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Cholinergic induction of theta-frequency oscillations in hippocampal inhibitory interneurons and pacing of pyramidal cell firing.

Cholinergic and GABAergic medial septal afferents contribute to hippocampal theta activity in part by actions on local interneurons. Interneurons near the border between stratum radiatum and stratum lacunosum-moleculare (LM) display intrinsic membrane potential oscillations at theta frequency when depolarized near threshold. First, whole-cell current-clamp recordings in rat hippocampal slices were used to examine effects of the cholinergic agonist carbachol on biocytin-labeled LM interneurons. At resting membrane potential, cells were depolarized by bath application of 25 microM carbachol, and the depolarization was sufficient to induce membrane potential oscillations (2.4 +/- 0.2 mV) that paced cell firing. Carbachol also depolarized LM interneurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione, (+/-)-2-amino-5-phosphonopentanoic acid, and bicuculline, indicating that cholinergic depolarization of LM cells does not depend on ionotropic glutamate or GABA(A) synaptic transmission in local circuits. Atropine blocked the depolarization, indicating that muscarinic receptors were involved. Minimal stimulation applied to visually identified LM interneurons was then used to determine if spontaneous activity in CA1 pyramidal cells can be paced by rhythmic inhibition generated by LM cells at theta frequency. Inhibitory postsynaptic potentials evoked in pyramidal cells by single minimal stimulations were followed by rebound depolarizations and action potentials. When trains of minimal stimulation were delivered, membrane potential oscillations of depolarized pyramidal cells followed the stimulation frequency. Minimal stimulation led pyramidal cell firing with an average phase of 177 degrees. Thus, muscarinic induction of theta-frequency membrane potential oscillations in LM interneurons may contribute to the generation of rhythmic inhibition that paces intrinsically generated theta activity in CA1 pyramidal cells.

2-Amino-5-phosphonovalerate↗

Extraction of sensory parameters from a neural map by primary sensory interneurons.

We examine the anatomical basis for the representation of stimulus parameters within a neural map and examine the extraction of these parameters by sensory interneurons (INs) in the cricket cercal sensory system. The extraction of air current direction by these sensory interneurons can be understood largely in terms of the anatomy of the system. There are two critical anatomical constraints. (1) The arborizations of afferents with similar directional tuning properties are located near each other within the neural map. Therefore, a continuous variation in stimulus direction causes a continuous variation in the spatial pattern of activation. (2) The restriction of the synaptic connections of an interneuron to a unique set of afferents results from the unique anatomy of that interneuron: its dendritic arbors are located within restricted regions of the afferent map containing afferents with a limited subset of directional sensitivities. The functional organization of the set of four interneurons studied here is equivalent to a Cartesian coordinate system for computing the stimulus direction vector. For any air current stimulus direction, the firing rates of the active interneurons could be decoded as Cartesian coordinates by neurons at successive processing stages. The implications of this Cartesian coordinate system are discussed with respect to optimal coding strategies and developmental constraints on the cellular implementation of this coding scheme.

Afferent Pathways↗

Muscarinic regulation of dendritic and axonal outputs of rat thalamic interneurons: a new cellular mechanism for uncoupling distal dendrites.

Inhibition is crucial for sharpening the sensory information relayed through the thalamus. To understand how the interneuron-mediated inhibition in the thalamus is regulated, we studied the muscarinic effects on interneurons in the lateral posterior nucleus and lateral geniculate nucleus of the thalamus. Here, we report that activation of muscarinic receptors switched the firing pattern in thalamic interneurons from bursting to tonic. Although neuromodulators switch the firing mode in several other types of neurons by altering their membrane potential, we found that activation of muscarinic subtype 2 receptors switched the fire mode in thalamic interneurons by selectively decreasing their input resistance. This is attributable to the muscarinic enhancement of a hyperpolarizing potassium conductance and two depolarizing cation conductances. The decrease in input resistance appeared to electrotonically uncouple the distal dendrites of thalamic interneurons, which effectively changed the inhibition pattern in thalamocortical cells. These results suggest a novel cellular mechanism for the cholinergic transformation of long-range, slow dendrite- and axon-originated inhibition into short-range, fast dendrite-originated inhibition in the thalamus observed in vivo. It is concluded that the electrotonic properties of the dendritic compartments of thalamic interneurons can be dynamically regulated by muscarinic activity.

Action Potentials↗

Reduced excitatory drive onto interneurons in the dentate gyrus after status epilepticus.

