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PubMed2005

Angiotensin receptors and actions in guinea pig enteric nervous system.

Actions of ANG II on electrical and synaptic behavior of enteric neurons in the guinea pig small intestine were studied. Exposure to ANG II depolarized the membrane potential and elevated neuronal excitability. The number of responding neurons was small, with responses to ANG II in 32% of submucosal neurons and 25% of myenteric neurons. Hyperpolarizing responses were evoked by ANG II in 45% of the neurons. The hyperpolarizing responses were suppressed by alpha2-noradrenergic receptor antagonists, which suggested that the hyperpolarizing responses reflected stimulation of norepinephrine release from sympathetic neurons. Exposure to ANG II enhanced the amplitude and prolonged the duration of noradrenergic inhibitory postsynaptic potentials and suppressed the amplitude of both fast and slow excitatory postsynaptic potentials. The selective ANG II(1) receptor (AT1R) antagonists, ZD-7115 and losartan, but not a selective AT2R antagonist (PD-123319), suppressed the actions of ANG II. Western blot analysis and RT-PCR confirmed expression of AT1R protein and the mRNA transcript for the AT1R in the enteric nervous system. No expression of AT2R protein or mRNA was found. Immunoreactivity for AT1R was expressed by the majority of neurons in the gastric antrum and small and large intestine. AT1R immunoreactivity was coexpressed with calbindin, choline acetyltransferase, calretinin, neuropeptide Y, and nitric oxide synthase in subpopulations of neurons. The results suggest that formation of ANG II might have paracrine-like actions in the enteric nervous system, which include alterations in neuronal excitability and facilitated release of norepinephrine from sympathetic postganglionic axons. The enhanced presence of norepinephrine is expected to suppress fast and slow excitatory neurotransmission in the enteric microcircuits and to suppress neurogenic mucosal secretion.

Angiotensin II↗
PubMed1999

Effects of diethylstilbestrol on mouse hippocampal evoked potentials in vitro.

1. Several steroids and related compounds can bind to central opiate receptors in whole-brain mouse homogenates. Among these drugs, the synthetic estrogen, diethylstilbestrol (DES), exhibits one of the highest affinities in binding experiments labeling opiate receptors with the nonselective opiate antagonist, [3H]diprenorphine. 2. In the search for a functional correlate to this biochemical finding, we have studied the effects of DES on the mouse hippocampal slice in vitro preparation. 3. Previously, binding studies were performed in hippocampal homogenates, labeling opiate receptors with [3H]diprenorphine or with the mu-selective opiate agonist, [3H]DAGO. DES inhibited [3H]diprenorphine and [3H]DAGO binding, the IC50 values obtained being (1.03 +/- 0.16) x 10(-5) and (1 +/- 0.8) x 10(-5) M, respectively. 4. In mice hippocampal slices, we measured the extracellular evoked potentials obtained in the CA1 pyramidal cell layer of the hippocampi and the field excitatory postsynaptic potentials (EPSP) obtained in the stratum radiatum. The presence of DES (10(-5) M) induced an increase in the amplitude of the population spikes measured in the pyramidal layer without modifying the field EPSP. This effect is similar to that obtained in the presence of DAGO in this preparation. The effect produced by DES was not modified by the presence of the opiate competitive antagonist, naloxone (10(-5) M), or by the opiate alkylating agent, beta-chlornaltrexamine (10(-5) M). Conversely, in the presence of the transcription inhibitor, actinomycin D (5 micrograms/ml), the effect produced by DES was inhibited. 5. Our results with DES support the general idea that estrogens increase central excitability. Although diethylstilbestrol can bind to opiate receptors in the hippocampus, the effect induced by this estrogen on hippocampal excitability seems unrelated to a direct action on opiate receptors, and an intracellular effect is suggested.

Animals↗
PubMed2005

Dynamics of excitatory synaptic components in sustained firing at low rates.

