Presynaptic inhibition is mediated by histamine and GABA in the crustacean escape reaction

1994 ◽  
Vol 71 (3) ◽  
pp. 1088-1095 ◽  
Author(s):  
A. el Manira ◽  
F. Clarac
Keyword(s):  
Presynaptic Inhibition ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Chordotonal Organ ◽  
Gamma Aminobutyric Acid ◽  
Giant Fiber ◽  
Sensory Transmission ◽  
Gaba Antagonist ◽  
Escape Reaction

1. Presynaptic inhibition of sensory transmission during the escape reaction in Crustacea has been studied using an in vitro preparation of the crayfish thoracic ganglia. Electrical stimulation of the medial giant fiber mediating the escape reaction induced depolarization in sensory afferent terminals of the coxo-basal chordotonal organ (CBCO). This depolarization was associated with an increase of the membrane conductance and was partially blocked by a gamma-aminobutyric acid (GABA) antagonist, picrotoxin, and by a histamine antagonist, cimetidine. 2. Pressure ejection of histamine on CBCO sensory terminals (CBT) recorded intracellularly, induced a depolarization of the membrane potential accompanied by a large increase of the conductance. Histamine-induced depolarization persisted after blockade of synaptic transmission mediated by Na+ spikes by tetrodotoxin. The amplitude of histamine-induced depolarization increased when negative current was injected into the sensory terminal through the recording electrode. Moreover, injection of chloride into the CBT, which shifts the reversal potential of chloride to a more positive value, resulted in an increase of the amplitude of the histamine-induced depolarization. 3. The existence of separate receptors for GABA and histamine on the CB sensory terminals was demonstrated using two complementary sets of experiments. The first one consisted of using specific blockers of GABA and histamine. Picrotoxin blocked selectively the GABA-induced depolarization of the CB sensory terminals, while it was ineffective in blocking the histamine-induced depolarization. Conversely, cimetidine blocked the histamine-induced depolarization totally, but did not affect the GABA response. The second set of experiments tested for of cross-desensitization between GABA and histamine responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Direct evidence for presynaptic inhibitory mechanisms in crayfish sensory afferents

1992 ◽  
Vol 67 (3) ◽  
pp. 610-624 ◽  
Author(s):  
D. Cattaert ◽  
A. el Manira ◽  
F. Clarac
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Chordotonal Organ ◽  
Gamma Aminobutyric Acid ◽  
Intracellular Recordings ◽  
Recording Site ◽  
Sensory Afferents ◽  
Spike Amplitude ◽  
Presynaptic Mechanisms

1. The central control of sensory inputs from a proprioceptor [chordotonal organ (CO)] in the second joint [coxo-basipodite (CB)] of the fifth leg was studied in crayfish in vitro preparations (Fig. 1A). Simultaneous intracellular recordings from CBCO terminals (CBT) and postsynaptic motoneurons (MNs) were performed along with micropipette pressure ejection or bath application of gamma-aminobutyric acid (GABA), to study the presynaptic mechanisms at work in the CBT (Fig. 1B). 2. Two intracellular recordings were used to show that the spikes never overshoot, and that the more central the recording site within the neuropile, the smaller the spikes (Fig. 2). Only electrotonic conduction occurs, therefore, in the sensory afferents within the ganglion. 3. Pressure ejection of GABA close to the recording site of CBTs in the ganglion (Fig. 3A) gave rise to a membrane depolarization, the reversal potential of which was about -25 mV (Fig. 7), as well as to an increase in the membrane conductance (Fig. 3C) and a decrease in the orthodromic spike amplitude; moreover, it did not elicit either hyperpolarization, or any change in the membrane conductance of the postsynaptic MN (Fig. 3B), which indicates that pressure ejection of GABA affected only a restricted area around the CBT and not the postsynaptic MNs. 4. In CBT, spontaneous primary afferent depolarizations (PADs) occurred irregularly when the activity of the preparation was not rhythmic (Fig. 4A), and in bursts when the preparation displayed fictive locomotion (Fig. 4B). In the latter case, antidromic spikes were sometimes superimposed on PADs (Fig. 4D). The amplitude of the PADs was reduced when picrotoxin (PTX), a GABA antagonist, was applied (Fig. 5), which suggests that GABA may be involved in spontaneous PADs. The reversal potential of PADs was about -25 mV (Figs. 6 and 7). 5. During simultaneous recordings from a CBT and a monosynaptically related MN, GABA applied by pressure ejection close to the CBT (Fig. 8A) completely suppressed the excitatory postsynaptic potentials (EPSPs) elicited by CBT spikes in the MN (Fig. 8, B and D). This was due to a presynaptic mechanism because no change in the membrane potential or membrane conductance was observed in the MN (Fig. 8C) and most of the CBTs associated with a given MN were affected (Fig. 9). 6. Simultaneously recording from a CBT and a monosynaptically related MN demonstrated that, during bouts of PADs, the spike amplitude decreased in proportion to the PAD amplitude (Fig. 10A).(ABSTRACT TRUNCATED AT 400 WORDS)