Impaired GABAergic inhibition may contribute to the development of hyperexcitability in epilepsy. We used the pilocarpine model of epilepsy to demonstrate that regulation of excitatory synaptic drive onto GABAergic interneurons is impaired during epileptogenesis. Synaptic input from granule cells (GCs), perforant path, and CA3 inputs onto hilar border interneurons of the dentate gyrus were examined in rat hippocampal slices during the latent period (1-8 d) after induction of status epilepticus (SE). Short-term depression (STD) of GC inputs to interneurons induced by brief (500-800 msec), repetitive (5-20 Hz) stimulation, as well as paired-pulse depression at both GC and CA3 inputs to interneurons, were significantly (p < 0.05) enhanced in SE-experienced rats. In contrast, we found no significant differences between SE-experienced and age-matched control rats in the properties of minimal EPSCs evoked at low frequency (0.3 Hz). Consistent with reduced GABAergic inhibition onto granule cells, paired-pulse depression of perforant path-evoked granule cell population spikes was lost in SE-experienced rats. Enhanced STD was partially mediated by group II metabotropic glutamate receptors, because the selective antagonist, 2S-2-amino-2-(1S,2S-2-carboxycyclopropyl-1-yl)-3-(xanth-9-yl)propanoic acid, attenuated STD in SE-experienced rats but had no effect on STD of GC inputs in the normal adult rat. The group II mGluR agonist, (2S',1R',2R',3R')-2-(2,3-dicarboxylcyclopropyl) glycine (1 micrometer), produced a greater depression of GC input to hilar border interneurons in SE-experienced rats than in controls. These results indicate that, in the SE-experienced rat, excitatory drive to hilar border inhibitory interneurons is weakened through a use-dependent mechanism involving group II metabotropic glutamate receptors.

Action Potentials↗

5-HT3 receptors mediate serotonergic fast synaptic excitation of neocortical vasoactive intestinal peptide/cholecystokinin interneurons.

Neocortical neurons expressing the serotonin 5-HT3 receptor (5-HT3R) were characterized in rat acute slices by using patch-clamp recordings combined with single-cell RT-PCR and histochemical labeling. The 5-HT3A receptor subunit was expressed selectively in a subset of GABAergic interneurons coexpressing cholecystokinin (CCK) and vasoactive intestinal peptide (VIP). The 5-HT3B subunit was never detected, indicating that 5-HT3Rs expressed by neocortical interneurons did not contain this subunit. In 5-HT3A-expressing VIP/CCK interneurons, serotonin induced fast membrane potential depolarizations by activating an inward current that was blocked by the selective 5-HT3R antagonist tropisetron. Furthermore, we observed close appositions between serotonergic fibers and the dendrites and somata of 5-HT3R-expressing neurons, suggestive of possible synaptic contacts. Indeed, in interneurons exhibiting rapid excitation by serotonin, local electrical stimulations evoked fast EPSCs of large amplitude that were blocked by tropisetron. Finally, 5-HT3R-expressing neurons were also excited by a nicotinic agonist, indicating that serotonergic and cholinergic fast synaptic transmission could converge onto VIP/CCK interneurons. Our results establish a clear correlation between the presence of the 5-HT3A receptor subunit in neocortical VIP/CCK GABAergic interneurons, its functional expression, and its synaptic activation by serotonergic afferent fibers from the brainstem raphe nuclei.

Animals↗

Coexistence of excitatory and inhibitory GABA synapses in the cerebellar interneuron network.

Functional GABA synapses are usually assumed to be inhibitory. However, we show here that inhibitory and excitatory GABA connections coexist in the cerebellar interneuron network. The reversal potential of GABAergic currents (E(GABA)) measured in interneurons is relatively depolarized and contrasts with the hyperpolarized value found in Purkinje cells (-58 and -85 mV respectively). This finding is not correlated to a specific developmental stage and is maintained in the adult animal. E(GABA) in interneurons is close to the mean membrane potential (-56.5 mV, as measured with a novel "equal firing potential" method), and both parameters vary enough among cells so that the driving force for GABA currents can be either inward or outward. Indeed, using noninvasive cell-attached recordings, we demonstrate inhibitory, excitatory, and sequential inhibitory and excitatory responses to interneuron stimulation [results obtained both in juvenile (postnatal days 12-14) and subadult (postnatal days 20-25) animals]. In hyperpolarized cells, single synaptic GABA currents can trigger spikes or trains of spikes, and subthreshold stimulations enhance the responsiveness to subsequent excitatory stimulation over at least 30 msec. We suggest that the coexistence of excitatory and inhibitory GABA synapses could either buffer the mean firing rate of the interneuron network or introduce different types of correlation between neighboring interneurons, or both.