Sustained firing is necessary for the persistent activity associated with working memory. The relative contributions of the reverberation of excitation and of the temporal dynamics of the excitatory postsynaptic potential (EPSP) to the maintenance of activity are difficult to evaluate in classical preparations. We used simplified models of synchronous excitatory networks, hippocampal autapses and pairs, to study the synaptic mechanisms underlying firing at low rates. Calcium imaging and cell attached recordings showed that these neurons spontaneously fired bursts of action potentials that lasted for seconds over a wide range of frequencies. In 2-wk-old cells, the median firing frequency was low (11 +/- 8.8 Hz), whereas in 3- to 4-wk-old cells, it decreased to a very low value (2 +/- 1.3 Hz). In both cases, we have shown that the slowest synaptic component supported firing. In 2-wk-old autapses, antagonists of N-methyl-d-aspartate receptors (NMDARs) induced rare isolated spikes showing that the NMDA component of the EPSP was essential for bursts at low frequency. In 3- to 4-wk-old neurons, the very low frequency firing was maintained without the NMDAR activation. However EGTA-AM or alpha-methyl-4-carboxyphenylglycine (MCPG) removed the very slow depolarizing component of the EPSP and prevented the sustained firing at very low rate. A metabotropic glutamate receptor (mGluR)-activated calcium sensitive conductance is therefore responsible for a very slow synaptic component associated with firing at very low rate. In addition, our observations suggested that the asynchronous release of glutamate might participate also in the recurring bursting.

Action Potentials↗
PubMed2006

Voltage-gated sodium channels in cerebellar Purkinje cells of mormyrid fish.

Cerebellar Purkinje cells of mormyrid fish differ in some morphological as well as physiological parameters from their counterparts in mammals. Morphologically, Purkinje cells of mormyrids have larger dendrites that are characterized by a lower degree of branching in the molecular layer. Physiologically, there are differences in electrophysiological response patterns that are related to sodium channel activity: first, sodium spikes in mormyrid Purkinje cells have low amplitudes, typically not exceeding 30 mV. Second, the response to climbing fiber stimulation in mormyrid Purkinje cells does not consist of a complex spike (with an initial fast sodium spike) as in mammals, but instead it consists of an all-or-none excitatory postsynaptic potential, the so-called climbing fiber response. Because of these unique properties, we have begun to characterize mormyrid Purkinje cells electrophysiologically. In this study, we provide a description of voltage-gated Na+ channels and conductances in Purkinje cells of the mormyrid fish Gnathonemus petersii. Various types of Na+ channel alpha-subunits, i.e., Nav1.1, Nav1.2, and Nav1.6, have been described in rodent Purkinje cells. Using immunohistochemical techniques, we found that these subunits are present in Purkinje cells of mormyrids. To test whether these Na+ channel subunits can mediate fast inactivating and resurgent Na+ currents in Gnathonemus Purkinje cells, we conducted patch-clamp recordings in acutely dissociated cells and in cerebellar slices. Both types of Na+ currents could be measured in rat and fish Purkinje cells. These data show that, despite prominent differences in electrophysiological response characteristics, Purkinje cells of rats and mormyrids share the same voltage-gated Na+ conductances.

Action Potentials↗
PubMed1991

Inhibition of an N-methyl-D-aspartate induced short-term potentiation in the rat hippocampal slice.

The effects of the phorbol ester 4 beta-phorbol-12,13 dibutyrate (PDBu) and the protein kinase (PK) inhibitors H-7 and sphingosine were investigated on the short-term potentiation (STP) of the population excitatory postsynaptic potential (EPSP) induced by perfusion of N-methyl-D-aspartate (NMDA) in the stratum radiatum of CA1 of the rat hippocampal slice. Bath perfusion of 130 microM NMDA for 10 s caused an initial depression of the population EPSP followed by a STP, which averaged 46% and lasted 16 min. PDBu (100 nM) perfused for 2 h completely inhibited the NMDA induced STP, suggesting that the stimulation of PKC inhibited an NMDA receptor activated process which induced the STP. The protein kinase inhibitors H-7 and sphingosine did not alter the NMDA induced STP.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Long-lasting potentiations evoked by a brief heterosynaptic tetanus in the guinea pig dentate gyrus in vitro.

The heterosynaptic effects induced by a brief afferent tetanization in the molecular layer of the dentate gyrus were investigated in the guinea pig hippocampal slice preparation using extracellular recording technique. At a brief interval (5 ms) between a single stimulation of the test afferents and the tetanus evoked in the conditioning afferents, a long-lasting (greater than 1 h) potentiation of the test field excitatory postsynaptic potential (EPSP) initial slope and amplitude was observed. This potentiation was occluded by prior homosynaptic tetanization of the test afferents, suggesting that it represents long-term potentiation (LTP). Thus, in the dentate gyrus, a single activation of a single test EPSP suffices to induce LTP when coinciding in time with a brief tetanus to other afferents. When not temporally paired with the test stimulation, i.e. at longer test-conditioning intervals (greater than 50 ms), the conditioning tetanus also elicited a long-lasting potentiation of the test field EPSP. This potentiation was, however, seen as a prolongation of the rising phase with no change in the field EPSP initial slope, and may represent a potentiation distinct from LTP.

