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At least 1,063 records · Page 59Linked to original sources
PubMed1989

Voltage-dependent properties of electrical synapses formed between identified leech neurones in vitro.

1. The voltage-dependent properties of rectifying and non-rectifying electrical synapses formed between identified leech neurones were quantified during their regeneration in vitro. 2. Junctional conductance increased with time in culture. This was evaluated by making comparisons between cell pairs maintained in vitro for differing amounts of time, as well as by taking repeated measurements from a single cell pair at different time intervals. 3. Non-rectifying electrical synapses were formed between certain identified neurones of the same type. Thus, Leydig cells cultured with Leydig cells established non-rectifying electrical connections, as did Retzius cells, longitudinal motoneurones (L cells) and anterior pagoda (AP) cells, each paired with its own cell type. 4. Rectifying synapses developed when sensory neurones (P cells or N cells) were paired with the other neurones mentioned above that form non-rectifying connections between themselves. The cell combinations examined were L cell-P cell. Leydig cell-N cell, and AP cell-P cell. The direction of current flow across these rectifying synapses was consistently from the sensory neurone to the other cell in the pair. 5. Non-rectifying connections early in the process of synapse regeneration (1-3 days) showed non-linearities greater than those observed in established non-rectifying synapses. There was a subtle, but clear, voltage dependence even at the later stages of synapse formation (4-18 days). 6. In contrast to non-rectifying connections, rectifying synapses formed between cells at early times in culture showed less voltage dependence than those observed at later times. 7. The marked non-linearities of the non-rectifying connections at early stages in synapse formation along with the reduced voltage dependence of the rectifying connections within the same time period revealed unexpected similarities between the two. At the early stages of synapse formation, the two types of electrical synapse were essentially indistinguishable for one direction of junctional current.

Animals↗
PubMed1990

Evidence for the uptake of neuronally derived choline by glial cells in the leech central nervous system.

1. With ion-sensitive microelectrodes based on the Corning exchanger 477317, the accumulation of an unidentified interfering substance was monitored in leech neuropile glial cells but not in neurons after a 10-fold increase in extracellular K+ concentration. Evidence is presented which shows that this substance may be choline. 2. The accumulation of interfering ions was not observed in Ca2(+)-free saline and was substantially reduced in the presence of eserine (a blocker of acetylcholinesterase). 3. In neuropile (and also packet) glial cells, extracellularly applied choline (10(-4) M) caused a steady increase in ion signal. This increase was not affected by removal of extracellular calcium, by hemicholinium-3 (a blocker of high-affinity choline uptake) or eserine. Shortly after the removal of choline from the saline the increase in ion signal stopped and the ion signal then decreased slowly to its original level. 4. Extracellular acetylcholine (10(-4) M) caused a similar increase in intracellular ion signal of neuropile glial cells to that caused by choline. This increase was blocked by eserine. 5. Extracellular choline caused a comparatively small increase in ion signal of Retzius neurones which was blocked by hemicholinium-3. In pressure neurones, choline or hemicholinium-3 had no effect on intracellular ion signal. 6. Autoradiographic analysis of [3H]choline uptake showed that most of the choline was taken up by glial cells in a time- and dose-dependent manner. Small but significant amounts of choline were taken up by neurones and connective tissue. 7. It is concluded that the neuropile and packet glial cells possess an effective choline uptake system which is activated by exogenous choline but also by choline that stems from enzymatic inactivation of acetylcholine released by neurones.

Acetylcholine↗
PubMed1990

Membrane potential dependence of intracellular pH regulation by identified glial cells in the leech central nervous system.