Action Potentials↗

ATP modulation of excitatory synapses onto interneurons.

Inhibitory interneurons play important roles in neuronal circuits, but the synaptic mechanisms that regulate excitatory input onto interneurons remain to be fully understood. We show that ATP-gated presynaptic P2X2 channels facilitate excitatory transmission onto stratum radiatum interneurons but not onto CA1 pyramidal neurons. ATP released endogenously during carbachol-induced oscillations facilitates excitatory synapses onto interneurons. Overall, these data provide evidence for the molecular identity, synaptic function, and interneuron synapse specificity of a presynaptic neurotransmitter-gated cation channel. The findings highlight a novel form of presynaptic facilitation for hippocampal interneurons and suggest a role for extracellular ATP in neuronal networks.

Adenosine Triphosphate↗

The spinal interneurons and properties of glutamatergic synapses in a primitive vertebrate cutaneous flexion reflex.

Unlike the monosynaptic "stretch" reflex, the exact neuronal pathway for a simple cutaneous reflex has not yet been defined in any vertebrate. In young frog tadpoles, we made whole-cell recordings from pairs of spinal neurons. We found direct, excitatory, glutamatergic synapses from touch-sensitive skin-sensory neurons to sensory pathway interneurons, and then from these sensory interneurons to motoneurons and premotor interneurons on the other side of the body. We conclude that the minimal pathway for this primitive reflex, in which stroking the skin on one side leads to flexion on the other side, is disynaptic. This detailed circuit information has allowed us to ask whether the properties of glutamatergic synapses during the first day of CNS development are tuned to their function in the tadpole's responses. Stroking the skin excites a few sensory neurons. These activate primarily AMPA receptors producing short, strong excitation that activates many sensory pathway interneurons but only allows temporal summation of closely synchronous inputs. In contrast, the excitation produced in contralateral neurons by the sensory pathway interneurons is weak and primarily mediated by NMDA receptors. As a result, considerable summation is required for this excitation to lead to postsynaptic neuron firing and a contralateral flexion. We conclude that from their early functioning, synapses from sensory neurons are strong and those from sensory pathway interneurons are weak. The distribution of glutamate receptors at synapses in this developing circuit is tuned so that synapses have properties suited to their roles in the whole animal's reflex responses.

Afferent Pathways↗

Networks of inhibitory and excitatory commissural interneurons mediating crossed reticulospinal actions.

Axonal projections and neurotransmitters used by commissural interneurons mediating crossed actions of reticulospinal neurons were investigated in adult cats. Eighteen interneurons, located in or close to lamina VIII in midlumbar segments, that were monosynaptically excited by reticulospinal tract fibres and projected to contralateral motor nuclei were labelled by intracellular injection of tetramethylrhodamine-dextran and Neurobiotin. The nine most completely labelled interneurons were analysed with combined confocal and light microscopy. None of the stem axons gave off ipsilateral axon collaterals. Seven cells had axon collaterals that arborized in the contralateral grey matter in the ventral horn of the same segments. Transmitters were identified by using antibodies raised against vesicular glutamate transporters 1 and 2, glutamic acid decarboxylase and the glycine transporter 2. The axons of two cells were immunoreactive for the glycine transporter 2 and hence were glycinergic. Three cells were immunoreactive for the vesicular glutamate transporter 2 and hence were glutamatergic. None of the axons displayed immunoreactivity for glutamic acid decarboxylase. Electron microscopy of two cells revealed direct synaptic connections with motoneurons and other neurons. Axonal swellings of one neuron formed synapses with profiles in motor nuclei whereas those of the other formed synapses with other structures, including cell bodies in lamina VII. The results show that this population of commissural interneurons includes both excitatory and inhibitory cells that may excite or inhibit contralateral motoneurons directly. They may also influence the activity of motoneurons indirectly by acting through interneurons located outside motor nuclei in the contralateral grey matter but are unlikely to have direct actions on interneurons in the ipsilateral grey matter.

Amino Acid Transport Systems, Neutral↗

Interneurons: an electron microscopic study of the cat's hippocampal formation, II.