Animals↗
PubMed1990

Acetylcholinesterase-containing neurons in the striatum, septum and hippocampus of the rat in embryonic culture and adult in situ.

Neurons of the rat brain, of either adult in situ or embryonic culture, have been studied by using a sensitive method for acetylcholinesterase (AChE) histochemistry. In the culture system, incubated for 6-18 days, AChE-positive neurons were found in tissues originating from the striatum and septum, but not in those from the hippocampus. These positive somata were morphometrically analyzed in terms of the cell size, i.e. the lengths of the major axis (Lmax) and the minor axis (Lmin) in cultured dishes of the striatum and septum; the mean Lmax was 20 and 22 microns, respectively. In in situ adult brain sections, a similar morphometric examination of AChE-positive neurons gave comparable results to those obtained in the culture system. An evaluation of both in vitro and in vivo through the histogramatical analysis revealed that the striatum contained more than two populations of AChE-positive cells differing in cell size. In contrast, a major single peak of Lmax was detected in the histogram of the septum. In both cases of striatum and septum in in situ adult brain, sagittal sections show larger size of Lmax, indicating that AChE-positive neurons are arranged in the sagittal direction. In studies on electrophysiological properties of large striatal cells in culture, both acetylcholine and glutamate induced changes in the membrane potential and/or the frequency of excitatory postsynaptic potential, while dopamine induced much smaller responses.

Acetylcholinesterase↗
PubMed1987

Effects of intracellular injections of phorbol ester and protein kinase C on cat spinal motoneurons in vivo.

In cat spinal motoneurons intracellular iontophoresis of phorbol 12, 13-diacetate or protein kinase C increases the afterhyperpolarization, the maximum rate of spike rise and the spike peak amplitude, without evident change in resting potential, input resistance and monosynaptic excitatory postsynaptic potential. Phorbol ester also reduces the accommodation of repetitive discharge evoked by intracellular current pulses. These data suggest that activation of protein kinase C facilitates the Ca2+-activated K+ current that mediates the afterhyperpolarization, as well as the fast Na+ current. These effects are quite different from those seen in some other mammalian central neurons.

Action Potentials↗
PubMed1992

Tumor necrosis factor alters synaptic transmission in rat hippocampal slices.

The effects of human recombinant tumor necrosis factor (TNF-alpha) on the synaptic transmission were studied in rat hippocampal slices by using extracellular field potential recordings. Population spikes and/or excitatory postsynaptic potentials were extracellularly recorded in hippocampus CA1 region from stratum pyramidale and stratum radiatum, respectively, and synaptic transmission was examined in the Schaffer collateral/commissural-CA1 pathway. Basal neurotransmission slightly and promptly increased in slices acutely exposed to TNF-alpha (1-100 nM). Examination of the long-term potentiation (LTP) revealed that a brief treatment with the cytokine did not influence LTP, while a long-lasting application of TNF-alpha (50 min or more) inhibited LTP in a dose-dependent way in the range of 1-100 nM. A role for TNF-alpha as a peptide of immunological significance belonging to the family of brain neuromodulators is discussed.

Animals↗
PubMed1996

Galanin inhibits long-term potentiation at Schaffer collateral-CA1 synapses in guinea-pig hippocampal slices.

The role of galanin on long-term potentiation (LTP) of the field excitatory postsynaptic potentials (fEPSPs) at Schaffer collateral-CA1 synapses was investigated in guinea-pig hippocampal slices. Application of galanin (10(-7) M) inhibited the magnitude of LTP without any changes in the amplitude of fEPSP prior to tetanic stimulation. A putative central nervous system (CNS) type galanin receptor antagonist, galanin(1-13)-Pro-Pro-(Ala-Leu)2-Ala-Amide (M40), did not modify the magnitude of LTP when applied alone. However, M40 significantly reversed the inhibition by galanin when applied with galanin simultaneously. These findings suggest that galanin plays an inhibitory role through the CNS type galanin receptors.