1. We have measured the intracellular pH (pHi) and membrane potential of identified glial cells in the central nervous system of the leech, Hirudo medicinalis, using double-barrelled pH-sensitive microelectrodes. 2. When extracellular K+ concentration was increased, the glial membrane potential decreased and pHi increased; lowering the extracellular K+ concentration hyperpolarized the glial membrane and decreased pHi. These pHi changes were largely dependent upon the presence of CO2-HCO3-; in nominally CO2-HCO3(-)-free saline solution, they were 50-80% smaller. 3. The steady-state pHi of the glial cells in CO2-HCO3(-)-buffered saline solution strongly correlated with the membrane potential between -40 and -90 mV. The slope of this relationship was 60 mV/pH unit. 4. The neurotransmitter 5-hydroxytryptamine (50 microM), which hyperpolarizes the glial membrane, also produced a large, CO2-HCO3(-)-dependent decrease in pHi. The size of the pHi change depended upon the amplitude of the membrane hyperpolarization. 5. The increase in pHi produced by the membrane depolarization in 20 mM-K+ was abolished in Na(+)-free saline. Removal of external Na+ in the presence of 20 mM-K+ reversed the pHi increase. 6. The pHi increase in 20 mM-K+ was also inhibited by the stilbene 4,4-diisothiocyanostilbene-2'-disulphonic acid (DIDS, 0.5 mM). In a DIDS-poisoned preparation a small decrease of pHi was observed in 20 mM-K+ both in the presence and nominal absence of CO2-HCO3-. 7. In neurones, neither CO2-HCO3- nor 20 mM-K+ produced an intracellular alkanization. The steady-state pHi of several identified neurones was not correlated with the membrane potential. 8. We conclude that in glial cells, but not in neurones, the pHi is dependent upon the membrane potential. This membrane potential dependence is due to the activity of the electrogenic Na(+)-HCO3- co-transporter in the glial cell membrane.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1990

Rapid co-transport of sodium and chloride ions in giant salivary gland cells of the leech Haementeria ghilianii.

1. Double-barrelled Cl(-)-selective microelectrodes were used to measure the apparent intracellular Cl- activity (aiCl) and membrane potential (Em) of leech salivary gland cells. In standard physiological solution buffered with HEPES (10 mM), intracellular Cl- activity (corrected for interference) was 38 +/- 8 mM (n = 11) compared to a value of 12.8 mM expected for passive Cl- distribution. The mean Em was -49.4 +/- 8.2 mV (n = 21) which was about 27 mV negative to the Cl- equilibrium potential. 2. Removal of external Cl- led to a slow fall in aiCl until a steady-state level of 4-11 mM was reached in 30-60 min. Recovery of aiCl on readdition of external Cl- took only 2-3 min. The uptake followed an exponential time course having a single rate constant of 1.73 +/- 0.1 min-1 (n = 5) whereas the loss appeared to occur in two phases. Changes in external Cl- produced immediate changes in Em which were the opposite of those expected for a high Cl- permeability, i.e. Cl- removal produced an immediate hyperpolarization (3-18 mV) and readdition of Cl- produced a transient depolarization (5-22 mV). 3. The intracellular accumulation of Cl- was dependent on the external Cl- activity. Even when the external Cl- concentration was reduced to 3%, the cells accumulated Cl- against an electrochemical gradient. 4. Cl- accumulation was temperature sensitive (Q10 approximately 2). 5. On removal of external Na+, aiCl fell to a level which was close to that expected for passive distribution. The active reaccumulation of Cl-, after intracellular Cl- depletion, was abolished in the absence of external Na+; aiCl slowly increased to its passive level. Steady-state aiCl or its recovery by Cl(-)-depleted cells was not affected by the absence of K+ in the bathing solution. 6. The reaccumulation of Cl- was not affected by furosemide (1-5 mM), bumetanide (10(-4) M), amiloride (10(-3) M) or 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS, 10(-4) M). 7. Removal of external Cl- caused a fall in intracellular Na+ activity (aiNa, measured with Na(+)-selective microelectrodes) from 15.9 +/- 6.8 mM (n = 9) to 2.5 +/- 1.3 mM (n = 3). When external Cl- was readded, aiNa rose to 46.5 +/- 6.6 mM (n = 3) before slowly recovering towards its original value. The maximal change in aiNa was 41.7 +/- 4.5 mM (n = 3) and the rate constant for Na+ uptake was 1.8 +/- 0.4 min-1 (n = 3).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Synaptic integration at a sensory-motor reflex in the leech.

