼36%. Its inactivation kinetic was accelerated slightly while the voltage dependence of steady-state inactivation was shifted by −6 mV to more negative potentials. All DAMGO effects were blocked by the preferential non-κ-opioid antagonist naloxone (10 μM). The κ-opioid agonist trans-(±)-3,4-dichloro- N-methyl- N(2-[1-pyrrolidinyl]cyclohexyl)benzeneacetamide (U50,488; 10 μM) strongly suppressed I K(V) by ∼57% and evoked a 20-mV hyperpolarizing shift and an acceleration of activation in both, DAMGO-sensitive and -insensitive putative vasopressinergic MCNs. U50,488 reduced I A by ∼29% and τ of inactivation by −20% in DAMGO-sensitive cells. In contrast, in DAMGO-insensitive cells U50,488 increased I A by ∼23% and strongly accelerated inactivation (τ −44%). The effects of U50,488 were suppressed by the selective κ-receptor antagonist nor-binaltorphimine (5 μM). We conclude that μ- and κ-opioidergic inputs decrease and increase excitability of oxytocinergic MCNs, respectively, through modulation of voltage-dependent K+ currents. In vasopressinergic MCNs, κ-opioidergic inputs differentially modulate these K+currents. The modulation of K+ currents is assumed to significantly contribute to opioidergic control of hormone release by MCNs within the supraoptic nucleus and from the axon terminals in the neural lobe.

Control of the Subthalamic Innervation of Substantia Nigra Pars Reticulata by D1 and D2 Dopamine Receptors

2006 ◽  
Vol 95 (3) ◽  
pp. 1800-1811 ◽  
Author(s):  
Osvaldo Ibañez-Sandoval ◽  
Adán Hernández ◽  
Benjamin Florán ◽  
Elvira Galarraga ◽  
Dagoberto Tapia ◽  
...  
Keyword(s):  
Dopamine Receptors ◽  
Receptor Agonist ◽  
Sch 23390 ◽  
Receptor Activation ◽  
Skf 38393 ◽  
Projection Neurons ◽  
Patch Clamp Technique ◽  
D2 Dopamine Receptors ◽  
Endogenous Dopamine ◽  
Whole Cell Patch Clamp

The effects of activating dopaminergic D1 and D2 class receptors of the subthalamic projections that innervate the pars reticulata of the subtantia nigra (SNr) were explored in slices of the rat brain using the whole cell patch-clamp technique. Excitatory postsynaptic currents (EPSCs) that could be blocked by 6-cyano-7-nitroquinoxalene-2,3-dione and d-(−)-2-amino-5-phosphonopentanoic acid were evoked onto reticulata GABAergic projection neurons by local field stimulation inside the subthalamic nucleus in the presence of bicuculline. Bath application of ( RS)-2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine hydrochloride (SKF-38393), a dopaminergic D1-class receptor agonist, increased evoked EPSCs by ∼30% whereas the D2-class receptor agonist, trans-(−)-4aR-4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-pyrazolo(3,4-g)quinoline (quinpirole), reduced EPSCs by ∼25%. These apparently opposing actions were blocked by the specific D1- and D2-class receptor antagonists: R-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetra-hydro-1H-3-benzazepinehydrochloride (SCH 23390) and S-(−)-5-anino-sulfonyl- N-[(1-ethyl-2-pyrrolidinyl)-methyl]-2-methoxybenzamide (sulpiride), respectively. Both effects were accompanied by changes in the paired-pulse ratio, indicative of a presynaptic site of action. The presynaptic location of dopamine receptors at the subthalamonigral projections was confirmed by mean-variance analysis. The effects of both SKF-38393 and quinpirole could be observed on terminals contacting the same postsynaptic neuron. Sulpiride and SCH 23390 enhanced and reduced the evoked EPSC, respectively, suggesting a constitutive receptor activation probably arising from endogenous dopamine. These data suggest that dopamine presynaptically modulates the subthalamic projection that targets GABAergic neurons of the SNr. Implications of this modulation for basal ganglia function are discussed.

