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PubMed1992

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

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.

Animals↗
PubMed1999

Excitatory amino acids and synaptic transmission in embryonic rat brainstem motoneurons in organotypic culture.

We used brainstem motoneurons recorded in organotypic slice co-cultures maintained for more than 18 days in vitro, together with multibarrel ionophoretic applications of glutamate receptor agonists and bath applications of specific blocking agents, to study the responses of rat brainstem motoneurons to glutamate receptor activation, and the contribution of these receptors to synaptic transmission. Differentiated brainstem motoneurons in vitro are depolarized by glutamate, N-methyl-d-aspartate (NMDA) and dl-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) iontophoresis, and express NMDA, AMPA and also specific kainate receptors, as evidenced by (+/-)2-amino-5-phosphonovaleric acid (APV)- and (-)1-(4-aminophenyl)-3-methyl-carbamoyl-4-methyl-7, 8-methylenedioxy-3,4-dihydro-5H-2,3-benzo-diazepine [GYKI 53784 (LY303070)]-resistant depolarizations. Electrical stimulations applied to the dorsal part of the explant trigger excitatory synaptic potentials with latencies distributed in three regularly spaced groups. Excitatory postsynaptic potentials (EPSPs) in the earliest group have a similar latency and time course and correspond to monosynaptic activation. EPSPs in later groups have more scattered latencies and time courses and correspond to polysynaptic activation. Monosynaptic EPSPs are insensitive to the specific NMDA blocker APV, and are completely and reversibly suppressed by the non-competitive AMPA receptor antagonist GYKI 53784 (LY303070). Detailed analysis of the spontaneous excitatory synaptic activity shows that APV decreases the frequency of spontaneous EPSPs without modifying their shape or amplitude. We conclude that excitatory synapses on brainstem motoneurons in vitro are mainly activated through AMPA receptors (AMPA-Rs). NMDA receptors (NMDA-Rs) are present in the membrane, but are located either at extrasynaptic sites or silent synapses, and are not directly involved in synaptic transmission on motoneurons. On the contrary, NMDA receptors contribute to synaptic transmission within the premotor interneuronal network.

Animals↗
PubMed1982

The ionic dependence of black widow spider venom action at the stretch receptor neuron and neuromuscular junction of crustaceans.

The effects of black widow spider venom (BWSV) on the crayfish stretch receptor and the lobster neuromuscular junction were examined. In crayfish stretch receptor neurons, BWSV caused a slight hyperpolarization followed by a large depolarization. The venom-induced depolarization of the stretch receptor was caused by an increase in membrane conductance to Na+ and Ca2+. Black widow spider venom also caused an increase in the frequency of miniature inhibitory postsynaptic potentials recorded in the stretch receptor. The ability of BWSV to increase the frequency of miniature excitatory postsynaptic potentials (MEPSPs) at the lobster neuromuscular junction was dependent on the divalent cation composition of the bathing medium. Ringer solutions containing Ca2+ supported the greatest venom-induced increase in MEPSP frequency, Mg2+ and Mn2+ supported a moderate increase in MEPSP frequency, while Co2+ and Zn2+ blocked this venom effect entirely. Black widow spider venom did not block axonal conduction in lobster walking leg axons or in the axon of the crayfish stretch receptor. The results suggest that in crustaceans, BWSV interacts specifically with membrane of the soma-dendritic region of the stretch receptor and with nerve terminal membrane, causing an increase in Na+ and Ca2+ conductance.

Animals↗
PubMed1989

Synaptic potentials induced by postganglionic stimulations in cat bladder parasympathetic neurones.

