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P Shinnick-Gallagher

Publications and source records attributed to P Shinnick-Gallagher.

At least 19 recordsLinked to original sources
PubMed1992

In vivo kindling does not alter afterhyperpolarizations (AHPs) following action potential firing in vitro in basolateral amygdala neurons.

Kindling in vivo results in enhanced glutamatergic synaptic transmission and epileptiform bursting in vitro in neurons of the basolateral amygdala (BLA). We tested the hypothesis that reduction of intrinsic inhibitory mechanisms, such as the slow- and medium-afterhyperpolarizations (s-AHPs, m-AHPs), contributes to the enhanced neuronal excitability observed in kindling-induced epileptogenesis using intracellular recording methodology. In these studies, neurons were recorded from the BLA contralateral to the kindling site. AHPs following depolarizing current-induced (100 ms, 1 nA) action potentials were recorded from BLA neurons of control and kindled animals. We found no difference in the amplitude of the s-AHP and m-AHP, or the duration of the s-AHP between control and kindled neurons. In addition, kindling did not alter the distribution of accommodating/non-accommodating BLA neurons (as assessed from neuronal responses during long (500 ms) depolarizing current injection). It is concluded that an alteration in the neuronal network within the BLA rather than a blockade of an intrinsic inhibitory mechanism underlies the enhanced excitability recorded in BLA neurons following kindling.

Action Potentials↗
PubMed1992

Trans-ACPD and L-APB presynaptically inhibit excitatory glutamatergic transmission in the basolateral amygdala (BLA).

Intracellular recordings were obtained from neurones of the basolateral nucleus of the amygdala (BLA) and glutamate-mediated EPSPs evoked by stimulation of the stria terminalis (ST). The conformationally restricted analogue of glutamate trans-1-aminocyclopentane-1,3-dicarboxylic acid (trans-ACPD) caused a dose-dependent reduction in EPSP amplitude, EC50 approximately 50 microM. This effect was mimicked by the glutamate autoreceptor agonist, L-aminophosphonobutyric acid (L-APB, 50 microM). Furthermore, the effects of submaximal concentrations (50 microM) of trans-ACPD and L-APB were additive. The reduction in EPSP amplitude is observed with concentrations of both drugs that have no effect on either the resting membrane potential or the input resistance of BLA neurones. In addition, these compounds can reduce EPSP amplitude but not the response to exogenous application of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-proprionate (AMPA) suggesting activation of presynaptic receptors. These findings suggest that both trans-ACPD and L-APB act at presynaptic glutamate receptors on glutamatergic afferents to reduce excitatory transmission in the BLA.

Aminobutyrates↗
PubMed1992

Kindling-induced long-lasting changes in synaptic transmission in the basolateral amygdala.

1. Intracellular current-clamp recordings were obtained from neurons of the basolateral amygdala (BLA) in an in vitro slice preparation from control and kindled animals. Postsynaptic potentials, elicited by stimulation of the stria terminalis (ST) or lateral amygdaloid nucleus (LA), were used to investigate the role of excitatory and inhibitory amino acid transmission in kindling-induced epileptiform activity. The contributions of glutamatergic and GABAergic receptor subtypes were analyzed by use of the non-N-methyl-D-aspartate (non-NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the NMDA antagonist DL-2-amino-5-phosphonovaleric acid (APV), and the GABAA antagonist bicuculline methiodide (BMI). 2. The synaptic waveform evoked in control neurons consisted of an excitatory postsynaptic potential (EPSP), a fast inhibitory postsynaptic potential (f-IPSP), and a slow inhibitory postsynaptic potential (s-IPSP). Stimulation of the ST or LA pathways evoked a burst-firing response in BLA neurons contralateral from the site of stimulation of kindled animals. 3. APV (50 microM) reduced, but CNQX (10 microM) completely blocked, the burst-firing response in BLA neurons from kindled animals and bicuculline-induced bursting in control neurons. 4. Kindling significantly increased the amplitude of both the slow NMDA- and the fast non-NMDA-receptor-mediated components of synaptic transmission (s- and f-EPSPs, respectively). Furthermore, the stimulus intensities required to evoke EPSPs just subthreshold for action potential generation were significantly lower in slices from kindled animals. 5. In kindled neurons no significant change was observed in the membrane input resistance and resting membrane potential or in the number of action potentials elicited in response to depolarizating current injection. 6. Kindling resulted in a pathway-specific loss of ST- and LA-evoked feedforward GABAergic synaptic transmission and of spontaneous IPSPs. In the same BLA neurons, direct GABAergic inhibition via stimulation of the LA was not affected by kindling. 7. The enhanced glutamatergic transmission was not due to disinhibition, because, in the presence of BMI (and CNQX to prevent BMI-induced bursting), the s-EPSP amplitude was still greater in kindled than in control neurons. 8. These results provide evidence that the epileptiform activity observed in BLA neurons after kindling results from an increase in excitatory NMDA- and non-NMDA-receptor-mediated glutamatergic transmission and a decrease in inhibitory gamma-aminobutyric acid (GABA)-receptor-mediated transmission; the enhanced excitatory transmission cannot be accounted for by reduced inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1992