The ultrastructure of interneurons was studied in the cat and it was found to differ from that of the pyramidal and granule cells. The size, shape and topographic situation of the cell body of interneurons were the criteria for approaching their identification with the cells found in Golgi material. Some interneuron dendrites are also described. The varicose and spindle-shaped dendritic profiles belonging to interneurons are different in size. In Golgi material the interneurons have beaded (varicose) or spindle-shaped dendrites. The arrangement of synaptic terminals on the interneuron dendritic surface seems to be their characteristic feature.

Animals↗

Cutaneous activation of the inhibitory L30 interneurons provides a mechanism for regulating adaptive gain control in the siphon withdrawal reflex of Aplysia.

The functional role of inhibition in the neural network underlying the siphon withdrawal response (SWR) of Aplysia was assessed by examining a recurrent circuit comprised of identified inhibitory interneurons (L30s), and excitatory interneurons (L29s). We previously showed that activity-dependent potentiation of the L30 inhibitory synapse onto L29 can regulate the net excitatory input elicited by tactile siphon stimulation onto siphon motor neurons (LFS cells) (Fischer and Carew, 1993a). To explore the functional significance of L30 potentiated inhibition, we have examined how a behaviorally relevant stimulus that activates the L30 interneurons modulates the SWR circuit. Utilizing a reduced preparation, we show that weak tactile stimulation of the tail strongly activates the L30s, and leads to significant potentiation of the L30 synapse. Next, we demonstrate that similar weak tail stimulation produces significant inhibition of siphon tap-evoked responses in both L29 interneurons and LFS motor neurons. We further show that this form of inhibition is transient, having a time course of approximately 60 sec. Finally, we directly tested the role of the L30s in mediating this form of inhibition by hyperpolarizing two (of three) L30 interneurons during tail stimulation. L30 inactivation significantly attenuated tail stimulation-induced inhibition of siphon-evoked input to both L29 interneurons and LFS motor neurons. Based on these results, we suggest that L30-potentiated inhibition may have an important adaptive role in optimizing the signal-to-noise ratio for activation of the SWR circuit by providing stabilization of SWR responsiveness under a wide range of environmental conditions.

Adaptation, Physiological↗

Convergence of mechanosensory afferents from different classes of exteroceptors onto spiking local interneurons in the locust.

Tactile stimuli to a leg of a locust are detected by two classes of exteroceptors: trichoid sensilla (tactile hairs), which are purely mechanoreceptors, and basiconic sensilla, which serve a dual role as mechano- and chemoreceptors. The trichoid sensilla have the longer shafts, but because the two types of receptors are intermingled over the surface of a leg, both can be excited when the leg contacts an obstacle. This article analyzes the mechanisms by which the tactile sensory information from these two classes of receptor is collated in the CNS so that spatial information is preserved. The mechanosensory afferents from both types of receptors on a hind leg make convergent connections that are excitatory and apparently direct with the same spiking local interneurons in a midline population of the metathoracic ganglion. The anatomy of the afferent projections suggests that the synapses from the two types of receptor are made onto the same region of branches of an interneuron. The slower conduction velocity of the spikes of the basiconic afferents compared to that of the trichoid afferents means that a mechanical stimulus to the tibia will first produce a depolarization caused by the trichoid afferents, followed up to 20 msec later by a depolarization caused by the basiconic sensilla. Each interneuron is excited by a contiguous and overlapping array of trichoid and basiconic receptors that form its receptive field. Different interneurons have different receptive fields such that the surface of the leg is mapped as a series of overlapping receptive fields. Within a receptive field the contribution of individual receptors can be markedly different: some basiconic receptors evoke large-amplitude EPSPs so that each afferent spike can cause a spike in the interneuron, whereas others generate small EPSPs that must sum with other inputs to evoke a spike. The amplitudes of the EPSPs generated by different receptors within a receptive field form gradients that are distributed according to the axes of the leg. The most effective basiconic and the most effective trichoid sensilla within a particular receptive field can be at the same or at different locations on the leg. Tactile sensory information from different types of receptor on one region of a leg is therefore collated initially by particular spiking local interneurons. This organization ensures summation between the inputs from the different types of receptors and should enhance sensitivity.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

Excitatory actions of norepinephrine on multiple classes of hippocampal CA1 interneurons.