Intracellular recording techniques were used to examine and compare synaptic potentials evoked by stimulating pre- and postganglionic nerve trunks in cat bladder parasympathetic ganglia. In the 76 ganglion cells examined, two types of responses were recorded on stimulating the postganglionic nerve: an antidromic action potential (type PostNS1; n = 30) or a fast excitatory postsynaptic potential (f-EPSP; type PostNS2; n = 46) which resulted in an orthodromic-like action potential. In some of the cells exhibiting a PostNS1 response (n = 19), a fast depolarization was superimposed on the antidromic spike. This depolarization was due to the synaptic activation of nicotinic receptors. In many of the cells exhibiting either PostNS1 or PostNS2 responses, repetitive stimulation of the postganglionic nerve induced a slow hyperpolarization. Applying nicotinic (hexamethonium, 0.5-1 mM) receptor muscarinic (atropine, 1 microM), alpha-adrenergic (phentolamine, 1 microM) and purinergic (caffeine, 0.5-1 mM) receptor antagonists completely inhibited the tetanus-induced slow hyperpolarization in some cells (n = 5). In other cells (n = 15), a slow hyperpolarization persisted in the presence of these antagonists. These results indicate that stimulation of the postganglionic nerve trunk of cat bladder parasympathetic ganglia can elicit not only an antidromic action potential, but also synaptic potentials which are mediated by the activation of cholinergic (nicotinic and muscarinic), noradrenergic and purinergic receptors, as well as non-cholinergic, non-alpha-adrenergic and non-purinergic synaptic potential.

Animals↗
PubMed1985

An intracellular analysis of the entopeduncular inputs on the centrum medianum-parafascicular nuclear complex in cats.

Intracellular recording from the CM-PF neurons was performed by stimulation of the EN, the caudate nucleus (Cd), the cerebellar nuclei (CN) and the motor cortex in the cat under Nembutal anesthesia. Twenty-seven neurons in the CM-PF nuclear complex and two neurons near the habenular nucleus received monosynaptic inhibitory postsynaptic potentials (IPSPs; latency of 1.0-4.0 ms, mean 2.3 ms) by EN stimulation. Cd stimulation evoked excitatory postsynaptic potentials (EPSPs) followed by long hyperpolarizations in most of the CM-PF neurons and produced antidromic activation in 7 neurons. Six neurons received EPSPs (latencies of 4-7 ms) by cortical stimulation. CN stimulation affected only two neurons in the present study. Intracellular HRP staining revealed that some CM-PF neurons have polygonal or spindle-shaped somata with fine, long and sparsely spinous dendrites.

Animals↗
PubMed1979

Effects of ACTH4-10 on synaptic transmission in frog sympathetic ganglion.

The influence of ACTH4-10, a behaviourally active fragment of adrenocorticotropic hormone (ACTH) devoid of endocrine activity, on synaptic transmission in the paravertebral sympathetic ganglion of the frog was investigated. Postsynaptic potentials evoked by electrical stimulation of pregnanglionic nerves were recorded using a sucrose gap method. Fast excitatory postsynaptic potentials (EPSPs), which are mediated via nicotinic cholinergic synapses, were not affected by 10(-6) M ACTH4-10. Application of ACTH4-10 in a concentration as low as 10(-8) M for 60 min caused a marked augmentation of the amplitude of slow inhibitory postsynaptic potentials (IPSPs) which are mediated via dopaminergic synapses. The increase in amplitude developed gradually after a latency of 60--90 min and outlasted the application of the peptide. In addition, ACTH4-10 at 10(-6) M increased the hyperpolarising response of the ganglion to exogenous dopamine, as studied by a micro-application method. There was no significant effect of ACTH4-10 on the muscarinic cholinergic depolarising response of the ganglion towards exogenous acetylcholine. The behaviourally active vasopressin fragment DG-LVP (10(-6) M) had no effect on slow IPSPs. The results demonstrate that ACTH4-10 specifically affects slow synaptic inhibition in frog sympathetic ganglion, probably by acting upon the postsynaptic membrane. The possibility is discussed that ACTH4-10 affects one of the intermediate steps between dopaminergic receptor interaction and generation of the slow IPSP.

Acetylcholine↗
PubMed1994

Cholecystokinin (CCK-8S) prolongs 'unsaturated' theta-pulse induced long-term potentiation in rat hippocampal CA1 in vitro.

The effects of bath-applied sulphated cholecystokinin octapeptide (CCK-8S; 500 nM) and the selective CCKB receptor antagonist PD 135158 (1 microM) on the induction and maintenance of an 'unsaturated' long-term potentiation (LTP) were examined using recordings of field excitatory postsynaptic potentials (fEPSP) and population spikes (PS) in the hippocampal CA1 region of the rat. LTP was induced by a single theta-pulse stimulation (10 pulses at 7 Hz) of the Schaffer collateral-commissural pathway. CCK-8S had minor effects on the induction of LTP but substantially prolonged LTP of both fEPSP and PS from about 1 to at least 3 h. The antagonist PD 135158 had no influence on the induction of potentiation of fEPSP slope, but decreased the potentiation of PS amplitude. The results support the view that CCK-8S may facilitate long-term changes in glutamatergic synaptic transmission of the hippocampus, such as LTP.