Epileptogenesis reduces the sensitivity of presynaptic gamma-aminobutyric acidB receptors on glutamatergic afferents in the amygdala.

Intracellular recordings were obtained from the basolateral amygdala in in vitro rat brain slice preparations to examine whether gamma-aminobutyric acid (GABA)B receptors are altered after in vivo kindling-induced epileptogenesis. Stimulating the stria terminalis evoked excitatory (EPSPs) and inhibitory (IPSPs) postsynaptic potentials in control neurons, and epileptiform bursting or enhanced EPSPs, but no IPSPs, in neurons from animals, 4 to 8 weeks after the last kindled seizure. Baclofen (0.1 nM-100 microM) depressed EPSPs in control and kindled basolateral amygdala neurons, but the EC50 appeared to be shifted 100-fold from 5 nM in control to 500 nM in kindled neurons. Further analysis suggested a high-affinity component may be affected in kind led neurons. The absence of IPSPs in kindled neurons could not account for this shift, because effects of baclofen on EPSP amplitude were reduced in kindled animals even when GABAA receptors were blocked with bicuculline methiodide (30 microM) and postsynpatic GABAB receptors with intracellular guanosine 5'-O-3-thiotriphosphate (10 mM); 6-cyano-2,3-dihydroxy-7-nitroquinoxaline (10 microM) was also present to block bicuculline methiodide-induced bursting. Membrane responses to exogenously applied N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid were not affected by baclofen. Baclofen also hyperpolarized basolateral amygdala neurons and reduced membrane input resistance with an EC50 of 1 microM in control and kindled neurons. Post- but not presynaptic effects of baclofen were blocked by 2-hydroxy-saclofen (100 microM) and pertussis toxin pretreatment. In conclusion, kindling-induced epileptogenesis reduces the sensitivity of presynaptic GABAB receptors, an effect which may contribute to the enhancement of excitatory transmission in kindled animals. Furthermore, different pharmacological properties of pre- and postsynaptic receptors in the amygdala suggest two distinct populations of GABAB receptors whose long-lasting responses to kindling-induced seizures are different.

Animals↗
PubMed1992

Differential actions of corticotropin releasing factor on basolateral and central amygdaloid neurones, in vitro.

Intracellular current- and voltage-clamp recordings were obtained from basolateral (BLA) and central (ACe) neurones of the rat amygdala in vitro. The effect of superfusion of rat corticotropin releasing factor (rCRF) was examined on the ACe and BLA, nuclei with a high density of CRF-immunoreactive cell bodies and CRF receptors, respectively. rCRF (12.5-250 nM) had no effect on either resting membrane potential or input resistance in BLA neurones. In contrast, at low nanomolar concentrations rCRF (10-50 nM) caused hyperpolarisation and decreased membrane input resistance in the majority of ACe neurones. The equilibrium potential for this effect was -84 mV in the presence of tetrodotoxin (0.5 microM), suggesting that this response may be mediated by a postsynaptic increase in K+ conductance. Furthermore, rCRF consistently reduced the amplitude of, and the current mediating, the slow after hyperpolarisation following evoked action potential firing in both nuclei. This effect was concentration-dependent with an EC50 of 40 nM in BLA neurones and was insensitive to tetrodotoxin and noradrenergic antagonists. In addition, the putative CRF antagonist alpha-helical CRF9-41 (5 microM) blocked the effect of rCRF and showed partial agonist action on slow after hyperpolarisations. In BLA neurones, rCRF (50 nM) prolonged the Ca(2+)-spike evoked in the presence of tetrodotoxin and tetraethylammonium (2 mM), suggesting that the blockade of the slow after hyperpolarisation occurs subsequent to Ca2+ entry. These results suggest that rCRF has a differential effect on the membrane properties of BLA and ACe neurones possibly by activation of a heterogeneous population of CRF receptors.

