PMID- 8930268
OWN - NLM
STAT- MEDLINE
DCOM- 19970313
LR  - 20171213
IS  - 0022-3077 (Print)
IS  - 0022-3077 (Linking)
VI  - 76
IP  - 5
DP  - 1996 Nov
TI  - Identification of a putative mechanosensory neuron in Lymnaea: characterization 
      of its synaptic and functional connections with the whole-body withdrawal 
      interneuron.
PG  - 3230-8
AB  - 1. In this study, we identified a putative mechanosensory neuron in the 
      freshwater pond snail Lymnaea stagnalis. This sensory neuron, termed right 
      parietal dorsal 3 (RPD3), mediates part of the whole-body withdrawal behavior via 
      the activation of a withdrawal interneuron. 2. RPD3 is located in the central 
      ring ganglia, where its soma is situated on the dorsal surface of the right 
      parietal ganglion. Intracellular injection of the dye Lucifer yellow revealed 
      that RPD3 has both central and peripheral axonal projections. 3. In isolated-CNS 
      preparations, RPD3 was quiescent. In semi-intact preparations, however, a 
      gentle/moderate mechanical touch (by a pair of blunt forceps) to the mantle 
      cavity or columellar musculature elicited action potentials in RPD3 in the 
      absence of prepotential activity. Furthermore, mechanical stimulus-induced action 
      potentials in RPD3 persisted in the presence of zero Ca2+/ high Mg2+ and high 
      Ca2+/high Mg2+ salines. Together, these data suggest that RPD3 is most likely to 
      be a primary sensory neuron. 4. In both isolated-CNS and semi-intact 
      preparations, intracellular depolarization of RPD3 excited the whole-body 
      withdrawal interneuron right pedal dorsal 11 (RPeD11). This synaptic connection 
      persisted in the presence of high Ca2+ and high Mg2+ saline, suggesting that it 
      is likely to be monosynaptic. Moreover, when stimulated electrically, the 
      interneuron RPeD11 induced an hyperpolarizing response in RPD3. The possibility 
      of this connection being monosynaptic was not tested, however, in the present 
      study. Together, these data demonstrate that RPD3 excites RPeD11, which in turn 
      may inhibit RPD3 activity. 5. In the semi-intact preparation, a mechanical touch 
      to the mantle edge excited RPD3, which in turn generated action potentials in 
      RPeD11. Zero Ca2+ saline blocked this synaptic connection between RPD3 and 
      RPeD11, suggesting that it is chemical. 6. To demonstrate that RPD3 was 
      sufficient to induce the withdrawal response and that the withdrawal behavior was 
      mediated indirectly via RPeD11, we made simultaneous intracellular recordings 
      from these two neurons while monitoring muscle contractions via a tension 
      transducer. Intracellular depolarization of RPD3 elicited action potentials in 
      RPeD11, followed by the contraction of the columellar muscle. Similar stimulation 
      of RPD3 failed to excite a simultaneously hyperpolarized RPeD11 and as a result, 
      no contraction of the columellar muscle occurred. Direct intracellular 
      depolarization of RPeD11, however, induced the contraction of the columellar 
      muscle. These data suggest that RPD3-induced withdrawal behavior is mediated in 
      part via RPeD11.
FAU - Inoue, T
AU  - Inoue T
AD  - Department of Anatomy, Faculty of Medicine, University of Calgary, Alberta, 
      Canada.
FAU - Takasaki, M
AU  - Takasaki M
FAU - Lukowiak, K
AU  - Lukowiak K
FAU - Syed, N I
AU  - Syed NI
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurophysiol
JT  - Journal of neurophysiology
JID - 0375404
SB  - IM
MH  - Animals
MH  - Interneurons/*physiology
MH  - Lymnaea
MH  - Mechanoreceptors/*physiology
MH  - Motor Activity/physiology
MH  - Neurons, Afferent/*physiology
MH  - Parietal Lobe/*physiology
MH  - Synaptic Transmission/*physiology
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
AID - 10.1152/jn.1996.76.5.3230 [doi]
PST - ppublish
SO  - J Neurophysiol. 1996 Nov;76(5):3230-8. doi: 10.1152/jn.1996.76.5.3230.