1. In the medicinal leech the distribution of synapses from the pressure sensory (P) neurone to the annulus erector (AE) motoneurone and the site of impulse initiation in the AE cell were determined to understand better the integration of sensory inputs by the motoneurone. 2. The axon of the AE cell bifurcates before leaving the ganglion. Laser photoablation experiments indicated that the axon proximal to the bifurcation is inexcitable. Two techniques, laser photoablation and measurement of impulse timing, each located the site of impulse initiation at the bifurcation. 3. The medial P cell makes a monosynaptic connection with the AE cell, eliciting an excitatory postsynaptic potential (EPSP) of 1-3 mV amplitude recorded in the AE cell soma. 4. Intracellular injection of dyes into separate cells showed that P cell branches appear to contact AE cell branches both ipsilaterally and contralaterally. Laser photoablation of selected portions of the P and AE cells' axons revealed functional contacts on both sides. 5. The primary axon bifurcation of the AE cell is the site of integration of synaptic potentials that spread passively from both sides of the ganglion. These summed synaptic potentials account for the concerted activity of the two AE cells in each ganglion.

Action Potentials↗
PubMed1993

Cyclic AMP mediates inhibition of the Na(+)-K+ electrogenic pump by serotonin in tactile sensory neurones of the leech.

1. Serotonin (5-HT) reduced the after-hyperpolarization (AHP) amplitude in tactile sensory neurones (T) but not in pressor (P) or nociceptive (N) cells of the leech. 2. Adenylate cyclase activators, phosphodiesterase inhibitors and membrane permeant analogues of cyclic adenosine monophosphate (cyclic AMP) mimicked the effect of 5-HT in reducing the AHP amplitude in T neurones. 3. Ionophoretic injection of cyclic AMP in T cells reduced the AHP amplitude, while cyclic guanosine monophosphate (cyclic GMP) or adenosine-5'-monophosphate (AMP) were without effect. 4. Inhibition of adenylate cyclase by the drug RMI 12330A (also known as MDL 12330A) suggested that 5-HT reduced the AHP amplitude through cyclic AMP. 5. 8-Bromoadenosine-3'-5'-cyclic monophosphate (8-Br-cyclic AMP) was still able to reduce the AHP amplitude after blocking the Ca(2+)-activated K+ conductance with CdCl2 and converted the normal hyperpolarization which follows the intracellular injection of Na+ into a depolarization. In addition, the cyclic AMP analogue slowed down and reduced the repolarization usually induced by CsCl after perfusion with K(+)-free solution. It is proposed that, in T sensory neurones, cyclic AMP mediates the inhibition of the Na(+)-K+ electrogenic pump induced by 5-HT application.

1-Methyl-3-isobutylxanthine↗
PubMed1993

pH recovery from intracellular alkalinization in Retzius neurones of the leech central nervous system.

1. Neutral-carrier pH-sensitive microelectrodes were used to investigate intracellular pH (pHi) recovery from alkalinization in leech Retzius neurones in Hepes- and in CO2-HCO3(-)-buffered solution. The Retzius neurones were alkaline loaded by the addition and subsequent removal of 16 mM acetate, by changing from 5% CO2-27 mM HCO3- to 2% CO2-11 mM HCO3- or by changing from CO2-HCO3(-)- to Hepes-buffered solution. 2. In Hepes-buffered solution (pH 7.4) the mean pHi was 7.29 +/- 0.11 and the mean membrane potential -44.7 +/- 5.9 mV (mean +/- S.D.; n = 83). 3. The rate of pHi recovery from alkalinization increased with decreasing pH of the bathing medium (pHb). pHi changed about 0.30 pH units for a pHb unit change. 4. A decrease of extracellular buffer concentration (Hepes concentration lowered from 20 to 5 mM) caused an acidification of extracellular and intracellular pH and an acceleration of pHi recovery from alkalinization. 5. A depolarization of the Retzius cell membrane-induced by increasing the K+ concentration of the bathing medium from 4 to 20 mM (delta Em = 16.5 +/- 5.5 mV) or from 4 to 40 mM (delta Em = 24.8 +/- 3.5 mV)--evoked a decrease of pHi and an acceleration of pHi recovery from alkalinization. 6. The H+ current blocker Zn2+ (0.5 mM) inhibited pHi recovery from alkalinization at resting membrane potential as well as during depolarization. The inhibition was more pronounced during depolarization. 7. In Cl(-)-free, CO2-HCO3(-)-buffered solution pHi recovery from an alkaline load by changing from 5% CO2-27 mM HCO3- to 2% CO2-11 mM HCO3- was slowed by 48-71%. The rate of pHi recovery from an alkaline load induced by changing from CO2-HCO3- to Hepes buffer was reduced by 33-56% in Cl(-)-free solution. The removal of external Cl- did not affect pHi recovery in Hepes-buffered solution. 8. The pHi recovery from alkalinization was DIDS-insensitive in CO2-HCO3(-)- as in Hepes-buffered solutions and was not slowed in the absence of external Na+. 9. It is concluded that in Retzius neurones pHi recovery from alkalinization is mediated by a passive voltage-dependent H+ influx along the electrochemical proton gradient. In the presence of CO2-HCO3- buffer a DIDS-insensitive Cl(-)-HCO3- exchanger additionally regulates pHi after an intracellular alkaline load. It cannot be excluded that intracellular processes (e.g. H+ release from organelles, metabolic H+ production) are also involved in pHi recovery from alkalinization.