BICUCULLINE/BACLOFEN-INSENSITIVE GABA RESPONSE IN CRUSTACEAN NEURONES IN CULTURE

1994 ◽  
Vol 191 (1) ◽  
pp. 167-193
Author(s):  
C Jackel ◽  
W Krenz ◽  
F Nagy
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Gamma Aminobutyric Acid ◽  
Action Potential Firing ◽  
Patch Clamp Technique ◽  
Conformationally Restricted ◽  
Whole Cell Patch Clamp ◽  
Gabac Receptor ◽  
Potential Firing ◽  
Sr 95531

Neurones were dissociated from thoracic ganglia of embryonic and adult lobsters and kept in primary culture. When gamma-aminobutyric acid (GABA) was applied by pressure ejection, depolarizing or hyperpolarizing responses were produced, depending on the membrane potential. They were accompanied by an increase in membrane conductance. When they were present, action potential firing was inhibited. The pharmacological profile and ionic mechanism of GABA-evoked current were investigated under voltage-clamp with the whole-cell patch-clamp technique. The reversal potential of GABA-evoked current depended on the intracellular and extracellular Cl- concentration but not on extracellular Na+ and K+. Blockade of Ca2+ channels by Mn2+ was also without effect. The GABA-evoked current was mimicked by application of the GABAA agonists muscimol and isoguvacine with an order of potency muscimol>GABA>isoguvacine. cis-4-aminocrotonic acid (CACA), a folded and conformationally restricted GABA analogue, supposed to be diagnostic for the vertebrate GABAC receptor, also induced a bicuculline-resistant chloride current, although with a potency about 10 times lower than that of GABA. The GABA-evoked current was largely blocked by picrotoxin, but was insensitive to the GABAA antagonists bicuculline, bicuculline methiodide and SR 95531 at concentrations of up to 100 µmol l-1. Diazepam and phenobarbital did not exert modulatory effects. The GABAB antagonist phaclophen did not affect the GABA-induced current, while the GABAB agonists baclophen and 3-aminopropylphosphonic acid (3-APA) never evoked any response. Our results suggest that lobster thoracic neurones in culture express a chloride-conducting GABA-receptor channel which conforms to neither the GABAA nor the GABAB types of vertebrates but shows a pharmacology close to that of the novel GABAC receptor described in the vertebrate retina.

Multimodal Convergence of Presynaptic Afferent Inhibition in Insect Proprioceptors

1999 ◽  
Vol 82 (1) ◽  
pp. 512-514 ◽  
Author(s):  
Wolfgang Stein ◽  
Josef Schmitz
Keyword(s):  
Presynaptic Inhibition ◽  
Sensory Information ◽  
Reversal Potential ◽  
Stick Insect ◽  
Chordotonal Organ ◽  
Primary Afferent Depolarization ◽  
Campaniform Sensilla ◽  
Sense Organs ◽  
Position Sensitive ◽  
Conductance Increase

In the leg motor system of insects, several proprioceptive sense organs provide the CNS with information about posture and movement. Within one sensory organ, presynaptic inhibition shapes the inflow of sensory information to the CNS. We show here that also different proprioceptive sense organs can exert a presynaptic inhibition on each other. The afferents of one leg proprioceptor in the stick insect, either the position-sensitive femoral chordotonal organ or the load-sensitive campaniform sensilla, receive a primary afferent depolarization (PAD) from two other leg proprioceptors, the campaniform sensilla and/or the coxal hairplate. The reversal potential of this PAD is about −59 mV, and the PAD is associated with a conductance increase. The properties of this presynaptic input support the hypothesis that this PAD acts as presynaptic inhibition. The PAD reduces the amplitude of afferent action potentials and thus likely also afferent transmitter release and synaptic efficacy. These findings imply that PAD mechanisms of arthropod proprioceptors might be as complex as in vertebrates.