Norepinephrine (NE) causes an increase in the frequency of inhibitory postsynaptic potentials in CA1 pyramidal neurons in vitro. The possibility that this increase in tonic inhibition is caused by an excitatory effect on inhibitory interneurons was investigated through whole-cell recordings from pyramidal cells and both whole-cell and cell-attached patch recordings from visualized interneurons in acute slices of rat hippocampus. Adrenergic agonists caused a large increase in the frequency and amplitude of spontaneous IPSCs recorded from pyramidal cells in the presence of ionotropic glutamate receptor blockers, but they had no effect on either the frequency or the amplitude of action potential-independent miniature IPSCs recorded in tetrodotoxin. This effect was mediated primarily by an alpha adrenoceptor, although a slight beta adrenoceptor-dependent increase in IPSCs was also observed. NE caused interneurons located in all strata to depolarize and begin firing action potentials. Many of these cells had axons that ramified throughout the stratum pyramidale, suggesting that they are responsible for the IPSCs observed in pyramidal neurons. This depolarization was also mediated by an alpha adrenoceptor and was blocked by a selective alpha 1- but not a selective alpha 2-adrenoceptor antagonist. However, a slight beta adrenoceptor-dependent depolarization was detected in those interneurons that displayed time-dependent inward rectification. In the presence of a beta antagonist, NE induced an inward current that reversed near the predicted K+ equilibrium potential and was not affected by changes in intracellular Cl- concentration. In the presence of an alpha 1 antagonist, NE induced an inwardly rectifying current at potentials negative to approximately -70 mV that did not reverse (between -130 and -60 mV), characteristics similar to the hyperpolarization-activated current (lh). However, the depolarizing action of NE is attributable primarily to the alpha 1 adrenoceptor-mediated decrease in K+ conductance and not the beta adrenoceptor-dependent increase in lh. These results provide evidence that NE increases action potential-dependent IPSCs in pyramidal neurons by depolarizing surrounding inhibitory interneurons. This potent excitatory action of NE on multiple classes of hippocampal interneurons may contribute to the NE-induced decrease in the spontaneous activity of pyramidal neurons and the antiepileptic effects of NE observed in vivo.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

Paradoxical effects of external modulation of inhibitory interneurons.

The neocortex, hippocampus, and several other brain regions contain populations of excitatory principal cells with recurrent connections and strong interactions with local inhibitory interneurons. To improve our understanding of the interactions among these cell types, we modeled the dynamic behavior of this type of network, including external inputs. A surprising finding was that increasing the direct external inhibitory input to the inhibitory interneurons, without directly affecting any other part of the network, can, in some circumstances, cause the interneurons to increase their firing rates. The main prerequisite for this paradoxical response to external input is that the recurrent connections among the excitatory cells are strong enough to make the excitatory network unstable when feedback inhibition is removed. Because this requirement is met in the neocortex and several regions of the hippocampus, these observations have important implications for understanding the responses of interneurons to a variety of pharmacological and electrical manipulations. The analysis can be extended to a scenario with periodically varying external input, where it predicts a systematic relationship between the phase shift and depth of modulation for each interneuron. This prediction was tested by recording from interneurons in the CA1 region of the rat hippocampus in vivo, and the results broadly confirmed the model. These findings have further implications for the function of inhibitory and neuromodulatory circuits, which can be tested experimentally.

Action Potentials↗

Synaptic communication among hippocampal interneurons: properties of spontaneous IPSCs in morphologically identified cells.

The properties of spontaneous IPSCs (sIPSCs) recorded with whole-cell patch-clamp techniques were investigated in various anatomically identified hippocampal CA1 interneurons and were compared with those recorded in pyramidal cells. Neurons labeled with biocytin or neurobiotin were classified on the basis of their dendritic and axonal arborizations, leading to the identification of previously unknown interneuron types projecting to the dendritic region of pyramidal cells. In most interneurons, the average sIPSCs decayed slower than did those observed in pyramidal cells. The properties of sIPSCs were homogeneous within a given morphologically identified neuron type. Many interneurons had comparable somatic size, location, and dendritic arbor but displayed extremely different axonal projections paralleled by distinct sIPSC properties. Thus, physiological comparisons are only meaningful after the complete morphological identification of the recorded cells. The decay of sIPSCs matched for amplitudes and rise times could vary over 10-fold in a given interneuron, consistent with electrotonic filtering and possibly with different GABAA receptor subunit assemblies present at distinct synapses. Our findings demonstrate an extensive connectivity among hippocampal interneurons through GABAA synapses of various properties that may underlie complex network oscillations at different frequencies.

Action Potentials↗

Somatodendritic depolarization-activated potassium currents in rat neostriatal cholinergic interneurons are predominantly of the A type and attributable to coexpression of Kv4.2 and Kv4.1 subunits.

