Inhibition of mechanosensory interneurons in the crayfish. I. Presynaptic inhibition from giant fibers

1980 ◽  
Vol 43 (6) ◽  
pp. 1495-1509 ◽  
Author(s):  
D. Kennedy ◽  
J. McVittie ◽  
R. Calabrese ◽  
R. A. Fricke ◽  
W. Craelius ◽  
...  
Keyword(s):  
Reversal Potential ◽  
Repetitive Firing ◽  
Primary Afferent Depolarization ◽  
Gamma Aminobutyric Acid ◽  
Giant Axons ◽  
Pharmacological Studies ◽  
Sucrose Gap ◽  
Conductance Increase ◽  
Tail Flip ◽  
Stimulation Of

1. Sucrose-gap and intracellular recordings were used to study the primary afferent depolarization (PAD) produced in mechanosensory afferents by impulses in lateral and medial giant axons, which are the command cells for the tail flip escape response in the crayfish. 2. The lateral and medial giant axons produce PAD through a polysynaptic interneuronal pathway. The response has a relatively long intraganglionic latency (7--11 ms), and command-evoked PAD can be recorded in ganglia from which the giant axons have been experimentally disconnected. 3. The final neurons of the pathway that delivers inhibition are few in number and extensive in distribution; most appear to be common to lateral and medial giant pathways. 4. At least some of the inhibitory interneurons have axons in the interganglionic connectives and probably produce both presynaptic and postsynaptic inhibition. 5. Stimulation of the lateral, but not the medial, giant axons causes a small, short-latency deplorization that is stable at high repetition rates. This small potential can be accounted for by transmission across known electrical synapses between mechanosensory afferents and the lateral giants in each abdominal ganglion. 6. Repetitive stimulation of the lateral giant axons causes substantial augmentation of PAD, apparently through recruitment of additional interneurons. PAD evoked by a single medial giant (MG) stimulus is generally much larger than that elicited by a single lateral giant (LG) spike. However, MG-PAD summates little and so the maximum PAD deltaV reached during repetitive firing is equivalent for the two types of giant axons. 7. Iontophoresis of gamma-aminobutyric acid (GABA) into the ganglionic neuropil depolarizes the primary afferents and blocks activity in neurons that have axons in the interganglionic connective. 8. The extrapolated PAD reversal potential and pharmacological studies suggest that a GABA-mediated chloride conductance increase is involved in the production of PAD.

Ammonia does not selectively block IPSPs in rat hippocampal pyramidal cells

1983 ◽  
Vol 49 (6) ◽  
pp. 1381-1391 ◽  
Author(s):  
B. E. Alger ◽  
R. A. Nicoll
Keyword(s):  
Reversal Potential ◽  
Pyramidal Cells ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Potentials ◽  
Calcium Dependent ◽  
Nonspecific Effects ◽  
Chloride Pump ◽  
High Concentrations ◽  
Conductance Increase ◽  
Potassium Response

Intracellular recordings from CA1 pyramidal cells in the rat hippocampal slice preparation have been used to study the action of ammonia on inhibitory postsynaptic potentials (IPSPs). Concentrations of ammonia less than 2 mM had little effect on IPSPs or the action of iontophoretically applied gamma-aminobutyric acid (GABA). This concentration has been reported to be fully effective in blocking hyperpolarizing IPSPs in spinal cord and neocortex. Concentrations above 2 mM did cause a depolarizing shift in the IPSP and GABA reversal potentials, but this effect was accompanied by several generalized effects. The conductance increase during the IPSP but not during the GABA response was depressed, indicating that ammonia has a presynaptic depressant effect on the IPSP. Ammonia also depressed excitatory postsynaptic potentials (EPSPs), presynaptic fiber potentials, and pyramidal cell population spikes. In addition, the calcium-dependent potassium response elicited by depolarizing current pulses was depressed. This depression was due, in part, to a depolarizing shift in the reversal potential for this response. Responses recorded with potassium-sensitive microelectrodes indicate that ammonia releases potassium into the extracellular space. The possibility is discussed that the shifts in IPSP reversal potential seen with high concentrations of ammonia are a consequence of generalized nonspecific effects. We conclude that the relative insensitivity of hippocampal IPSPs to blockade by ammonia suggests that a mechanism fundamentally unlike an ammonia-sensitive chloride pump must maintain the hippocampal IPSP gradient.