Animals↗
PubMed1991

Studies on substances that induce long-term potentiation in guinea-pig hippocampal slices.

Fluids were collected from the rabbit neocortex during a tetanic stimulation of the cortical surface. When these samples from the neocortex were applied on the guinea-pig hippocampal slices, only those fractions containing substances with molecular weights less than 3000, 3000-10,000 and greater than 50,000 and not with other molecular weights, could induce long-term potentiation of population spikes in the CAI area in response to stratum radiatum stimulation. Intracellular recordings from the CAI neurons revealed that the long-term potentiation-inducing substances increased the excitatory postsynaptic potential without changing the membrane potential and the input resistance of these cells. A pretreatment of the rabbits with MK-801 prevented the release of the long-term potentiation-inducing substances. 2-Amino-5-phosphonovalerate was unable to block the long-term potentiation-inducing action of the substances from the rabbit neocortex. Gel-electrophoresis of the substances collected from the rabbit neocortex revealed the presence of an acidic peptide with a molecular weight of about 69,000. These results indicate that tetanic stimulation of rabbit neocortex results in a release of substances with molecular weights of less than 3000, 3000-10,000 and greater than 50,000 that could induce long-term potentiation in guinea-pig hippocampal slices. The release, but not the long-term potentiation-inducing action, of these substances appears to depend on the activation of N-methyl-D-aspartate receptors. The long-term potentiation-inducing substance in the greater than 50,000 mol. wt fraction may be an acidic peptide with a molecular weight of about 69,000.

2-Amino-5-phosphonovalerate↗
PubMed2005

Divergent effects of Abeta1-42 on ionotropic glutamate receptor-mediated responses in CA1 neurons in vivo.

Aggregated Abeta1-42 is hypothesized to be the central cause of Alzheimer's disease. However, early changes in synaptic activity may be detected in the disease long before a significant cell loss is manifested. Despite the fact that Abeta1-42 interference with long-term potentiation (LTP) and the field excitatory postsynaptic potential (fEPSP) is well documented, the exact mechanism of these events remains to be clarified. Here we studied the effects of iontophoretically applied Abeta1-42 on the neuronal firing evoked in vivo on the CA1 hippocampal neurons of Wistar rats by different agonists of the ionotropic glutamate receptors: N-methyl-d-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) and kainic acid (KA). NMDA elicited firing enhanced in all of the measured cells; in contrast, the AMPA-mediated responses decreased significantly after Abeta1-42 ejection. The changes in KA-evoked responses to Abeta1-42 revealed two types of cells. In the first type, the KA-mediated firing remained at the control level, while in the second type, Abeta1-42 attenuated the KA-evoked responses. A protective pentapeptide, Leu-Pro-Tyr-Phe-Asp-amide, was used to verify the specificity of these beta-amyloid-elicited effects. The pentapeptide protected against the modulatory effects of Abeta1-42 on the NMDA and AMPA responses. In conclusion, we have shown that Abeta1-42 exerts divergent effects on the activity of the ionotropic glutamate receptors in vivo. These results suggest that the LTP disruption and fEPSP attenuation seen after Abeta1-42 application are in part due to the altered function of these receptors.

Amyloid beta-Peptides↗
PubMed1998

Nerve-induced release of nitric oxide exerts dual effects on nicotinic transmission within the coeliac ganglion in the rabbit.