Unlike other neostriatal neurons, cholinergic interneurons exhibit spontaneous, low-frequency, repetitive firing. To gain an understanding of the K+ channels regulating this behavior, acutely isolated adult rat cholinergic interneurons were studied using whole-cell voltage-clamp and single-cell reverse transcription-PCR techniques. Cholinergic interneurons were identified by the presence of choline acetyltransferase (ChAT) mRNA. Depolarization-activated potassium currents in cholinergic interneurons were dominated by a rapidly inactivating, K+-selective A current that became active at subthreshold potentials. Depolarizing prepulses inactivated this component of the current, leaving a delayed, rectifier-like current. Micromolar concentrations of Cd2+ dramatically shifted the voltage dependence of the A current without significantly affecting the delayed rectifier. The A-channel antagonist 4-aminopyridine (4-AP) produced a voltage-dependent block (IC50, approximately 1 mM) with a prominent crossover at millimolar concentrations. On the other hand, TEA preferentially blocked the sustained current component at concentrations <10 mM. Single-cell mRNA profiling of subunits known to give rise to rapidly inactivating K+ currents revealed the coexpression of Kv4.1, Kv4.2, and Kv1.4 mRNAs but low or undetectable levels of Kv4.3 and Kv3.4 mRNAs. Kv1.1, beta1, and beta2 subunit mRNAs, but not beta3, were also commonly detected. The inactivation recovery kinetics of the A-type current were found to match those of Kv4.2 and 4.1 channels and not those of Kv1.4 or Kv1. 1 and beta1 channels. Immunocytochemical analysis confirmed the presence of Kv4.2 but not Kv1.4 subunits in the somatodendritic membrane of ChAT-immunoreactive neurons. These results argue that the depolarization-activated somatodendritic K+ currents in cholinergic interneurons are dominated by Kv4.2- and Kv4. 1-containing channels. The properties of these channels are consistent with their playing a prominent role in governing the slow, repetitive discharge of interneurons seen in vivo.

4-Aminopyridine↗

Parallel effects of joint receptors on motor neurones and intersegmental interneurones in the locust.

At the distal end of a mesothoracic tibia of the locust, Schistocerca gregaria, is a chordotonal organ which monitors the position and movement of the tarsus relative to the tibia. It contains approximately 35 receptors that variously encode different spatial and temporal parameters (position, velocity and direction of movement). Some excite intersegmental interneurones that respond phasically or tonically, with directional sensitivity to active or imposed movements of the tarsus. Some of these interneurones are also excited by intrinsic movements of the tarsal segments. Others, besides being excited by tarsal proprioceptive inputs, are also excited by exteroreceptors on the tarsus. When stimulated mechanically or electrically, chordotonal afferents evoke excitatory postsynaptic potentials with a central latency of between 0.9 and 1.4 ms simultaneously in the intersegmental interneurones and in tarsal motor neurones. The central arborizations of the afferents, the intersegmental interneurones and the tarsal motor neurones overlap in certain neuropilar regions of the mesothoracic ganglion. Other afferents cause an inhibition of the motor neurones, with a longer and non-consistent latency suggesting the involvement of other intercalated interneurones. These results indicate that proprioceptive inputs from the tarsal joint receptors are transmitted in parallel and monosynaptically to tarsal motor neurones and to the intersegmental interneurones.

Animals↗

Synaptic effects in lumbar alpha-motoneurones evoked from group II muscle afferents via two different interneuronal pathways in the cat.

Conditioning of monosynaptic reflexes was used to investigate group II excitation from quadriceps (Q) and sartorius (Sart) in posterior biceps-semitendinosus (PBSt) motoneurones and different lesions were made to analyze the interneuronal pathways. The purpose of the investigation was to find if the excitation from group II Q and Sart afferents, which enter the spinal cord in L4-L6, is relayed to motoneurones by interneurones located in these segments and/or in the same segments (L7-S1) as the PBSt motoneurones. In some experiments a transection of the dorsal column in L6, which interrupts the group II input from Sart and Q to interneurones in the L7-S1 segments, resulted in a marked decrease (by about 2/3) of group II excitation from these nerves. In other experiments the same lesion did not reduce the group II effect. In the latter cases the effect could be abolished by a second lesion of the lateral funiculus (LF) in L5-L6. It is postulated that potent effects from Q and Sart group II afferents can be evoked by interneurones located in L7-S1, i.e. in the same segments as the PBSt motoneurones (L7-S1), and/or via interneurones in more rostral segments. The axons of the more rostrally located group II interneurones appear to descend mainly in the middle part of the LF.

Animals↗