Amygdala↗
PubMed1991

Decrease of GABA-immunoreactive neurons in the amygdala after electrical kindling in the rat.

The present study was designed to investigate the effects of electrical kindling in vivo on GABA immunoreactivity (GABA-IR) of the lateral and basolateral amygdaloid nuclei 2-6 months post-stimulation. Male Sprague-Dawley rats were implanted with bipolar electrodes in the basolateral nucleus and stimulated once per day until 3-5 stage 5 seizures were observed. Coronal sections containing the amygdala were processed for GABA-IR using the contralateral side of the brain. Results indicate that, in comparison to controls, fully kindled animals showed a significant decrease in total number of GABA-IR amygdala neurons. Decreases in GABA-positive punctate structures surrounding unlabeled pyramidal cells were also observed, but not quantified. The present data suggest that epileptogenesis of the amygdala is associated with a significant reduction of GABA-IR in the lateral and basolateral areas throughout the contralateral amygdaloid nucleus.

3,3'-Diaminobenzidine↗
PubMed1991

Excitatory transmission in the basolateral amygdala.

1. Intracellular current-clamp recordings obtained from neurons of the basolateral nucleus of the amygdala (BLA) were used to characterize postsynaptic potentials elicited through stimulation of the stria terminalis (ST) or the lateral amygdala (LA). The contribution of glutamatergic receptor subtypes to excitatory postsynaptic potentials (EPSPs) were analyzed by the use of the non N-methyl-D-aspartate (non-NMDA) antagonist, 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), and the NMDA antagonist, (DL)-2-amino-5-phosphonovaleric acid (APV). 2. Basic membrane properties of BLA neurons determined from membrane responses to transient current injection showed that at the mean resting membrane potential (RMP; -67.2 mV) the input resistance (RN) and time constant for membrane charging (tau) were near maximal, and that both values were reduced with membrane hyperpolarization, suggesting an intrinsic regulation of synaptic efficacy. 3. Responses to stimulation of the ST or LA consisted of an EPSP followed by either a fast inhibitory postsynaptic potential (f-IPSP) only, or by a fast- and subsequent slow-IPSP (s-IPSP). The EPSP was graded in nature, increasing in amplitude with increased stimulus intensity, and with membrane hyperpolarization after DC current injection. Spontaneous EPSPs were also observed either as discrete events or as EPSP/IPSP waveforms. 4. In physiological Mg2+ concentrations (1.2 mM), at the mean RMP, the EPSP consisted of dual, fast and slow, glutamatergic components. The fast-EPSP (f-EPSP) possessed characteristics of kainate/quisqualate receptor activation, namely, the EPSP increased in amplitude with membrane hyperpolarization, was insensitive to the NMDA receptor antagonist, APV (50 microM), and was blocked by the non-NMDA receptor antagonist, CNQX (10 microM). In contrast, the slow-EPSP (s-EPSP) decreased in amplitude with membrane hyperpolarization, was insensitive to CNQX (10 microM), and was blocked by APV (50 microM), indicating mediation by NMDA receptor activation. 5. In the presence of CNQX (10 microM), ST stimulation evoked an APV-sensitive s-EPSP. In contrast, LA stimulation evoked a f-IPSP, which when blocked by subsequent addition of bicuculline methiodide (BMI; 30 microM) revealed a temporally overlapping APV-sensitive s-EPSP. These data suggest that EPSP amplitude and duration are determined, in part, by the shunting of membrane conductance caused by a concomitant IPSP. 6. Superfusion of either CNQX or APV in BLA neurons caused membrane hyperpolarization and blockade of spontaneous EPSPs and IPSPs, suggesting that these compounds may act to block tonic excitatory amino acid (EAA) release within the nucleus, and that a degree of feed-forward inhibition occurs within the nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1991

Inhibitory transmission in the basolateral amygdala.