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.

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)

Inhibitory transmission in the basolateral amygdala

1991 ◽  
Vol 66 (3) ◽  
pp. 999-1009 ◽  
Author(s):  
D. G. Rainnie ◽  
E. K. Asprodini ◽  
P. Shinnick-Gallagher
Keyword(s):  
Reversal Potential ◽  
Nmda Antagonist ◽  
Gabab Receptors ◽  
Excitatory Postsynaptic Potential ◽  
Sodium Pentobarbital ◽  
Gamma Aminobutyric Acid ◽  
Gabaa Receptor Antagonist ◽  
Basolateral Nucleus ◽  
Stimulation Of ◽  
Synaptic Responses

1. Intracellular recording techniques were used to characterize synaptic inhibitory postsynaptic potentials (IPSPs) recorded from neurons of the basolateral nucleus of the amygdala (BLA). Bipolar electrodes positioned in the stria terminalis (ST) or lateral amygdala (LA) were used to evoke synaptic responses at a frequency of 0.25 Hz. 2. Two synaptic waveforms having IPSP components could be evoked by electrical stimulation of either pathway: a biphasic, excitatory postsynaptic potential (EPSP), fast-IPSP (f-IPSP) waveform, and a multiphasic, EPSP, f-IPSP, and subsequent slow-IPSP (s-IPSP) waveform. Expression of either waveform was dependent on the site of stimulation. ST stimulation evoked a similar number of biphasic (45%) and multiphasic (50%) synaptic responses. In contrast, stimulation of the LA pathway evoked mainly (80%) multiphasic synaptic responses. 3. Both the f- and s-IPSP elicited by ST stimulation could be reduced in amplitude in the presence of the glutamatergic, N-methyl-D-aspartate (NMDA) antagonist, (DL)-2-amino-5-phosphonovaleric acid (APV, 50 microM), and were abolished by the glutamatergic, non-NMDA antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM). In contrast, a CNQX-resistant f-IPSP was evoked with LA stimulation and abolished by subsequent addition of bicuculline methiodide (BMI), a gamma-aminobutyric acid (GABAA) receptor antagonist, suggesting direct inhibition of BLA neurons by GABAergic LA interneurons. The sensitivity of the s-IPSPs and the f-IPSPs to glutamatergic antagonists suggests the presence of feed-forward inhibition onto BLA neurons. 4. The f-IPSP possessed characteristics of potentials mediated by GABAA receptors linked to Cl- channels, namely, a reversal potential of -70 mV, a decrease in membrane resistance (13.5 M omega) recorded at -60 mV, a block by BMI, and potentiation by sodium pentobarbital (NaPB). 5. The s-IPSP was associated with a resistance decrease of 4.5 M omega, a reversal potential of -95 mV, and was reversibly depressed (approximately 66%) by 2-hydroxy-saclofen (100 microM), suggesting activation of GABAB receptors. 6. The large resistance change associated with the f-IPSP, its temporal overlap with evoked EPSPs, and the development of both spontaneous and evoked burst firing in the presence of BMI suggests that the f-IPSP determines the primary state of excitability in BLA neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Presynaptic inhibition of exteroceptive afferents by proprioceptive afferents in the terminal abdominal ganglion of the crayfish

1996 ◽  
Vol 76 (2) ◽  
pp. 1047-1058 ◽  
Author(s):  
P. L. Newland ◽  
H. Aonuma ◽  
M. Sato ◽  
T. Nagayama
Keyword(s):  
Sensory Neurons ◽  
Sensory Nerve ◽  
Abdominal Ganglion ◽  
Resting Potential ◽  
Primary Afferent Depolarization ◽  
Gamma Aminobutyric Acid ◽  
Water Displacement ◽  
Conductance Increase ◽  
Proprioceptive Afferents ◽  
Chemical Synapses

