Vasopressin and oxytocin in sensory neurones: expression, exocytotic release and regulation by lactation

The hair plate proprioceptors at the thoraco-coxal joint of insect limbs provide information about the movements of the most basal joint of the legs. The ventral coxal hair plate of a middle leg consists of group of 10-15 long hairs (70 microns) and 20-30 short hairs (30 microns). The long hairs are deflected by the trochantin as the leg is swung forward during the swing phase of walking, and their sensory neurones respond phasically during an imposed deflection and tonically if the deflection is maintained. Selective stimulation of the long hairs elicits a resistance reflex that rotates the coxa posteriorly and is similar to that occurring at the transition from the swing to the stance phase of walking. The motor neurones innervating the posterior rotator and adductor coxae muscles are excited, and those to the antagonistic anterior rotator muscle are inhibited. By contrast, selective stimulation of the short hairs leads only to a weak inhibition of the anterior rotator. The excitatory effects of the long hairs are mediated, in part, by direct connections between their sensory neurones and particular motor neurones. A spike in a sensory neurone elicits a short-latency depolarising postsynaptic potential (PSP) in posterior rotator and adductor motor neurones whose amplitude is enhanced by hyperpolarising current injected into the motor neurone. When the calcium in the saline is replaced with magnesium, the amplitude of the PSP is reduced gradually, and not abruptly as would be expected if an interneurone were interposed in the pathway. Several sensory neurones from long hairs converge to excite an individual motor neurone, evoking spikes in some motor neurones. The projections of the sensory neurones overlap with some of the branches of the motor neurones in the lateral association centre of the neuropile. It is suggested that these pathways would limit the extent of the swing phase of walking and contribute to the switch to the stance phase in a negative feedback loop that relieves the excitation of the hairs by rotating the coxa backwards.

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Na+, K+ and Ca2+ currents in identified leech neurones in culture

Journal of Experimental Biology ◽

10.1242/jeb.141.1.1 ◽

1989 ◽

Vol 141 (1) ◽

pp. 1-20

Author(s):

R. R. Stewart ◽

J. G. Nicholls ◽

W. B. Adams

Keyword(s):

Minor Component ◽

Outward Current ◽

Membrane Properties ◽

Delayed Rectifier ◽

Inactivation Kinetics ◽

Channel Blockers ◽

Sensory Neurones ◽

K Current ◽

The Individual ◽

K Currents

1. Na+, K+ and Ca2+ currents have been measured by voltage-clamp in Retzius (R), anterior pagoda (AP) and sensory (pressure, touch and nociceptive) cells dissected from the central nervous system (CNS) of the leech. These cells maintain their distinctive membrane properties and action potential configurations in culture. Currents carried by the individual ions were analysed by the use of channel blockers and by their kinetics. Since the cells are isopotential they can be voltage-clamped effectively. 2. Depolarization, as expected, gave rise to an early inward Na+ current followed by a delayed outward K+ current. In Na+-free medium containing tetraethylammonium (TEA+), and in the presence of 4-aminopyridine (4-AP), inward Ca2+ currents were revealed that inactivated slowly and were blocked by Cd2+ and Mn2+. 3. Na+ and Ca2+ currents were similar in their characteristics in R. AP and sensory neurones. In contrast, K+ currents showed marked differences. Three principal K+ currents were identified. These differed in their time courses of activation and inactivation and in their responses to Ca2+ channel blockers. 4. K+ currents of the A-type (IA) activated and inactivated rapidly, were not affected by Ca2+ channel blockers and were eliminated by steady-state inactivation at holding potentials of −30 mV. A-type K+ currents were found in AP cells and as a minor component of the outward current in R cells. A Ca2+-activated K+ current (IC), that inactivated more slowly and was reduced by Ca2+ channel blockers, constituted the major outward current in R cells. The third K+ current resembled the delayed rectifier currents (IK1 and IK2) of squid axons with slow activation and inactivation kinetics. Such currents were found in R cells and in the sensory neurones (T, P and N). 5. The principal differences in membrane properties of identified leech neurones can be explained in terms of the numbers of Na+ channels and the distinctive kinetics of K+ channels in each type of cell.

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Development of synapses between identified sensory neurones and giant interneurones in the cockroach Periplaneta americana

Development ◽

10.1242/dev.86.1.227 ◽

1985 ◽

Vol 86 (1) ◽

pp. 227-246

Author(s):

J. M. Blagburn ◽

D. J. Beadle ◽

D. B. Sattelle

Keyword(s):

Periplaneta Americana ◽

Synapse Formation ◽

Primary Dendrite ◽

Lateral Side ◽

Synaptic Density ◽

Sensory Neurones ◽

Guidance Cues ◽

First Instar ◽

Sensory Processes ◽

Giant Interneurone

The cereal afferent, giant interneurone pathway in Periplaneta americana was used as a model for synapse formation. The morphology of the two identified filiform hair sensory neurones (FHSNs) and of two giant interneurones (GI2 and GI3) was followed throughout embryogenesis by cobalt injection. The FHSN axons enter the CNS at the 45 % stage of embryogenesis, branch at 50 % and form complete arborizations by 70 %. The giant interneurones send out a primary dendrite at 45 %. Secondary branches form between 50 % and 60 % and elaboration of the branching pattern takes place until 80 % embryogenesis. At early stages the FHSN axons are within filopodial range of GI dendrites which may use these sensory processes as guidance cues. Synapse formation between the main FHSN axon shafts and GI dendrites was investigated by injection of the latter with HRP. From 55 % to 65 % the process is initiated by desmosome—like filopodial contacts, with subsequent vesicle clustering and formation of a small synaptic density. Numbers of contacts did not significantly increase after about 70 %, but the number of synapses doubled between 65 % and 75 %, with each GI process becoming postsynaptic to two FHSN synapses and the presynaptic densities lengthening to become bars. From 75 % embryogenesis to hatching there is a further small increase in synaptic bar length. In the first instar GI3 is postsynaptic to both FHSN axons, whereas GI2 forms very few synapses with the axon of the lateral FHSN (LFHSN). This imbalance of contacts is present throughout synaptogenesis, apart from some early filopodial contacts. GI3 forms synapses with the lateral side of the LFHSN axon from 60 % embryogenesis but these are totally absent at hatching. The growth of glia along this side of the axon during the last 30 % of development appears to be associated with degeneration of synapses in this region. Thus, as the dendrites of the GIs grow to form a miniature version of the adult without loss of branches, there is little evidence of an initial overproduction of FHSN—GI synapses. Similarly there is no evidence that GI2 forms ‘incorrect’ synapses with the axon of LFHSN. However, GI3 contacts are removed from an inappropriate region of a correct synaptic partner, LFHSN.

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