Animals↗
PubMedDate not supplied

Complex composition of synaptic potentials of the rubrospinal neurons to corticofugal impulses.

Complex, multicomponent excitatory postsynaptic potentials (EPSPs) of the red nucleus rubrospinal neurons evoked by stimulation of the sensorimotor cortex and associative field of the parietal cortex were studied in acute experiments on pentobarbitalized cats by the intracellular recording technique. Complex cortical EPSPs were recorded in two-thirds of the studied number of neurons. Monosynaptic nature of the first two components of EPSPs evoked by corticofugal impulses propagating at an average velocity of 18.5 ms and 7.5 ms was revealed. Participation of the corticospinal input in the genesis of EPSPs mentioned was revealed by selective activation of corticospinal fibers on the level of medullary pyramids as well as by studying peculiarities of their interaction with effects of cortical stimulation. It was shown that both corticospinal and corticorubral (predominantly slow conducting) neurons participate in the genesis of the first two components of complex EPSPs.

Animals↗
PubMed1987

Postnatal transient expression of long-lasting descending inhibitory effect on spinal reflexes in the rat.

In the spinal cord isolated from neonatal rats, stimulation of the ipsilateral lateral column at the thoracic level strongly inhibited monosynaptic segmental reflex in the lumbar cord for about 60 s. The descending inhibition was not associated with any changes in the membrane potential or conductance in lumbar motoneurons when the excitatory postsynaptic potentials in response to stimulation of the dorsal root were depressed. The descending inhibition was diminished with age and could not be detected at 5 months of age. It is suggested that certain inhibitory pathways in the descending spinal tract are rearranged during postnatal development of rats.

Age Factors↗
PubMed1991

Cyclic AMP induces long-term increase in synaptic efficacy in CA1 region of rat hippocampus.

The membrane permeable cyclic AMP analogue dibutyryl cAMP was found to have a biphasic effect on the amplitude of population spikes recorded in area CA1 of rat hippocampal slices in response to 0.05 Hz stimulation of the Schaffer collateral/commissural path. While dbcAMP was present the population spike was depressed and after washout of dbcAMP the population spike showed potentiation lasting at least 2 h. The population excitatory postsynaptic potential (EPSP) was unaffected. Addition of picrotoxin throughout the experiment caused no change in the depression but reduced the potentiation caused by dbcAMP. We conclude that cAMP may play a role in long-term potentiation (LTP).

Animals↗
PubMed1991

Properties of associative long-lasting potentiation induced by cellular conditioning in the motor cortex of conscious cats.

Mechanisms of long-lasting potentiation of synaptic responses induced in the thalamocortical and recurrent collateral pathways of the pyramidal tract were studied in intracellular recordings from the motor cortex of unanesthetized, chronically implanted cats. The observations provide the first description of long-lasting potentiation in the unanesthetized neocortex in vivo. Monosynaptic excitatory postsynaptic potentials of 2-5 mV in amplitude were evoked as test responses by stimulation of the pyramidal tract and thalamic ventrolateral nucleus at 0.1-0.5 Hz frequency. Pressure microinjections of drugs and ions were also performed during intracellular recordings. In the first series of experiments, test synaptic responses were paired with intracellular current injection-induced action potentials at an interstimulus interval set between 0-200 ms and 0.1-0.5 Hz frequency. Pairings (30-100 x) induced long-lasting potentiation of the test responses in 58% of cells. The increased synaptic responses typically initiated action potentials and their potentiation usually lasted over the period of recordings. Increases in amplitude of synaptic responses were not correlated with statistically significant changes in electrical membrane properties (resting potential, input resistance, time constant, spike threshold) or parameters of action potentials and their afterpotentials. The failure to induce increases in synaptic efficacy by unpaired stimuli (pseudoconditioning) demonstrated the associative property of the long-lasting potentiation. In a second series of experiments, differential cell conditioning was employed. This paradigm induced long-lasting potentiation of the explicitly paired synaptic response without noticeable modification of unpaired or pseudorandomly paired synaptic responses tested conjointly in the same neuron. These observations demonstrated the input-specificity of long-lasting potentiation. In a third series of experiments, subthreshold depolarizing current pulses were summated with synaptic responses to induce firing in the recorded neuron during pairing. Long-lasting potentiation occurred in 55% of the summated synaptic inputs. Pseudoconditioning did not induce synaptic potentiation in these cells. In a fourth series of experiments, conditioning was employed in neurons in which firing activity was suppressed by an intracellularly injected lidocaine derivative. Long-lasting potentiation was induced in 50% of the attempts when synaptic responses were paired with current-induced depolarizations greater than 30 mV. These results suggest that postsynaptic induction of long-lasting synaptic potentiation can be successful in the absence of postsynaptic sodium spikes in neurons of the motor cortex in vivo. In a fifth series of experiments, homosynaptic high-frequency tetanization (80-200 Hz for 5-15 s) was applied to the thalamocortical and recurrent pyramidal afferents.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1995