Neuronal diversity in the subiculum: correlations with the effects of somatostatin on intrinsic properties and on GABA-mediated IPSPs in vitro

1996 ◽  
Vol 76 (3) ◽  
pp. 1657-1666 ◽  
Author(s):  
J. R. Greene ◽  
A. Mason
Keyword(s):  
Cell Layer ◽  
Hippocampal Formation ◽  
Reversal Potential ◽  
Cell Types ◽  
Gamma Aminobutyric Acid ◽  
Cell Type ◽  
Bathing Medium ◽  
Current Pulses ◽  
Series Of Experiments

1. We used intracellular current-clamp techniques to record from 33 ventral subicular neurons in slices or rat hippocampal formation. Presumed pyramidal neurons were characterized by their responses to depolarizing current pulses as either intrinsically burst firing (IB) or regular spiking (RS). Within the subiculum, IB cells were encountered most frequently in the deep cell layer, whereas RS cells were encountered most frequently in the superficial cell layer. IB cells had more depolarized resting potentials, lower input resistances, and more sag in their voltage responses to hyperpolarizing current pulses. 2. Somatostatin (5 microM) applied in the bathing medium caused a hyperpolarization and reduction in input resistance. These effects were of greater magnitude in IB cells. Somatostatin had no effect on sag in either cell type. These effects of somatostatin were unchanged in the presence of gamma-aminobutyric acid (GABA) receptor antagonists. 3. In a series of experiments conducted in RS cells only, somatostatin reduced the amplitude of the late but not the early component of evoked biphasic inhibitory postsynaptic potentials (IPSPs). 4. A second series of experiments was conducted in RS and IB cells. Somatostatin reduced the amplitude of pharmacologically isolated GABAA IPSPS in both cell types. In IB cells but not RS cells there was a correlation between this effect and the somatostatin-induced hyperpolarization. Somatostatin also reduced the amplitude of isolated GABAB IPSPS in both cell types, but more so in IB cells. 5. Somatostatin had no effect on the reversal potential of either IPSP in either cell type and no effect on the GABAA-mediated conductance in either cell type. In contrast, the GABAB-mediated conductance was reduced, especially in IB cells. 6. The effects of somatostatin on GABAA IPSPS are principally a result of membrane shunting and reductions in ionic driving force, but these mechanisms do not account for the reduction in GABAB IPSPS. 7. We suggest that the combined effects of somatostatin are likely to alter the balance between fast and slow inhibition and to do so more in IB cells than in RS cells.

Synaptic responses of guinea pig and rat central amygdala neurons in vitro

1991 ◽  
Vol 65 (5) ◽  
pp. 1227-1241 ◽  
Author(s):  
I. Nose ◽  
H. Higashi ◽  
H. Inokuchi ◽  
S. Nishi
Keyword(s):  
Guinea Pig ◽  
Reversal Potential ◽  
Input Resistance ◽  
Short Latency ◽  
Central Nucleus ◽  
Gamma Aminobutyric Acid ◽  
Basal Nucleus ◽  
Long Latency ◽  
Stimulation Of