The involvement of nitric oxide in the modulation of nicotinic activation was investigated in vitro in isolated rabbit coeliac ganglion. The electrical activity of the ganglionic neurons was recorded using intracellular recording techniques. When a train of pulses of supramaximum intensity was applied to the splanchnic nerves, gradual depression of fast nicotinic activation occurred: the pulses do not systematically elicit action potentials, but very often elicit excitatory postsynaptic potentials only. This phenomenon appeared between 15 and 20 Hz and increased with the frequency of stimulation. It was not related to any change in the membrane potential of the ganglionic neurons. For a given frequency, the depression appeared progressively and it was particularly strong at the end of the train. The use of pharmacological agents that interfere with the nitric oxide pathway, such as L-arginine (precursor of nitric oxide), D-arginine (non-precursor of nitric oxide) N(omega_-nitro-L-arginine and N(omega)-nitro-L-arginine methyl ester (inhibitors of nitric oxide synthase), and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (nitric oxide scavenger), demonstrated that nitric oxide modulated this depression phenomenon by exerting a dual effect on the nicotinic activation, i.e. facilitation or inhibition. Agents interfering with the guanosine 3',5'-cyclic monophosphate pathway, such as oxadiazolo[4,3-a] quinoxalin-1-one (selective inhibitor of the nitric oxide-activated soluble guanylate cyclase) and zaprinast (selective inhibitor of the phosphodiesterases involved in the guanosine 3',5'-cyclic monophosphate pathway) demonstrated that only the facilitatory effect of nitric oxide on the nicotinic activation was mediated through the guanosine 3',5'-cyclic monophosphate pathway. The mechanism sustaining the inhibitory effect remains to be determined. By modulating the nicotinic activation, nitric oxide plays a role in the integrative properties of the prevertebral ganglia. This opens new perspectives with regard to the control of visceral functions by the prevertebral level of regulation.

Animals↗
PubMed2000

Muscarinic receptor activation is a prerequisite for the endogenous release of nitric oxide modulating nicotinic transmission within the coeliac ganglion in the rabbit.

The aim of the present study was to investigate whether the activation of muscarinic receptors is a preliminary step to the endogenous release of nitric oxide modulating nicotinic transmission within the prevertebral ganglia. This work has been performed in vitro in isolated rabbit coeliac ganglion. The electrical activity of the ganglionic neurons was recorded using intracellular recording techniques. When a train of pulses of supramaximal intensity was applied to the splanchnic nerves, gradual depression of fast nicotinic transmission occurred: the pulses do not systematically elicit action potentials, but very often elicit excitatory postsynaptic potentials only. The use of pharmacological agents that interfere with the nitric oxide pathway such as L-arginine (precursor of nitric oxide) or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (nitric oxide scavenger) demonstrated that nitric oxide modulates this depression phenomenon by facilitating or inhibiting the nicotinic transmission of the ganglionic neurons. A nitric oxide donor (diethylamine/nitric oxide complex) induced an inhibition of the nicotinic synaptic transmission. In the presence of the muscarinic receptors antagonist atropine, L-arginine and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide failed to modify the nicotinic transmission of the ganglionic neurons but diethylamine/nitric oxide complex was still able to inhibit it. These results demonstrate that in the coeliac ganglion, the activation of muscarinic cholinergic receptors is a prerequisite for the activation of neuronal nitric oxide synthase in preganglionic fibres. The nitric oxide released then exerts a facilitation or an inhibition of the nicotinic transmission of the ganglionic neurons. Atropine triggered a facilitation of the nicotinic transmission when superfused alone and an inhibition when superfused in the presence of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. These results confirm that muscarinic receptors activate the nitric oxide pathway modulating the nicotinic transmission of the prevertebral neurons. Our results also demonstrate that when the nitric oxide pathway is blocked, activation of muscarinic receptors leads to facilitation of the nicotinic transmission. Our study brings new insights concerning the modulation by nitric oxide and by muscarinic receptors of the synaptic transmission within the prevertebral ganglia.

Animals↗
PubMed1996

Long-term modifications of synaptic efficacy in the human inferior and middle temporal cortex.

The primate temporal cortex has been demonstrated to play an important role in visual memory and pattern recognition. It is of particular interest to investigate whether activity-dependent modification of synaptic efficacy, a presumptive mechanism for learning and memory, is present in this cortical region. Here we address this issue by examining the induction of synaptic plasticity in surgically resected human inferior and middle temporal cortex. The results show that synaptic strength in the human temporal cortex could undergo bidirectional modifications, depending on the pattern of conditioning stimulation. High frequency stimulation (100 or 40 Hz) in layer IV induced long-term potentiation (LTP) of both intracellular excitatory postsynaptic potentials and evoked field potentials in layers II/III. The LTP induced by 100 Hz tetanus was blocked by 50-100 microM DL-2-amino-5-phosphonovaleric acid, suggesting that N-methyl-D-aspartate receptors were responsible for its induction. Long-term depression (LTD) was elicited by prolonged low frequency stimulation (1 Hz, 15 min). It was reduced, but not completely blocked, by DL-2-amino-5-phosphonovaleric acid, implying that some other mechanisms in addition to N-methyl-DL-aspartate receptors were involved in LTD induction. LTD was input-specific, i.e., low frequency stimulation of one pathway produced LTD of synaptic transmission in that pathway only. Finally, the LTP and LTD could reverse each other, suggesting that they can act cooperatively to modify the functional state of cortical network. These results suggest that LTP and LTD are possible mechanisms for the visual memory and pattern recognition functions performed in the human temporal cortex.

