Two papers about cellular mechanisms for prepulse inhibition studied in Tritonia

 

A cellular mechanism for prepulse inhibition (2003)

by William N. Frost, Li-Ming Tian, Travis A. Hoppe, Donna L. Mongeluzi, and Jean Wang

This paper shows the first cellular-level evidence for prepulse inhibition in Tritonia. A weak sensory stimulus has both excitatory and inhibitory effects on S-cells. The inhibitory effects shunt the synaptic output of some S-cells.

Prepulse inhibition (PPI):

Strong, unexpected stimuli elicit startle responses in all animals, but it can be markedly attenuated if closely preceded by a weak stimulus. 

Schizophrenics show abnormally low level of PPI.

Tritonia PPI

A prepulse stimulus was given by vibrated stick before an electric shock to elicit the swim

The prepulse acts to hyperpolarize two cell types in the swim circuit

Tactile stimuli hyperpolarized DSI and S-cells, but it also cause a lot of excitatory responses in other neurons.

The prepulse shortens and narrows the S cell action potential

Spike narrowing seen in the S cell AP.

Identification of a neuron, Pl 9, mediating the prepulse-elicited S cell inhibition

Pl 9 appears to receive direct EPSPs from most or all ipsilateral S cells and inturn produces direct IPSPs bilaterally onto the entire S cell population, as well as onto the Tr1, DRI, and VSI-B interneurons.

Pl 9 mediates prepulse-elicited hyperpolarizing inhibition of the S cells.

Evidence that Pl 9 mediates PPI

Intracellular stimulation of a single Pl 9 blocked the swim motor program.

Killing a single Pl 9 reduced PPI

Pl 9 inhibits S cell synaptic efficacy

S cell-evoked EPSPs in the swim network neurons were reduced in size when S cells were activated. 

Pl 9 reduces S cell synaptic efficacy via presynaptic inhibition of S cell transmitter release

Pl 9-evoked IPSPs are mediated by Chloride ion, blocked by d-tubocurarine

Pl 9 caused reduction of presynaptic action potentials of S cells in duration and amplitude

The S cell synaptic efficacy depended on its membrane potential

Identification of a neuron, Pl 10, involved in prespulse-elicite postsynaptic inhibition of the DSIs

PI 9 had no direct contact onto DSI, but Pl 10 does.

Pl 10 can block the swim

This study above looking at change in synaptic efficacy of S cells

The next study then looked at change in spike propagation

Axonal conduction block as a novel mechanism of prepulse inhibition

by Anne H. Lee, Evgenia V. Megalou, Jean Wang, and William N. Frost

Prepulse nerve stimuli produce PPI of the swim motor program, and conduction block of S-cell action potential trains

PdN3 alone (swim) vs PdN3 preceded by CN1,4,5 (prepulse) - in all cases CN1,4,5 stim prevented the swim.

Stim of CN1,4,5 caused conduction failure of S-cells evoked by PdN3 stim

Sometimes saw incomplete blockade

Prepulse-elicited conduction block has the temporal features of behavioral PPI in Tritonia

Conduction failure seen when stim was given with 250-500 ms latency (stim, 400 ms)

Conduction block also occurs in response to skin prepulse

Evidence that interneuron Pl-9 mediates PPI of S-cell conduction block

Peak Pl firing was 43 and 59 Hz in response to the tactile stimulation

photoinnactivation of Pl-9 blocked PPI