1. To investigate postsynaptic potentials (PSPs), we made intracellular recordings from neurons of the amygdaloid central nucleus in slices from the guinea pig and rat brains maintained in vitro. The results from guinea pigs and rats were very similar. 2. In the presence of bicuculline (20 microM), focal electrical stimulation of the amygdaloid basal nucleus with low intensities elicited short-latency excitatory PSPs (EPSPs) followed by long-latency EPSPs. The short-latency EPSP was selectively blocked by 6-cyano-7-nitroquinoxaline-2,3-dion (CNQX; 10-20 microM). The long-latency EPSP was preferentially abolished by D,L-2-amino-5-phosphonovaleric acid (D,L-APV; 40 microM) and was augmented by removal of extracellular Mg2+. The compound EPSP reversed at -4 mV, which was close to -1 mV, the reversal potential for pressure-ejected glutamate (Glu). 3. When the intensity of the focal stimulation was increased in the presence of bicuculline (20 microM), CNQX (20 microM), and D,L-APV (50 microM), a second EPSP with a short latency and a prolonged duration could be evoked in approximately 65% of the neurons. The EPSPs were reversibly blocked by d-tubocurarine (50 microM) or hexamethonium (200 microM) but were unaffected by atropine (1 microM) or a 5-hydroxytryptamine type 3 receptor antagonist, ICS-205930 (5-10 microM). In these neurons, acetylcholine (ACh; 1-3 mM) caused a depolarization, associated with a decreased input resistance. 4. In the presence of CNQX (20 microM) and D,L-APV (50 microM), single focal stimulation of the dorsolateral subdivision in the central nucleus with low intensities elicited a depolarizing inhibitory PSP (IPSP). The IPSP was reversibly abolished by bicuculline (20-40 microM). The reversal potential (-63 mV) for the IPSP was similar to the reversal potential (-61 mV) for the response to gamma-aminobutyric acid (GABA) applied by pressure ejection. 5. In the presence of bicuculline (20-40 microM) and CNQX (20 microM), a repetitive focal stimulus with high intensities delivered to the dorsolateral subdivision produced a hyperpolarizing PSP followed by a slow depolarization in most neurons. Of putative inhibitory amino acid transmitters, glycine (Gly; 3 mM) produced only a hyperpolarization, associated with a decrease in input resistance. Strychnine (1-2 microM) reversibly blocked both the Gly hyperpolarization and the synaptically evoked hyperpolarization. The reversal potential of -81 mV for the hyperpolarizing PSP was close to -82 mV for the Gly hyperpolarization. The reversal potential for the Gly response was shifted to less negative values by increasing the external K+ concentration or decreasing the extracellular Cl- concentration.(ABSTRACT TRUNCATED AT 400 WORDS)

GABA as an inhibitory neurotransmitter in human cerebral cortex

1989 ◽  
Vol 62 (5) ◽  
pp. 1018-1027 ◽  
Author(s):  
D. A. McCormick
Keyword(s):  
Cerebral Cortex ◽  
Cortical Neurons ◽  
Epileptiform Activity ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Pyramidal Cells ◽  
Excitatory Postsynaptic Potential ◽  
Gamma Aminobutyric Acid ◽  
Human Cerebral Cortex ◽  
Inhibitory Neurotransmitter

1. The possible role of gamma-aminobutyric acid (GABA) as an inhibitory neurotransmitter in the human cerebral cortex was investigated with the use of intracellular recordings from neocortical slices maintained in vitro. 2. Electrical stimulation of afferents to presumed pyramidal cells resulted in an initial excitatory postsynaptic potential (EPSP) followed by fast and slow inhibitory postsynaptic potentials (IPSPs). The early IPSP had an average reversal potential of -68 mV, was associated with a mean 67-nS increase in membrane conductance, was reduced by the GABAA antagonist bicuculline, was sensitive to the intracellular injection of Cl-, and was mimicked by the GABAA agonist muscimol. 3. The late IPSP, in contrast, had an average reversal potential of -95 mV, was associated with a mean 12-nS increase in membrane conductance, was reduced by the GABAB antagonist phaclofen, and was mimicked by the GABAB agonist baclofen. 4. Block of the early IPSP by bicuculline or picrotoxin led to the generation of paroxysmal epileptiform activity, which could be further enhanced by reduction of the late IPSP. 5. These data strongly support the hypothesis that GABA is a major inhibitory neurotransmitter in the human cerebral cortex and that GABAergic IPSPs play an important role in controlling the excitability and responsiveness of cortical neurons.

GABA-activated whole-cell currents in isolated retinal ganglion cells

1988 ◽  
Vol 60 (2) ◽  
pp. 381-396 ◽  
Author(s):  
A. T. Ishida ◽  
B. N. Cohen
Keyword(s):  
Ganglion Cell ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Noise Analysis ◽  
Reversal Potential ◽  
Retinal Ganglion ◽  
Gamma Aminobutyric Acid ◽  
Whole Cell