2-Amino-5-phosphonovalerate↗
PubMed1997

Synaptic interactions in neocortical local circuits: dual intracellular recordings in vitro.

Properties of local synaptic connections in neocortex, studied with dual intracellular recordings in vitro and correlated with cell and synaptic morphology are summarized. The different durations and sensitivities to somatic membrane potential of pyramid-pyramid excitatory postsynaptic potentials (EPSPs) apparently reflect the positions of the synapses on the postsynaptic dendrites. Their time-, frequency- and voltage-dependent properties enable supra-linear summation of several low-frequency inputs arising in the same dendritic region, even if only loosely coincident, but they depress during repetitive firing in any one input. Pyramidal input to classical fast spiking and low threshold spiking interneurones are strikingly different. Here low presynaptic firing rates results in many transmission failures. EPSPs are brief and inputs must be near coincident for summation. However, these synapses display pronounced. frequency-dependent, incrementing facilitation at higher presynaptic frequencies. Once initiated by a brief high-frequency burst, this facilitation is maintained at lower frequencies. GABAA receptor-mediated inhibitory postsynaptic potentials (IPSPs) arising proximally are of very different durations depending on the type of interneurone activated and can prevent and subsequently synchronize firing in their many postsynaptic partners with very different delays (eg. 10-100 ms). Low threshold spiking interneurones, in contrast, generate brief IPSPs only in more distal dendritic regions and have little effect on somatic excitability acting to shunt input distally.

Animals↗
PubMed1997

Dopaminergic modulation of LTP induction in the dentate gyrus of intact brain.

The effect of the dopamine system on the induction of long-term potentiation (LTP) in the dentate gyrus was studied in anesthetized rats. A subthreshold tetanic train (seven pulses at 100 Hz) given to the perforant pathway, which usually fails to elicit LTP, potentiated a slope of field excitatory postsynaptic potentiation (fEPSP) measured from the hilus of the dentate gyrus when a precursor for catecholamine, L-3,4-dihydroxyphenylalanine (L-DOPA), was administered orally to rats. The increase in the fEPSP slope persisted for at least 60 min. Intraventricular injection of a specific dopamine D1/D5 agonist, SKF38393, mimicked the effect of L-DOPA, suggesting an involvement of D1/D5 receptors in the induction of dentate gyrus LTP. Consistent with this, intraventricular administration of the D1/D5 antagonist SCH23390 resulted in complete inhibition of LTP induction by a longer tetanus (100 pulses at 100 Hz), which usually elicits a robust LTP. Thus, D1/D5 receptor activation appears to modulate LTP induction in vivo.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Presynaptic inhibition by neuropeptide Y in rat hippocampal slice in vitro is mediated by a Y2 receptor.

1. The action of analogues and C-terminal fragments of neuropeptide Y (NPY) was examined on excitatory synaptic transmission in area CA1 of the rat hippocampal slice in vitro, by use of intracellular and extracellular recordings, to determine by agonist profile the NPY receptor subtype mediating presynaptic inhibition. 2. Neither NPY, analogues nor fragments of NPY affected the passive or active properties of the post-synaptic CA1 pyramidal neurones, indicating their action is at a presynaptic site. 3. The full-sequence analogues, peptide YY (PYY) and human NPY (hNPY), were equipotent with NPY at the presynaptic receptor, while desamido hNPY was without activity. 4. NPY2-36 was equipotent with NPY. Fragments as short as NPY 13-36 were active, but gradually lost activity with decreasing length. NPY 16-36 had no effect on extracellular field potentials, but still significantly inhibited excitatory postsynaptic potential amplitudes. Fragments shorter than NPY 16-36 had no measurable effect on synaptic transmission. 5. The presynaptic NPY receptor in hippocampal CA1 therefore shares an identical agonist profile with the presynaptic Y2 receptor at the peripheral sympathetic neuroeffector junction.

Action Potentials↗