Neurophysiological changes of spiny neurons in rat neostriatum after transient forebrain ischemia: an in vivo intracellular recording and staining study.

The spontaneous activities, evoked postsynaptic potentials and membrane properties of spiny neurons in rat neostriatum were compared before, during and after 5-8 min ischemia using intracellular recording and staining techniques in vivo. Severe forebrain ischemia was induced with the four-vessel occlusion method. Approximately 2.5 min after the onset of ischemia the baseline membrane potential quickly depolarized to -20 mV and remained at this level during ischemia. Repolarization began within 2 min after recirculation. The onset of ischemic depolarization was directly related to the severity of ischemia and its latency was inversely related to brain temperature. Spontaneous firing and membrane potential fluctuation of spiny neurons ceased immediately after ischemia and slowly recovered several hours after recirculation. No neuronal hyperactivity was observed up to 7 h after recirculation. Cortically evoked inhibitory postsynaptic potentials and late depolarizations disappeared earlier after ischemia and recovered later following recirculation than the initial excitatory postsynaptic potentials. Membrane input resistance of spiny neurons was significantly increased but the time constant remained the same following recirculation. The rheobase and spike threshold of spiny neurons were significantly increased and the repetitive firing evoked by depolarizing current pulse was suppressed shortly after recirculation. The results of the present study indicated that the spontaneous activity and evoked postsynaptic responses of spiny neurons are suppressed and the excitability of spiny neurons is decreased after transient ischemia. The polysynaptic responses are more sensitive to ischemia than the monosynaptic ones.

Animals↗
PubMed1995

Membrane potential oscillations of neonatal rat spinal motoneurons evoked by electrical stimulation of dorsal root fibres.

Intracellular recording from lumbar motoneurons of the neonatal rat isolated spinal cord bathed in standard saline solution was used to study membrane potential oscillations which accompanied the decay phase of excitatory postsynaptic potentials (EPSP) induced by single electrical pulses to an adjacent dorsal root. About 60% of motoneurons displayed rhythmic oscillations of 10 +/- 2 mV maximal amplitude and 7 +/- 0.5 Hz frequency. Ability to generate oscillations could not be correlated to the cell membrane properties or to the age of the preparation (5-13 days). The oscillation frequency was independent of membrane potential (-100 to -45 mV) or of the intensity of dorsal root stimuli. The oscillation amplitude was linearly related to the cell potential within the same voltage level. Fast Fourier transform analysis showed that the power spectrum of oscillations peaked at approximately 8 Hz. Electrically evoked activities and spontaneous events displayed similar cut-off frequencies. When the cell membrane potential was steadily depolarized, a hyperpolarizing pulse applied during the decay phase of the EPSP promptly revealed the presence of oscillatory behaviour. Pharmacological block of neurokinin-1 or N-methyl-D-aspartate receptors depressed the decay phase of the EPSP and the associated oscillatory responses. It is suggested that rhythmic oscillations were probably due to summated synaptic potentials generated at the premotoneuron level and are perhaps of functional relevance to motoneuron behaviour.

Animals↗
PubMed1984

Effects of caroverine and diltiazem on synaptic responses, L-glutamate-induced depolarization and potassium efflux in the frog spinal cord.