1. We have begun to analyze neurotransmitter-activated conductances in retinal ganglion cells by measuring the response of single voltage-clamped adult goldfish ganglion cells to gamma-aminobutyric acid (GABA). Here we describe 1) our method of identifying ganglion cells in vitro after their dissociation from papain-treated retinas, and 2) the response of these cells to GABA in the tight-seal whole cell configuration of the patch-clamp method (cf. 41) after 1-4 days of primary cell culture. 2. Ganglion cell somata were backfilled in situ by injections of horseradish peroxidase (HRP) into the optic nerve. After dissociation of the retinas containing these cells, HRP reaction product was localized to cells that retained the size, shape, and an intracellular organelle characteristic of ganglion cells in situ. These features enabled us thereafter to identify ganglion cells in vitro without retrograde marker transport. 3. GABA (3-10 microM) elicited inward currents and substantial noise increases in almost all ganglion cells at negative holding potentials. Reversal potential measurements in salines containing different chloride concentrations indicated that GABA produces a chloride-selective conductance increase in ganglion cells. Bicuculline (10 microM) reversibly inhibited ganglion cell GABA responses. Baclofen (10 microM) alone elicited no responses in ganglion cells. 4. Noise analysis of GABA-activated whole cell currents yielded elementary conductance estimates of 16 pS, with a slow time constant of 30 ms plus a faster component of 1-2 ms. No significant voltage dependence of these values was observed between -20 and -80 mV. 5. We have thus devised a means of identifying ganglion cells dissociated from adult retinas, identified GABAA receptors (cf. 16) on these cells, and found that the responses mediated by these receptors resemble those found in other regions of central nervous system (CNS). These results are consistent with the notion that GABA may function as an inhibitory transmitter at synapses on ganglion cells.

Effects of ethanol and other drugs on excitatory and inhibitory neurotransmission in the crayfish

1992 ◽  
Vol 67 (3) ◽  
pp. 576-587 ◽  
Author(s):  
J. A. Blundon ◽  
G. D. Bittner
Keyword(s):  
Presynaptic Inhibition ◽  
Time Course ◽  
Muscle Fibers ◽  
Gabab Receptors ◽  
Inhibitory Synapses ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Potentials ◽  
Postsynaptic Currents ◽  
Gabaa Antagonist

1. Crayfish exposed to 434 mM ethanol (EtOH) showed signs of hyperactivity within 0.5-2 h, at which times crayfish hemolymph EtOH concentration had reached 60-90 mM. 2. A 10-min exposure to 60-90 mM EtOH reduced presynaptic inhibition of excitatory postsynaptic currents (EPSCs) at the crayfish opener neuromuscular junction (NMJ) in vitro but did not significantly alter excitatory neurotransmission. The same concentrations of EtOH did not alter other potentials or currents associated with inhibition at this synapse, such as presynaptic inhibitory potentials (PIPs), inhibitory postsynaptic potentials (IPSPs), and inhibitory postsynaptic currents (IPSCs). 3. Intermediate EtOH concentrations (120-180 mM) applied for 10 min in vitro reduced the amplitude of excitatory postsynaptic potentials (EPSPs) by decreasing the membrane resistance of opener muscle fibers and by reducing the amplitude of EPSCs. 4. High EtOH concentrations (434 mM) applied for 10 min in vitro had yet greater depressive effects on measures of postsynaptic properties described above. The time course of EPSCs was also significantly reduced. In addition, presynaptic properties such as action-potential (AP) amplitude and frequency of spontaneous release of neurotransmitter were reduced by 434 mM EtOH. 5. Presynaptic inhibition, gamma-aminobutyric acid (GABA; 250-500 microM), muscimol (50 microM), and baclofen (75 microM) all reduced the depolarizing afterpotential of APs in the excitor axon and reduced EPSPs in opener muscle fibers. GABA (500 microM) and baclofen (75 microM) significantly reduced presynaptic AP amplitudes, whereas presynaptic inhibition, GABA (250 microM), and muscimol (50 microM) had no effect on AP amplitude. Bicuculline (250-500 microM), a GABAA antagonist, did not entirely eliminate presynaptic inhibition, whereas picrotoxin (50 microM), another GABAA antagonist, completely removed presynaptic inhibition. Thus presynaptic inhibitory mechanisms may involve both GABAA and GABAB receptors on the opener excitor axon. 6. Our data suggest that the behavioral hyperactivity seen at hemolymph EtOH concentrations of 60-90 mM is not accompanied by a change in excitatory synaptic transmission observed at the opener NMJ. Rather, crayfish hyperactivity may be due to depressive effects of EtOH on inhibitory synapses in the CNS similar to the disinhibition evoked by EtOH at the opener NMJ.