1. Exteroceptive hairs that are sensitive to water displacement and touch are distributed over the surface of the tailfan of crayfish. We show that the sensory neurons innervating these hairs receive a primary afferent depolarization (PAD) from sensory neurons innervating a proprioceptor that monitors movements of the endopodite and protopodite of the tailfan. This PAD occurs only during high-velocity movements of the exopodite, which are similar to those that occur during swimming. The effects that the proprioceptor mediate are widespread, so that afferents in four sensory nerve roots of the terminal abdominal ganglion, innervating hairs on the protopodite, exopodite, endopodite, and telson, receive a PAD. The PAD is unlikely to be mediated through monosynaptic pathways because there is no anatomic overlap between the central projections of chordotonal afferents and many of the exteroceptive afferents. The depolarization is associated with a conductance increase and can be increased by the injection of hyperpolarizing current or reversed (approximately 10 mV above resting potential) by injection of depolarizing current. The properties of the presynaptic input are, therefore, consistent with being mediated through chemical synapses. This is supported by the observation in the electron microscope that the exteroceptive afferents receive chemical input synapses. The depolarization is mimicked by gamma-aminobutyric acid and reduced by bath application of picrotoxin or bicuculline, suggesting that it is a depolarizing inhibitory postsynaptic potential. The PAD reduces the amplitude of exteroceptive afferent spikes, an action that is thus likely to reduce transmitter release and the efficacy of synaptic transmission.

GABAb receptors are coupled to a barium-insensitive outward rectifying potassium conductance in premotor respiratory neurons

1993 ◽  
Vol 69 (1) ◽  
pp. 286-289 ◽  
Author(s):  
P. G. Wagner ◽  
M. S. Dekin
Keyword(s):  
Single Channel ◽  
Gabab Receptor ◽  
Potassium Conductance ◽  
Reversal Potential ◽  
Gabab Receptors ◽  
Respiratory Neurons ◽  
Repetitive Firing ◽  
K Channel ◽  
Gamma Aminobutyric Acid ◽  
Bath Application

1. Labeled premotor respiratory neurons from neonatal rats in culture were used to study the effects of (+/-)baclofen, a selective gamma-aminobutyric acid (GABA)b receptor agonist known to inhibit rhythmic breathing movements in mammals. Bath application of (+/-)baclofen-activated outward currents in cell-attached patches, suggesting that a second messenger system linked the (+/-)baclofen-activated conductance (GBac) to the GABAb receptor. 2.GBac channels exhibited outward rectification and were insensitive to blockade by Ba2+ and Cs+. The single-channel conductance was 100 pS in symmetrical K+ solutions and decreased as [K+]o was reduced. The reversal potential for the GBac channel shifted 45 mV/decade when [K+]o was changed indicating that it was predominantly selective for K+ ions. These properties were similar to those of the S-channel in Aplysia sensory neurons. 3. The properties of GBac channels were distinct from those associated with the GABAb mediated slow inhibitory postsynaptic potential (IPSP), indicating that GABAb receptors can be associated with more than one type of K+ channel. We propose that GBac channels modulate the repetitive firing activity of premotor respiratory neurons and may also participate in presynaptic inhibition.

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.

Actions of norepinephrine on rat hypoglossal motoneurons

1995 ◽  
Vol 74 (5) ◽  
pp. 1911-1919 ◽  
Author(s):  
M. A. Parkis ◽  
D. A. Bayliss ◽  
A. J. Berger
Keyword(s):  
Choline Chloride ◽  
Reversal Potential ◽  
Repetitive Firing ◽  
Inward Current ◽  
Hypoglossal Motoneurons ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Perfusion Solution ◽  
Adrenoceptor Agonist ◽  
Firing Properties