Alkalies↗
PubMed1993

Selection of transmitter responses at sites of neurite contact during synapse formation between identified leech neurons.

1. Pressure sensitive (P) neurons of the leech Hirudo medicinalis show both an inhibitory, Cl(-)-dependent response and a depolarizing, cationic response to pipette application of serotonin (5-HT). Serotonergic Retzius (R) neurons in culture reform inhibitory, Cl(-)-dependent synapses with P neurons but fail to elicit the extrasynaptic, depolarizing response to 5-HT. We have examined the localization of the selection of 5-HT responses by testing the sensitivity of P cell growth cones and neurites to 5-HT application. 2. As measured by intracellular recording at the P cell soma, synaptic release of 5-HT from R cell processes activated only the Cl(-)-dependent response in P cell neurites. Focal application of 5-HT from a micropipette depolarized uncontacted P cell growth cones and neurites. In contrast, processes from the same P cells that were contacted by R cells were rarely depolarized by 5-HT application unless the application pipette was moved along the neurites away from the sites of contact. 3. The channels underlying the depolarizing response to 5-HT were identified in patch clamp recordings from P cell growth cones. These cation channels showed rare, brief openings in the absence of 5-HT. Application of 5-HT in the bath (outside the patch pipette) increased channel activity in uncontacted P cell growth cones but not in growth cones of the same P cells contacted by R cells. 4. We conclude that the selection of transmitter responses during synapse formation was localized to discrete sites of contact between the synaptic partners.

Action Potentials↗
PubMed1994

Sodium-bicarbonate cotransport current in identified leech glial cells.

1. The membrane current associated with the cotransport of Na+ and HCO3- was investigated in neuropil glial cells in isolated ganglia of the leech Hirudo medicinalis L. using the two-electrode voltage-clamp technique. 2. The addition of 5% CO2-24 mM HCO3- evoked an outward current, which slowly decayed, and which was dependent upon the presence of external Na+. Removal of CO2-HCO3- elicited a transient inward current. Re-addition of Na+ to Na(+)-free saline in the presence of CO2-HCO3- also produced an outward current. Under these conditions an intracellular alkalinization and a rise in intracellular [Na+] were recorded using triple-barrelled, ion-sensitive microelectrodes. Addition or removal of HCO3-, in the absence of external Na+, caused little or no change in membrane voltage, membrane current and intracellular pH, indicating that the glial membrane has a very low HCO3- conductance. 3. Voltage steps revealed nearly linear current-voltage relationships both in the absence and presence of CO2-HCO3-, with an intersection at the assumed reversal potential of the HCO(3-)-dependent current. These results suggest a cotransport stoichiometry of 2HCO3-: 1 Na+. The HCO(3-)-dependent current could be inhibited by diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS). 4. Simultaneous recording of current and intracellular pH showed a correlation of the maximal acid-base flux with the transient HCO(3-)-dependent current during voltage steps in the presence of CO2-HCO3-. The maximum rate of acid-base flux and the HCO(3-)-dependent peak current showed a similar dependence on membrane voltage. Lowering the external pH from 7.4 to 7.0 produced an inward current, which increased twofold in the presence of CO2-HCO3-. This current was largely inhibited by DIDS, indicating outward-going electrogenic Na(+)-HCO3- cotransport during external acidification. 5. When external Na+ was replaced by Li+, a similar outward current and intracellular alkalinization were observed in the presence of CO2-HCO3-. The Li(+)-induced intracellular alkalinization was not inhibited by amiloride, a blocker of Na+(Li+)-H+ exchange, but was sensitive to DIDS. These results suggest that Li+ could, at least partly, substitute for Na+ at the cotransporter site. 6. Our results indicate that the Na(+)-HCO3- cotransport produces a current across the glial cell membrane in both directions with a reversal potential near the membrane resting potential, rendering pHi a function of the glial membrane potential.