Functional and Ionic Properties of a Slow Afterhyperpolarization in Ferret Perigeniculate Neurons In Vitro

1998 ◽  
Vol 80 (3) ◽  
pp. 1222-1235 ◽  
Author(s):  
Uhnoh Kim ◽  
David A. Mccormick
Keyword(s):  
Low Frequency ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Intracellular Recordings ◽  
Persistent Currents ◽  
Current Application ◽  
Plateau Potential ◽  
Frequency Components ◽  
Low Threshold

Kim, Uhnoh and David A. McCormick. Functional and ionic properties of a slow afterhyperpolarization in ferret perigeniculate neurons in vitro. J. Neurophysiol. 80: 1222–1235, 1998. Intracellular recordings from spontaneously spindling GABAergic neurons of the ferret perigeniculate nucleus in vitro revealed a fast afterhyperpolarization after each action potential, a medium-duration afterhyperpolarization after each low-threshold Ca2+ spike, and a slow afterhyperpolarization after the cessation of spindle waves. The slow afterhyperpolarization was associated with an increase in membrane conductance, and the reversal potential was sensitive to extracellular [K+]o, indicating that it is mediated at least in part by the activation of a K+ conductance. However, the block of Ca2+ channels did not block the slow afterhyperpolarization, whereas the block of Na+ channels did block this event, even after the generation of repetitive Ca2+ spikes, indicating that it is mediated by a Na+-activated K+ current. Application of apamin reduced the afterhyperpolarization and enhanced a plateau potential after each low-threshold Ca2+ spike. This plateau potential could result in a prolonged depolarization of perigeniculate neurons, even before the application of apamin, resulting in the generation of tonic discharge. The plateau potential was blocked by the local application of tetrodotoxin, indicating that it is mediated by a persistent Na+ current. The activation and interaction of these slowly developing and persistent currents contributes significantly to low-frequency components of spindle wave generation. In particular, we suggest that the activation of the slow afterhyperpolarization may contribute to the generation of the spindle wave refractory period in vitro.

Cholecystokinin depolarizes rat thalamic reticular neurons by suppressing a K+ conductance

1995 ◽  
Vol 74 (3) ◽  
pp. 990-1000 ◽  
Author(s):  
C. L. Cox ◽  
J. R. Huguenard ◽  
D. A. Prince
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Membrane Depolarization ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Equilibrium Potential ◽  
K Channel ◽  
Neuron Activity ◽  
Cck Receptors

1. The thalamic reticular nucleus (nRt) is innervated by cholecystokinin (CCK)-containing neurons and contains CCK binding sites. We used tight-seal, whole cell recording techniques with in vitro rat thalamic slices to investigate the action of CCK on neurons in nRt and ventrobasal thalamus (VB). 2. Brief applications of the CCK agonist cholecystokinin octapeptide (26-33) sulfated (CCK8S) evoked prolonged spike discharges in nRt neurons but had no direct effects on VB neuron activity. This selective excitatory action of CCK8S in nRt resulted from a long-lasting membrane depolarization (2-10 min) associated with an increased input resistance. Voltage-clamp recordings revealed that CCK8S reduced membrane conductance by 0.6-3.8 nS, which amounted to 5-54% of the resting conductance of these neurons. 3. The conductance blocked by CCK8S was linear over the range of -50 to -100 mV and reversed near the potassium equilibrium potential. Modifications of extracellular K+ concentration altered the reversal potential of the conductance as predicted by the Nernst equation. The K+ channel blocker Cs+, applied either intracellularly or combined intra- and extracellularly, blocked the response to CCK8S. 4. The CCK8S-induced depolarization persisted after suppression of synaptic transmission by either tetrodotoxin or a low-Ca2+, high-Mg2+ extracellular solution, indicating that the depolarization was primarily due to activation of postsynaptic CCK receptors and not mediated through the release of other neurotransmitters. 5. The selective CCKA antagonists L364,718 and Cam-1481 attenuated the CCK8S-induced depolarization, whereas the CCKB antagonist L365,260 had little or no effect on the depolarization. 6. Our findings indicate that CCK8S, acting via CCKA-type receptors, reduces a K+ leak current, resulting in a long-lasting membrane depolarization that can presumably modify the firing mode of nRt neurons. Through this effect, CCK actions in nRt may strongly influence thalamocortical function.

Sign in / Sign up

Export Citation Format

Share Document