1. We used conventional intracellular recording techniques in 400-microns-thick slices from the brain stems of juvenile rats to investigate the action of norepinephrine (NE) on subthreshold and firing properties of hypoglossal motoneurons (HMs). 2. In recordings in current-clamp mode, 50 or 100 microM NE elicited a reversible depolarization accompanied by an increase in input resistance (RN) in all HMs tested (n = 74). In recordings in single-electrode voltage-clamp mode, NE induced a reversible inward current (INE) accompanied by a reduction in input conductance. The average reversal potential for INE was -104 mV. The NE responses could be elicited in a Ca(2+)-free solution containing tetrodotoxin, indicating that they were postsynaptic. 3. The NE response could be blocked by the alpha-adrenoceptor antagonist prazosin, but not by the beta-adrenoceptor antagonist propranolol, and could be mimicked by the alpha 1-adrenoceptor agonist phenylephrine but not by the alpha 2-adrenoceptor agonist UK 14,304 or by the beta-adrenoceptor agonist isoproterenol when alpha-adrenoceptors were blocked. 4. Substitution of barium for calcium in the perfusion solution blocked the increase in RN in response to NE without completely blocking the depolarization. Replacement of sodium chloride with choline chloride in the barium-substituted perfusion solution blocked the remaining depolarization. 5. The neuropeptide thyrotropin-releasing hormone (TRH), which also depolarizes and increases the RN of HMs, occluded the response of HMs to NE. 6. NE altered HM firing properties in three ways: it always lowered the minimum amount of injected current needed to elicit repetitive firing, it increased the slope of the firing frequency versus injected current relation in 8 of 14 cells tested, and it increased the delay from the onset of the depolarizing current pulse to the first evoked spike in all cells tested. 7. We conclude that NE acts directly on alpha 1-adrenoceptors to increase the excitability of HMs. It does this by reducing a barium-sensitive resting potassium current and activating a barium-insensitive inward current carried primarily by sodium ions. A portion of the intracellular pathway for these actions is shared by TRH. In addition, there is evidence that NE alters HM firing patterns by affecting currents that are activated following depolarization.

Properties of Unitary IPSCs in Hippocampal Pyramidal Cells Originating From Different Types of Interneurons in Young Rats

1997 ◽  
Vol 77 (4) ◽  
pp. 1939-1949 ◽  
Author(s):  
Mohamed Ouardouz ◽  
Jean-Claude Lacaille
Keyword(s):  
Reversal Potential ◽  
Pyramidal Cells ◽  
Mean Amplitude ◽  
Paired Pulse ◽  
Young Rats ◽  
Different Types ◽  
The Mean ◽  
Paired Pulse Depression ◽  
Types Of Interneurons ◽  
Stimulation Of

Ouardouz, Mohamed and Jean-Claude Lacaille. Properties of unitary IPSCs in hippocampal pyramidal cells originating from different types of interneurons in young rats. J. Neurophysiol. 77: 1939–1949, 1997. Whole cell recordings were used in hippocampal slices of young rats to examine unitary inhibitory postsynaptic currents (uIPSCs) evoked in CA1 pyramidal cells at room temperature. Loose cell-attached stimulation was applied to activate single interneurons of different subtypes located in stratum oriens (OR), near stratum pyramidale (PYR), and at the border of stratum radiatum and lacunosum-moleculare (LM). uIPSCs evoked by stimulation of PYR and OR interneurons had similar onset latency, rise time, peak amplitude, and decay. In contrast, uIPSCs elicited by activation of LM interneurons were significantly smaller in amplitude and had a slower time course. The mean reversal potential of uIPSCs was −53.1 ± 2.1 (SE) mV during recordings with intracellular solution containing potassium gluconate. With the use of recording solution containing the potassium channel blocker cesium, the reversal potential of uIPSCs was not significantly different (−58.5 ± 2.6 mV), suggesting that these synaptic currents were not mediated by potassium conductances. Bath application of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline (25 μM) reversibly blocked uIPSCs evoked by stimulation of all interneuron subtypes. In bicuculline, the mean peak amplitude of uIPSCs recorded with potassium gluconate was reduced to 3.5 ± 4.4% of control ( n = 7). Similarly, with cesium methanesulfonate, the mean amplitude in bicuculline was 2.9 ± 3.1% of control ( n = 13). Application of the GABAB receptor antagonist CGP 55845A (5 μM) resulted in a significant and reversible increase in the mean amplitude of uIPSCs recorded with cesium-containing intracellular solution. Thus uIPSCs from all cell types appeared under tonic presynaptic inhibition by GABAB receptors. Paired stimulation of individual interneurons at 100- to 200-ms intervals did not result in paired pulse depression of uIPSCs. For individual responses, a significant negative correlation was observed between the amplitude of the first and second uIPSCs. A significant paired pulse facilitation (154.0 ± 8.0%) was observed when the first uIPSC was smaller than the mean of all first uIPSCs. A small, but not significant, paired pulse depression (90.8 ± 4.0%) was found when the first uIPSC was larger than the mean of all first uIPSCs. Our results indicate that these different subtypes of hippocampal interneurons generate Cl−-mediated GABAA uIPSCs. uIPSCs originating from different types of interneurons may have heterogeneous properties and may be subject to tonic presynaptic inhibition via heterosynaptic GABAB receptors. These results suggest a specialization of function for inhibitory interneurons and point to complex presynaptic modulation of interneuron function.