Animals↗
PubMed1994

Evidence that glial cells modulate extracellular pH transients induced by neuronal activity in the leech central nervous system.

1. The role of the giant neuropile glial cells in the buffering of activity-related extracellular pH changes was studied in segmental ganglia of the leech Hirudo medicinalis L. using pH-sensitive microelectrodes and a slow, two-electrode voltage-clamp system. Neuronal activity was induced by electrical stimulation of a ganglionic side nerve (20 Hz, 1 min). 2. In CO2-HCO3(-)-buffered saline the glial cells were depolarized by 6.5 +/- 2.3 mV and alkalinized by 0.024 +/- 0.006 pH units (mean +/- SD) during the stimulation. The stimulation induced an acidification of 0.032 +/- 0.006 pH units in the extracellular spaces (ECS). 3. Voltage clamping the glial cells suppressed the stimulus-induced glial depolarization and turned the intraglial alkalinization into an acidification of 0.045 +/- 0.021 pH units (n = 6) that closely resembled the acidification observed in the presence of the anion transport blocker DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid, 0.5 mM), and in CO2-HCO(3-)-free saline. 4. Voltage clamping the glial cell resulted in the appearance of a distinct stimulus-induced extracellular alkalinization of 0.024 +/- 0.013 pH units at the onset of the stimulation, as also observed during DIDS application and in the absence of CO2-HCO3-. 5. The results suggest that glial uptake of bicarbonate is mediated by depolarization-induced activation of the electrogenic Na(+)-HCO3- cotransport, which suppresses the profound alkalinization of the ECS during neuronal activity. This is the first direct evidence the glial cells actively modulate extracellular pH changes in a voltage-dependent manner.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1995

Tyrosine phosphorylation during synapse formation between identified leech neurons.

1. We have examined whether tyrosine phosphorylation is required for synapse formation between identified neurons from the central nervous system of the leech in culture. 2. Within a few hours of contact with the cell body of the serotonergic Retzius neuron (R cell), the soma of the postsynaptic pressure-sensitive neuron (P cell), but not the R cell, could be labelled intracellularly with an antibody against phosphotyrosine residues. The labelling seemed specific for P cells contacted by R cells, as it was greatly reduced in pairs of either R or P cells and in single cells. Genistein (20 microM) and lavendustin A (10 microM), selective inhibitors of tyrosine kinases, blocked the labelling of contacted P cells, whereas their ineffective analogues (genistein and lavendustin B) had no effect on labelling. 3. R cell contact also induced the loss of an extrasynaptic, depolarizing response (due to modulation of cation channels) to serotonin (5-HT) in the P cell within a few days of juxtaposing cell bodies and within an hour of contact with growth cones. Treatment of the neurons with the tyrosine kinase inhibitors (but not the ineffective analogues) prevented the loss of the depolarizing response and of single cation channel modulation by 5-HT. 4. R cells formed inhibitory, Cl(-)-dependent synapses with P cells. Synapse formation was prevented by the tyrosine kinase inhibitors but not by their ineffective analogues. These compounds had no obvious effect on neurite outgrowth or cell adhesion. We conclude that tyrosine phosphorylation is a signal during the formation of this synapse.

Animals↗
PubMed1997

Channel modulation by tyrosine phosphorylation in an identified leech neuron.

1. We have examined the effects of tyrosine phosphorylation on a spontaneously active cation channel that also participates in the modulation of pressure-sensitive (P) neurons in the leech. Cation channel activity in cell-attached or isolated, inside-out membrane patches from P cells in culture was monitored before and after treatments that altered the level of tyrosine phosphorylation. 2. In cell-attached recordings from intact P cells, bath application of genistein, an inhibitor of tyrosine kinases, resulted in a 6.6 +/- 2.6-fold increase in channel activity with no change in the mean open time or amplitude. Daidzein, an inactive form of genistein, was without effect. Addition of pervanadate, a membrane-permeant inhibitor of tyrosine phosphatases, had no effect on its own and blocked the effect of subsequent addition of genistein. 3. In inside-out P cell membrane patch recordings, exposure to a catalytically active fragment of a tyrosine phosphatase resulted in a 10.3 +/- 3.6-fold increase in channel activity with no change in the mean open time or amplitude. Orthovanadate had no effect on channel activity and, when added with the phosphatase, prevented the increase in activity. 4. Our results demonstrate that the basal activity of cation channels is increased by tyrosine dephosphorylation, suggesting a constitutive modulation of channel activity under resting conditions.