The frog spinal cord was used to determine the characteristics of the actions of caroverine and diltiazem, two organic Ca2+-antagonists, on synaptic responses and L-glutamate-induced depolarization. Caroverine and diltiazem (10(-4)M) depressed the dorsal root potential (DR-DRP) induced by electrical stimulation of an adjacent dorsal root. Diltiazem also depressed the ventral root potential (DR-VRP), whereas caroverine augmented both the polysynaptic component in the ventral root reflex and the size of the DR-VRP. The root potentials induced by high frequency stimulation (20 Hz, for 1 s) were markedly depressed by these Ca2+-antagonists at a concentration of 10(-4)M. When the preparation was perfused with normal medium, the compounds depressed L-glutamate-induced depolarizations in ventral and dorsal roots. In preparations treated with tetrodotoxin (TTX) (2 X 10(-7)M), the antagonizing actions of the drugs against L-glutamate-induced depolarizations in the ventral root were markedly reduced or abolished, while significant antagonizing actions on the depolarization in the dorsal root were still observed. The increase in extracellular K+ activity induced by L-glutamate in the TTX-treated preparation was significantly reduced by the compounds. Caroverine and diltiazem had no effect on the presynaptic nerve spike and on the focal synaptic potential induced by a single stimulation of a dorsal root; however, the focal synaptic potential induced by high frequency stimulation (20 Hz, 1 s) was attenuated. Motoneuronal action potentials were abolished by the drugs, while the excitatory postsynaptic potential remained unaffected. 9 The present results suggest that caroverine and diltiazem are not specific L-glutamate antagonists in the frog spinal cord, but that they block the initiation of an action potential without affecting presynaptic nerve conduction, transmitter release or transmitter-receptor interactions. The inhibitory effects of these compounds on L-glutamate-induced K+-efflux are discussed with reference to their Ca2+-antagonizing actions.

Animals↗
PubMed1996

Depression of glutamatergic transmission by nociceptin in the neonatal rat hemisected spinal cord preparation in vitro.

The present study explored the action of nociceptin, the putative endogenous ligand for the orphan opioid receptor (ORL1), on the rat hemisected spinal cord preparation. Electrical stimulation of a dorsal root evokes a glutamatergic population ventral root potential (DR-VRP) in the corresponding ventral root. Low intensity stimulation evokes two A fibre-mediated components; a compound action potential of motoneurones superimposed on a population e.p.s.p. (excitatory postsynaptic potential); at higher stimulus intensities sufficient to activate C fibres a more prolonged population e.p.s.p. is evoked. All three components were depressed by nociceptin in a concentration-dependent manner with IC50 values (s.e.mean) of 119 +/- 2 nM (n = 4), 241 +/- 3 nM (n = 4) and 32 +/- 2 nM (n = 4), respectively. The depressant actions of nociceptin (30 nM and 300 nM) were not reversed by the opioid antagonist naloxone (1 microM). Nociceptin (100 nM and 300 nM) had no effect on the afferent volleys in the dorsal root. Nociceptin therefore appears to be acting as an inhibitory peptide at the spinal level through a naloxone-insensitive opioid receptor.

Amino Acid Sequence↗
PubMed1992

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

1. Intracellular recordings were obtained from pyramidal-type neurons in the basolateral amygdaloid nucleus (BLA) in slices of rat ventral forebrain and used to compare the actions of exogenously applied cholinomimetics to the effects produced by electrical stimulation of amygdalopetal cholinergic afferents from basal forebrain. 2. Bath application of carbachol depolarized pyramidal cells with an associated increase in input resistance (Ri), reduced the slow after-hyperpolarization (AHP) that followed a series of current-evoked action potentials and blocked spike frequency accommodation. All of these effects were reversed by the muscarinic antagonist atropine but not by the nicotinic antagonist hexamethonium. 3. Electrical stimulation of amygdaloid afferents within the external capsule evoked a series of synaptic potentials consisting of a non-cholinergic fast excitatory postsynaptic potential (EPSP), followed by early and late inhibitory postsynaptic potentials (IPSPs). Each of these synaptic potentials was reduced by carbachol in an atropine-sensitive manner. 4. Local application of carbachol to pyramidal cells produced a short-latency hyperpolarization followed by a prolonged depolarization. The hyperpolarization and depolarization to carbachol were blocked by atropine but not hexamethonium. 5. The carbachol-induced hyperpolarization was associated with a decrease in Ri and had a reversal potential nearly identical to that of the early IPSP. The inhibitory response was blocked by perfusion of medium containing tetrodotoxin (TTX), bicuculline or picrotoxin, while the subsequent depolarization was unaffected. On the basis of these data, it is concluded that the muscarinic hyperpolarization is mediated through the rapid excitation of presynaptic GABAergic interneurons in the slice. 6. The findings that the carbachol-induced depolarization was associated with an increase in Ri, often had a reversal potential below -80 mV, was sensitive to changes in extracellular potassium concentration and was blocked by intracellular ionophoresis of the potassium channel blocker caesium suggest that it resulted from a muscarinic blockade of one or more potassium conductances. 7. Repetitive stimulation of sites within the slice containing cholinergic afferents evoked a series of fast EPSPs followed by IPSPs. These non-cholinergic potentials were followed by a slow EPSP that lasted from 10 s-4 min. The slow EPSP was enhanced by eserine and blocked by atropine. It was also blocked by TTX or cadmium, indicating that it was dependent on spike propagation and calcium-dependent release of acetylcholine (ACh). 8. Stimulation of cholinergic afferents in the slice mimicked other effects produced by carbachol including blockade of the slow AHP and accommodation of action potential discharge and these actions were potentiated by eserine and blocked by atropine.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1994