Dopaminergic control of angiotensin II-induced vasopressin secretion in vitro

1998 ◽  
Vol 275 (4) ◽  
pp. E687-E693 ◽  
Author(s):  
Noreen F. Rossi
Keyword(s):  
Angiotensin Ii ◽  
Sch 23390 ◽  
Receptor Activation ◽  
Significant Rise ◽  
Skf 38393 ◽  
Receptor Subtype ◽  
Adrenergic Blockade ◽  
Adrenergic Antagonist ◽  
Vasopressin Secretion

Because dopamine influences arginine vasopressin (AVP) release, the present studies were designed to ascertain the dopamine receptor subtype that potentiates angiotensin II-induced AVP secretion in cultured hypothalamo-neurohypophysial explants. Dopamine (a nonselective D1/D2 agonist), apomorphine (a D2 ≫ D1 agonist), and SKF-38393 (a selective D1 agonist) dose dependently increased AVP secretion. Maximal AVP release was observed with 5 μM dopamine, 307 ± 66% ⋅ explant−1 ⋅ h−1, 1 μM SKF-38393, 369 ± 41% ⋅ explant−1 ⋅ h−1, and 0.1 μM apomorphine, 374 ± 67% ⋅ explant−1 ⋅ h−1. Selective D1 antagonism with 1 μM SCH-23390 blocked AVP secretion to values no different from basal. Domperidone (D2 antagonist), phenoxybenzamine (nonselective adrenergic antagonist), and prazosin (α1-antagonist) failed to prevent release. D1 antagonism also prevented AVP secretion to 1 μM angiotensin II [angiotensin II, 422 ± 87% ⋅ explant−1 ⋅ h−1vs. angiotensin II plus SCH-23390, 169 ± 28% ⋅ explant−1 ⋅ h−1( P < 0.05)], but D2 and α1-adrenergic blockade did not. In contrast, AT1 receptor inhibition with 0.5 μM losartan blocked angiotensin II- but not dopamine-induced AVP release. AT2antagonism had no effect. Although subthreshold doses of the agonists did not increase AVP secretion (0.05 μM dopamine, 133 ± 44% ⋅ explant−1 ⋅ h−1; 0.01 μM SKF-38393, 116 ± 26% ⋅ explant−1 ⋅ h−1;and 0.001 μM angiotensin II, 104 ± 29% ⋅ explant−1 ⋅ h−1), the combination of dopamine and angiotensin II provoked a significant rise in AVP [420 ± 83% ⋅ explant−1 ⋅ h−1( P < 0.01)]. Similar results were observed with SKF-38393 and angiotensin II, and the AVP response was blocked to basal levels by either D1 or AT1 antagonism. These findings support a role for D1 receptor activation to increase AVP release and mediate angiotensin II-induced AVP release within the hypothalamo-neurohypophysial system. The data also suggest that the combined subthreshold stimulation of receptors that use distinct intracellular pathways can prompt substantial AVP release.

Dopamine D-1/D-5 Receptor Activation Is Required for Long-Term Potentiation in the Rat Neostriatum In Vitro

2001 ◽  
Vol 85 (1) ◽  
pp. 117-124 ◽  
Author(s):  
J.N.D. Kerr ◽  
J. R. Wickens
Keyword(s):  
Receptor Antagonist ◽  
Learning And Memory ◽  
Sch 23390 ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Striatal Neurons ◽  
Theoretical Understanding ◽  
Endogenous Dopamine ◽  
Term Potentiation

Dopamine and glutamate are key neurotransmitters involved in learning and memory mechanisms of the brain. These two neurotransmitter systems converge on nerve cells in the neostriatum. Dopamine modulation of activity-dependent plasticity at glutamatergic corticostriatal synapses has been proposed as a cellular mechanism for learning in the neostriatum. The present research investigated the role of specific subtypes of dopamine receptors in long-term potentiation (LTP) in the corticostriatal pathway, using intracellular recording from striatal neurons in a corticostriatal slice preparation. In agreement with previous reports, LTP could be induced reliably under Mg2+-free conditions. This Mg2+-free LTP was blocked by dopamine depletion and by the dopamine D-1/D-5 receptor antagonist SCH 23390 but was not blocked by the dopamine D-2 receptor antagonist remoxipride or the GABAA antagonist picrotoxin. In dopamine-depleted slices, the ability to induce LTP could be restored by bath application of the dopamine D-1/D-5 receptor agonist, SKF 38393. These results show that activation of dopamine D-1/D-5 receptors by either endogenous dopamine or exogenous dopamine agonists is a requirement for the induction of LTP in the corticostriatal pathway. These findings have significance for current understanding of learning and memory mechanisms of the neostriatum and for theoretical understanding of the mechanism of action of drugs used in the treatment of psychotic illnesses and Parkinson's disease.