Characterization of synaptically mediated fast and slow inhibitory processes in piriform cortex in an in vitro slice preparation

1988 ◽  
Vol 59 (5) ◽  
pp. 1352-1376 ◽  
Author(s):  
G. F. Tseng ◽  
L. B. Haberly
Keyword(s):  
Membrane Potential ◽  
Piriform Cortex ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Membrane Depolarization ◽  
Resting Membrane Potential ◽  
Excitatory Postsynaptic Potential ◽  
Pentobarbital Sodium ◽  
Postsynaptic Potential ◽  
Conductance Increase

1. Intracellular recordings were obtained from anatomically verified layer II pyramidal cells in slices from rat piriform cortex cut perpendicular to the surface. 2. Responses to afferent and association fiber stimulation at resting membrane potential consisted of a depolarizing potential followed by a late hyperpolarizing potential (LHP). Membrane polarization by current injection revealed two components in the depolarizing potential: an initial excitatory postsynaptic potential (EPSP) followed at brief latency by an inhibitory postsynaptic potential (IPSP) that inverted with membrane depolarization and truncated the duration of the EPSP. 3. The early IPSP displayed the following characteristics suggesting mediation by gamma-aminobutyric acid (GABA) receptors linked to Cl- channels: associated conductance increase, sensitivity to increases in internal Cl- concentration, blockage by picrotoxin and bicuculline, and potentiation by pentobarbital sodium. The reversal potential was in the depolarizing direction with respect to resting membrane potential so that the inhibitory effect was exclusively via current shunting. 4. The LHP had an associated conductance increase and a reversal potential of -90 mV in normal bathing medium that shifted according to Nernst predictions for a K+ potential with changes in external K+ over the range 4.5-8 mM indicating mediation by the opening of K+ channels and ruling out an electrogenic pump origin. 5. Lack of effect of bath-applied 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) or internally applied ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) on the LHP and failure of high amplitude, direct membrane depolarization to evoke a comparable potential, argue against endogenous mediation of the LHP by a Ca2+ activated K+ conductance [gK(Ca)]. However, an apparent endogenously mediated gK(Ca) with a duration much greater than the LHP was observed in a low percent of layer II pyramidal cells. Lack of effect of 8-Br-cAMP also indicates a lack of dependence of the LHP on cAMP. 6. Other characteristics of the LHP that were demonstrated include: a lack of blockage by GABAA receptor antagonists, a probable voltage sensitivity (decrease in amplitude in the depolarizing direction), and an apparent brief onset latency (less than 10 ms) when the early IPSP was blocked by picrotoxin. The LHP was unaffected by pentobarbital sodium when the early IPSP was blocked by picrotoxin. 7. Both the LHP and early IPSP were blocked by low Ca2+/high Mg2+, consistent with disynaptic mediation.(ABSTRACT TRUNCATED AT 400 WORDS)

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