Relationships between morphology and physiology of pyramid-pyramid single axon connections in rat neocortex in vitro.

1. Double intracellular recordings were made from 1163 pairs of pyramidal neurones in layer V-VI of the rat somatomotor cortex in vitro using sharp electrodes filled with biocytin. Monosynaptically connected pairs of cells were identified when an action potential in one could elicit a constant latency excitatory postsynaptic potential (EPSP) in the other and the cells were filled with biocytin. Labelled cells were subsequently identified histologically with avidin-horseradish peroxidase. 2. Thirty-four pairs of cells were found to be monosynaptically connected. Fifteen of these pairs were sufficiently stable for electrophysiological recordings and three of these were recovered sufficiently to permit full morphological reconstruction. 3. The EPSP recorded between the first pair of pyramids varied in amplitude between 0 and 3 mV (mean 1.33 +/- 1.06 mV) and fluctuated considerably (coefficient of variation, 0.796). This was largely due to a high incidence of apparent failures of transmission. On reconstruction two boutons from the presynaptic pyramid axon were in close apposition to the proximal portions of basal dendrites of the postsynaptic cell. 4. In the second pair of pyramids the EPSP had a mean amplitude of 1.06 mV, and displayed a 10-90% rise time of 2.8 ms and a width at half-amplitude of 23 ms. This EPSP did not alter significantly with changes in membrane potential at the soma. The presynaptic axon closely apposed the distal apical dendrite of the postsynaptic cell in eight places. 5. In the third pair of pyramids, the EPSPs, recorded at a relatively depolarized membrane potential, were long lasting and could elicit slow dendritic spikes with long and variable latencies. These slow spikes suggested that the postsynaptic recording site was dendritic and on reconstruction a possible location was identified on the apical dendrite. A total of five presynaptic boutons closely apposed three separate, proximal branches of the postsynaptic apical dendrite. 6. These results provide the first illustration of a morphological basis for variations in functional properties of pyramid-pyramid connections in the neocortex.

Animals↗
PubMed1990

Glutamate, the dominant excitatory transmitter in neuroendocrine regulation.

Glutamate has been found to play an unexpectedly important role in neuroendocrine regulation in the hypothalamus, as revealed in converging experiments with ultrastructural immunocytochemistry, optical physiology with a calcium-sensitive dye, and intracellular electrical recording. There were large amounts of glutamate in boutons making synaptic contact with neuroendocrine neurons in the arcuate, paraventricular, and supraoptic nuclei. Almost all medial hypothalamic neurons responded to glutamate and to the glutamate agonists quisqualate and kainate with a consistent increase in intracellular calcium. In all magnocellular and parvocellular neurons of the paraventricular and arcuate nuclei tested, the non-NMDA (non-N-methyl-D-aspartate) glutamate antagonist CNQX (cyano-2,3-dihydroxy-7-nitroquinoxaline) reduced electrically stimulated and spontaneous excitatory postsynaptic potentials, suggesting that the endogenous neurotransmitter is an excitatory amino acid acting primarily on non-NMDA receptors. These results indicate that glutamate plays a major, widespread role in the control of neuroendocrine neurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