Animals↗
PubMed2003

Somatic exocytosis of serotonin mediated by L-type calcium channels in cultured leech neurones.

We studied somatic exocytosis of serotonin and its mediation by L-type calcium (Ca2+) channels in cultured Retzius neurones of the leech. Exocytosis was induced by trains of impulses at different frequencies or by depolarisation with 40 mM potassium (K+), and was quantified by use of the fluorescent dye FM 1-43. Stimulation increased the membrane fluorescence and produced a pattern of FM 1-43 fluorescent spots of 1.28 +/- 0.01 microm in diameter, provided that Ca2+ was present in the bathing fluid. Individual spots lost their stain during depolarisation with 40 mM K+. Electron micrographs showed clusters of dense core vesicles, some of which were in contact with the cell membrane. Presynaptic structures with clear vesicles were absent from the soma. The number of fluorescent spots per soma, but not their diameter or their fluorescence intensity, depended on the frequency of stimulation. Trains at 1 Hz produced 19.5 +/- 5 spots per soma, 77.9 +/- 13.9 spots per soma were produced at 10 Hz and 91.5 +/- 16.9 spots per soma at 20 Hz. Staining patterns were similar for neurones in culture and in situ. In the presence of the L-type Ca2+ channel blocker nimodipine (10 microM), a 20 Hz train produced only 22.9 +/- 6.4 spots per soma, representing a 75 % reduction compared to control cells (P < 0.05). Subsequent incubation with 10 mM caffeine to induce Ca2+ release from intracellular stores increased the number of spots to 73.22 +/- 12.5. Blockers of N-, P-, Q- or invertebrate Ca2+ channels did not affect somatic exocytosis. Our results suggest that somatic exocytosis by neurones shares common mechanisms with excitable endocrine cells.

Animals↗
PubMed1969

Excitatory and inhibitory motoneurons in the central nervous system of the leech.

The locomotion and reflex responses of the leech are brought about by inmuscles that are arranged in a regular, simple pattern in the body wall and that flatten, shorten, lengthen, or bend the animal. In the segmental ganglia, it is possible to recognize by morphological and physiological criteria the individual motoneurons that cause contractions and relaxations of these muscles.

Action Potentials↗
PubMed1973

Retzius cells: neuroeffectors controlling mucus release by the leech.

Mucus release from the skin of leeches is under the control of the pair of large Retzius cells in each segmental ganglion. The rate of mucus release increases with the impulse activity of Retzius cells and with the concentration of their putative neurotransmitter, 5-hydroxytryptamine, to which the skin is exposed.

Action Potentials↗
PubMed1991

A neuron-silicon junction: a Retzius cell of the leech on an insulated-gate field-effect transistor.

An identified neuron of the leech, a Retzius cell, has been attached to the open gate of a p-channel field-effect transistor. Action potentials, spontaneous or stimulated, modulate directly the source-drain current in silicon. The electronic signals match the shape of the action potential. The average voltage on the gate was up to 25 percent of the intracellular voltage change. Occasionally weak signals that resemble the first derivative of the action potential were observed. The junctions can be described by a model that includes capacitive coupling of the plasma membrane and the gate oxide and that accounts for variable resistance of the seal.

Action Potentials↗
PubMed1989

Central synaptic inputs to identified leech neurons determined by peripheral targets.

Developing Retzius (Rz) neurons in different segments of the central nervous system of the medicinal leech have different peripheral targets: Rz cells in standard segments innervate the body wall, whereas Rz cells in the reproductive segments innervate reproductive tissue. Early removal of reproductive tissue primordia causes reproductive Rz cells to develop morphologically like their standard segmental homologs, suggesting that Rz cells depend on peripheral targets for signals that determine their central and peripheral morphology. Furthermore, after removal of reproductive tissue, reproductive Rz cells also receive synaptic inputs normally appropriate for standard Rz cells. These results suggest that the functional identity of these neurons is specified by the target they contact during embryogenesis.

Action Potentials↗