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)

2-Amino-5-phosphonovalerate↗
PubMed1990

Slow inward and late slow outward currents induced by hyperpolarizing pre-pulses in cat bladder parasympathetic neurones.

Single-electrode voltage-clamp techniques were used to examine membrane currents recorded as a result of hyperpolarizing pre-pulses in cat bladder parasympathetic neurones. In 84 ganglion cells examined, two types of current were observed in response to hyperpolarizing pre-pulses of 10 ms to 1 s duration from holding potentials of -30 to -60 mV to test potentials of -90 to -130 mV. In 46 cells, a short-duration pulse induced a slow inward current (SIC); with longer pulse durations, an outward current was superimposed on the SIC, resulting in a late slow outward current (LSOC). In the remaining cells, either a SIC (n = 12) or an LSOC (n = 26) was recorded over a range of hyperpolarizing pre-pulse durations. The more depolarized the holding potential, the more hyperpolarized the test potential and the longer the pulse duration, the larger the amplitude of the SIC and LSOC. The SIC and LSOC were associated with an increase in input conductance. The extrapolated reversal potential (Vrev) for the LSOC obtained at a holding potential of -60 mV (where the LSOC seemed to be less contaminated with the SIC) was -89 +/- 4 mV (mean +/- standard error of the mean; n = 5), which is close to the equilibrium potential for the K ion. The LSOC was depressed by a high-K (10-20 mM) solution and potentiated by a low-K (0.47 mM) solution. The SIC was depressed by a low-Na (26.2 mM) solution, but was not affected significantly by a low-Cl (12.2 mM) solution. A low-Ca (0.1 mM)/high-Mg (5 mM) solution depressed the LSOC, while a high-Ca (5 mM) solution potentiated it. Cd (0.5 mM) blocked the SIC almost completely, and suppressed the LSOC. The LSOC but not the SIC was suppressed by tetraethylammonium chloride (10 mM). Superfusing Cs (3 mM) did not affect either the LSOC or the SIC. 4-Aminopyridine (1 mM) and muscarine (10 microM) depressed or replaced the SIC with an outward current, while potentiating the LSOC. These results suggest that a hyperpolarizing pre-pulse induces slow inward Na- and late slow outward Ca-dependent K currents, which are inactivated at depolarized potentials and are de-inactivated by hyperpolarizing pulses in a time-dependent manner.

4-Aminopyridine↗
PubMed1990

Action of an irreversible acetylcholine esterase inhibitor, soman, on muscarinic hyperpolarization in cat bladder parasympathetic ganglia.

1. Intracellular recording techniques were used to examine the action of an irreversible acetylcholine esterase (AChE) inhibitor, soman, on the hyperpolarizations mediated through muscarinic cholinoceptors in cat bladder parasympathetic neurones. 2. Soman (0.1-10 microM) depressed the amplitude and prolonged the duration of the muscarinic slow inhibitory postsynaptic potential (s-i.p.s.p.) elicited by a preganglionic tetanus (40 Hz for 1 s) in the presence of mecamylamine (20 microM), phentolamine (1 microM) and caffeine (1 mM), in a dose-dependent manner. The effect of soman on the amplitude of the s-i.p.s.p. was partially reversible, while the effect on the duration was irreversible. 3. Soman hyperpolarized the membrane and decreased input resistance, but this effect could not account for soman-induced inhibition of the s-i.p.s.p. 4. Soman depressed the amplitude and prolonged the duration of a muscarinic hyperpolarization induced by pressure application of acetylcholine (ACh) in the presence of mecamylamine, phentolamine and caffeine. The time course of this effect paralleled that on the synaptically-evoked muscarinic s-i.p.s.p. 5. A reversible AChE inhibitor, pyridostigmine (10-100 microM), also depressed the amplitude and prolonged the duration of a muscarinic hyperpolarization induced by either preganglionic stimulation or ACh pressure application. These actions were reversible, and not accompanied by a significant change in membrane potential or input resistance. 6. The inhibitory action of soman (1 microM) on the muscarinic hyperpolarization was prevented by pyridostigmine (10 microM), but not by atropine (1 microM). 7. These results demonstrate that soman prolongs not only the muscarinic hyperpolarization, but also inhibits its amplitude through a postsynaptic action, probably through AChE inhibition, in cat bladder parasympathetic neurones.