Different Inhibitory Inputs Onto Neostriatal Projection Neurons as Revealed by Field Stimulation

2005 ◽  
Vol 93 (2) ◽  
pp. 1119-1126 ◽  
Author(s):  
Fatuel Tecuapetla ◽  
Luis Carrillo-Reid ◽  
Jaime N. Guzmán ◽  
Elvira Galarraga ◽  
José Bargas
Keyword(s):  
Channel Blocker ◽  
Inhibitory Synapses ◽  
Projection Neurons ◽  
Medium Spiny Neurons ◽  
Field Stimulation ◽  
Paired Pulse ◽  
Postsynaptic Currents ◽  
Spiny Neurons ◽  
Short Time ◽  
Paired Pulse Depression

This work investigated if diverse properties could be ascribed to evoked inhibitory postsynaptic currents (IPSCs) recorded on rat neostriatal neurons when field stimulation was delivered at two different locations: the globus pallidus (GP) and the neostriatum (NS). Previous work stated that stimulation in the GP could antidromically excite projection axons from medium spiny neurons. This maneuver would predominantly activate the inhibitory synapses that interconnect spiny cells. In contrast, intrastriatal stimulation would preferentially activate inhibitory synapses provided by interneurons. This study shows that, in fact, intensity-amplitude experiments are able to reveal different properties for IPSCs evoked from these two locations (GP and NS). In addition, while all IPSCs evoked from the GP were always sensitive to ω-conotoxin GVIA (CaV2.22.2 or N-channel blocker), one-half of the inhibition evoked from the NS exhibited little sensitivity to ω-conotoxin GVIA. Characteristically, all ω-conotoxin GVIA–insensitive IPSCs exhibited strong paired pulse depression, whereas ω-conotoxin GVIA–sensitive IPSCs evoked from either the GP or the NS could exhibit short-time depression or facilitation. ω-Agatoxin TK (CaV2.12.1+ or P/Q-channel blocker) blocked IPSCs evoked from both locations. Therefore 1) distinct inhibitory inputs onto projection neostriatal cells can be differentially stimulated with field electrodes; 2) N-type Ca2+ channels are not equally expressed in inhibitory terminals activated in the NS; and 3) synapses that interconnect spiny neurons use both N- and P/Q-type Ca2+ channels.

scholarly journals Influences of Morphine on the Spontaneous and Evoked Excitatory Postsynaptic Currents in Lateral Amygdala of Rats

2016 ◽  
pp. 165-169 ◽  
Author(s):  
J.-J. ZHANG ◽  
X.-D. LIU ◽  
L.-C. YU
Keyword(s):  
Synaptic Transmission ◽  
Excitatory Synaptic Transmission ◽  
Morphine Treatment ◽  
Lateral Amygdala ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Whole Cell Patch Clamp ◽  
The Central Nervous System ◽  
Underlying Mechanisms

Acute morphine exposure induces antinociceptive activity, but the underlying mechanisms in the central nervous system are unclear. Using whole-cell patch clamp recordings, we explore the role of morphine in the modulation of excitatory synaptic transmission in lateral amygdala neurons of rats. The results demonstrate that perfusion of 10 μM of morphine to the lateral amygdala inhibits the discharge frequency significantly. We further find that there are no significant influences of morphine on the amplitude of spontaneous excitatory postsynaptic currents (sEPSCs). Interestingly, morphine shows no marked influence on the evoked excitatory postsynaptic currents (eEPSCs) in the lateral amygdala neurons. These results indicate that acute morphine treatment plays an important role in the modulation on the excitatory synaptic transmission in lateral amygdala neurons of rats.

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