Acetylcholine↗
PubMed1989

Spontaneous epileptiform activity and alteration of GABA- and of NMDA-mediated neurotransmission in amygdala neurons kindled in vivo.

This study was designed to analyze in vitro the changes in synaptic potentials that occur in neurons of the basolateral amygdala 4-6 weeks after kindling in vivo. The following 3 phenomena were observed in basolateral neurons which were contralateral to the kindling site: (1) spontaneous epileptiform bursting; (2) evoked epileptiform bursting or 'extra' evoked synaptic potentials; and (3) the absence of GABAergic inhibitory postsynaptic potentials either spontaneous or evoked. Epileptiform bursting, spontaneous and evoked, and 'extra' evoked synaptic potentials were depressed by NMDA receptor antagonists and were recorded in normal physiological solution. These data suggest that the amygdala is an area of the brain particularly sensitive to epileptogenesis.

Animals↗
PubMed1989

The transient potassium current, the A-current, is involved in spike frequency adaptation in rat amygdala neurons.

The possible functional roles of the transient K+ current, IA, in basolateral amygdala (BLA) neurons were studied using a rat brain slice preparation and conventional intracellular recording techniques. Conditioning depolarization, which inactivates IA, slowed the action potential repolarization while conditioning hyperpolarization accelerated the action potential repolarization. 4-Aminopyridine (4-AP, 100 microM), a specific IA antagonist, also caused a clear delay in spike repolarization similar to the effect of conditioning depolarization suggesting that IA is involved in the action potential repolarization. When BLA neurons were excited by injecting long depolarizing current pulses (500 ms), they responded with an initial rapid discharge of action potentials which slowed or accommodated; an afterhyperpolarization (AHP) followed the depolarizing current pulses. Superfusion of 4-AP (100 microM) blocked accommodation resulting in an increase in action potential discharge in 74% (32 out of 43) neurons tested. The remaining 11 cells responded with an increased frequency of discharge of the first few action potentials. Unlike the effect of cadmium (Cd2+, 100 microM), a calcium channel blocker, 4-AP did not reduce the AHP. In the presence of norepinephrine (NE, 10 microM), a neurotransmitter which has been shown to block calcium-activated potassium conductance, 4-AP caused a further increase in the number and frequency of action potential discharge. In addition, in BLA neurons, spontaneous interictal and ictal-like events were observed at low and high concentrations of 4-AP, respectively. We conclude that IA is involved in the action potential repolarization as well as spike frequency adaptation in BLA neurons and that these actions may contribute to the convulsant effect of 4-AP.

4-Aminopyridine↗
PubMed1989

Primary afferent excitatory transmission recorded intracellularly in vitro from rat medial vestibular neurons.

Intracellular recordings were made from rat medial vestibular nucleus (MVN) neurons in transverse brain slices containing the root of the vestibular nerve (N. VIII). Electrical stimuli applied to the N. VIII tract evoked an orthodromic excitatory postsynaptic potential (EPSP) that lasted about 50 ms following a 0.5 to 1.5 ms delay between the stimulus artifact and synaptic potential. These orthodromic EPSPs were insensitive to the following antagonists: atropine, hexamethonium, diphenhydramine, and caffeine. Based on these results we conclude that the primary afferent excitatory transmitter is not acetylcholine, histamine, or adenosine, respectively. However, kynurenic acid, a general excitatory amino acid receptor antagonist, blocked the orthodromic EPSP while having no effect on the resting membrane potential, input resistance, or action potential configuration of MVN neurons. Our data suggest that an excitatory amino acid, or amino acid-like substance, is responsible for primary afferent excitatory transmission in the rat medial vestibular nucleus.

Action Potentials↗
PubMed1989

Fast hyperpolarization following an excitatory postsynaptic potential in cat bladder parasympathetic neurons.

Intracellular recording techniques were used to study a fast hyperpolarizing potential following the fast excitatory postsynaptic potential evoked by an orthodromic nerve stimulation in cat bladder parasympathetic ganglion cells. In the 61 ganglion cells examined, two types of responses were recorded on stimulating the preganglionic nerve; one had only a fast excitatory postsynaptic potential (type SI, n = 20) and the other had a fast excitatory postsynaptic potential followed by a fast hyperpolarizing potential (type SII, n = 41). In type SII neurons, the half-maximum duration of the afterhyperpolarizing potential following an orthodromic spike was longer than that of a direct spike produced by injecting a depolarizing current pulse through the recording electrode; the half-maximum durations for afterhyperpolarizing potentials following orthodromic and direct action potentials were comparable in type SI cells. Blocking the initiation of an orthodromic spike by hyperpolarizing the membrane in type SII cells revealed a fast excitatory postsynaptic potential followed by a fast hyperpolarizing potential which was similar to that observed at the resting potential. The fast hyperpolarizing potential had a duration comparable to that of an afterhyperpolarizing potential following an orthodromic action potential. The fast excitatory postsynaptic potential-fast hyperpolarizing potential sequence was blocked completely and reversibly by nicotinic receptor antagonists (hexamethonium and D-tubocurarine). Atropine, alpha-2 noradrenergic (yohimbine and phentolamine), and purinergic (caffeine) antagonists had no effect on the fast hyperpolarizing potential. In cells which show type SII responses, spontaneous excitatory postsynaptic potentials were not followed by a hyperpolarization. Depolarizing the membrane (by passing a cathodal current through the recording electrode) to an amplitude comparable to that of a fast excitatory postsynaptic potential also did not elicit a membrane hyperpolarization in type SII cells. In some cells, stimulating one preganglionic nerve trunk elicited a fast hyperpolarizing potential, but activating another nerve trunk innervating the same ganglion cell did not. There was no correlation between the variations in the amplitudes of the fast excitatory postsynaptic potential and the fast hyperpolarizing potential in type SII cells, but increasing the stimulus intensity applied to the presynaptic nerve fiber potentiated the amplitude of the fast excitatory postsynaptic potential and the fast hyperpolarizing potential. The fast hyperpolarizing potential was not associated with appreciable changes in input resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1988

Soman enhances nicotinic depolarizations, and depresses muscarinic hyperpolarizations in parasympathetic neurons.

Intracellular recording techniques were used to study the action of an irreversible anticholinesterase, soman, on cholinergic transmission in cat bladder parasympathetic neurons. With soman (0.1-10 microM) treatment, nicotinic depolarizations were increased in amplitude and prolonged in duration, whereas muscarinic hyperpolarizations showed either a depressed amplitude and prolonged duration, or were completely blocked. These data suggest that the final result of soman action is different at nicotinic and muscarinic receptor-channel complexes in parasympathetic neurons.

Animals↗
PubMed1988

Estrogen priming affects active membrane properties of medial amygdala neurons.

The medial nucleus of the amygdala (MNA) in the rat is a target tissue for estrogen binding and a sexually dimorphic structure. We used an in vivo slice preparation and intracellular recording techniques to study the effects of beta-estradiol priming on active and passive membrane properties of MNA neurons. Two groups of adult female rats were used; ovariectomized (OVX) non-primed rats and OVX rats that were estrogen-primed at least 24 h prior to recording. Estrogen priming increased the occurrence of spontaneous excitatory postsynaptic potentials (EPSPs) in MNA neurons, and of depolarizing afterpotentials (DAPs) observed with a cathodally triggered action potential, and was associated with a lack of accommodation in these cells. Overall, long-term exposure to estrogen markedly increased the spontaneous activity and excitability of the MNA neurons.

Action Potentials↗
PubMed1988

Disinhibition in the rat septum mediated by M1 muscarinic receptors.

Acetylcholine (ACh) has been documented as an important central neurotransmitter. We have investigated the actions of ACh within the dorsolateral septal nucleus of the rat to examine its actions within this nucleus, specifically how it may interact to modulate the inhibitory action of gamma-aminobutyric acid (GABA), the known inhibitory transmitter in this area. Our results demonstrate that ACh, acting on M1 muscarinic receptors leads to disinhibition by decreasing GABA release.

Action Potentials↗