Effects of scaphognathite nerve stimulation on the acutely deafferented crab ventilatory central pattern generator

Abstract

Sensory axons from crab (Carcinus maenas)scaphognathites enter the thoracic ganglion primarily via the LNb branch of the levator nerve. The LNa branch of the levator nerve and the depressor nerve each contain relatively few sensory axons.2. Acutely deafferented ventilatory central pattern generators show a free running burst rate which is lower than that observed in intact crabs. Electrical stimulation of the levator nerve, or of its LNb branch, increases the burst rate in a frequency dependent manner. Stimulation at high enough intensity to recruit afferents will restart a paused motor rhythm. Stimulation of the levator nerve with short pulse trains phase resets and can entrain the rhythm.3. In addition to increasing the burst rate, LNb stimulation also causes a progressive elimination of motor neurons from the bursts as the stimulating frequency increases, probably due to depolarization of the 3 oval organ 'giant' afferent axons in this branch. Intracellular depolarization of single oval organ afferents will also inhibit some motor neurons as well as slow or stop the rhythm.4. Continuous stimulation of the depressor nerve does not affect the ganglionic burst rate and this nerve contains only a few small diameter afferent axons; however, brief trains of stimuli can reset the rhythm in a phase-dependent manner.

Degeneration of afferent neurons and long-term stability of the ventilatory central pattern generator in chronically deafferented crabs

“…The observations that LN stimulation following chronic deafferentation does not increase CPG V burst rate supports the argument made in the previous paper (Wilkens and DiCaprio 1994) that the accelerating effects arise from impulses carried by the small afferent neurons only. Stimulation of LN on the 22nd and 60th days after chronic deafferentation fails to speed the CPG v rhythm.…”

“…The proposed inhibitory input of the OOAs onto the CPG~ is supported by the observation that current injection into single oval organ terminals within the thoracic ganglion can reset (trains of stimuli), slow or stop the rhythm (repeat-mode stimuli), and when the rhythm is stopped stimuli inhibit all levator motor neurons and cause the depressor motor neurons to fire tonically (Wilkens and DiCaprio 1994). The level of OOA activity required to inhibit the CPG~ following small afferent degeneration is somewhat lower than that required in acute preparations.…”

“…Sixty days after nerve section when all small afferents have degenerated LN stimulation at 20 Hz induced pausing in each of three ganglia (Fig. 1), while 50 Hz stimulation caused pausing in only 2 or 10 acutely deafferented ganglia (Wilkens and DiCaprio 1994). It is not known if the surviving OOA axons increase their synaptic efficacy onto follower cells in the ganglion, but increase in synaptic efficacy of surviving afferents onto interneuronS following partial deafferentation has been documented in other arthropod cases (Murphey and Lemere 1984;Murphey and Levine 1980;Shepherd and Murphey 1986;Volman 1989).…”

“…Following this the rate of bursting usually increases until by 30-60 min regular bursting became reestablished. Bursting in quiescent CPGvs can often be started by delivering electrical stimuli to the circumesophageal connectives, adding dopamine to the perfusate, reducing the oxygen tension of the perfusate, or stimulating the levator nerve (Simmers and Bush 1983;DiCaprio and Fourtner 1984;Wilkens et al 1989;Rajashekhar and Wilkens 1992;Wilkens and DiCaprio 1994). In marked contrast, the operated-side CPG v which has been without afferent input for several days does not respond negatively to the surgical isolation of the ganglion.…”

“…At 60 days LN stimulation still caused the elimination of motor units from the depressor burst. This is assumed to arise from impulses carried by the OOA axons (Wilkens and DiCaprio 1994), since these axons do not degenerate following scaphognathectomy. The rate of loss of afferent efficacy is similar to the rate of loss of afferent axons (52% in one week) in an abdominal sensory nerve in crayfish following nerve section (Govind et al 1992).…”

Degeneration of afferent neurons and long-term stability of the ventilatory central pattern generator in chronically deafferented crabs

“…The observations that LN stimulation following chronic deafferentation does not increase CPG V burst rate supports the argument made in the previous paper (Wilkens and DiCaprio 1994) that the accelerating effects arise from impulses carried by the small afferent neurons only. Stimulation of LN on the 22nd and 60th days after chronic deafferentation fails to speed the CPG v rhythm.…”

“…The proposed inhibitory input of the OOAs onto the CPG~ is supported by the observation that current injection into single oval organ terminals within the thoracic ganglion can reset (trains of stimuli), slow or stop the rhythm (repeat-mode stimuli), and when the rhythm is stopped stimuli inhibit all levator motor neurons and cause the depressor motor neurons to fire tonically (Wilkens and DiCaprio 1994). The level of OOA activity required to inhibit the CPG~ following small afferent degeneration is somewhat lower than that required in acute preparations.…”

“…Sixty days after nerve section when all small afferents have degenerated LN stimulation at 20 Hz induced pausing in each of three ganglia (Fig. 1), while 50 Hz stimulation caused pausing in only 2 or 10 acutely deafferented ganglia (Wilkens and DiCaprio 1994). It is not known if the surviving OOA axons increase their synaptic efficacy onto follower cells in the ganglion, but increase in synaptic efficacy of surviving afferents onto interneuronS following partial deafferentation has been documented in other arthropod cases (Murphey and Lemere 1984;Murphey and Levine 1980;Shepherd and Murphey 1986;Volman 1989).…”

“…Following this the rate of bursting usually increases until by 30-60 min regular bursting became reestablished. Bursting in quiescent CPGvs can often be started by delivering electrical stimuli to the circumesophageal connectives, adding dopamine to the perfusate, reducing the oxygen tension of the perfusate, or stimulating the levator nerve (Simmers and Bush 1983;DiCaprio and Fourtner 1984;Wilkens et al 1989;Rajashekhar and Wilkens 1992;Wilkens and DiCaprio 1994). In marked contrast, the operated-side CPG v which has been without afferent input for several days does not respond negatively to the surgical isolation of the ganglion.…”

“…At 60 days LN stimulation still caused the elimination of motor units from the depressor burst. This is assumed to arise from impulses carried by the OOA axons (Wilkens and DiCaprio 1994), since these axons do not degenerate following scaphognathectomy. The rate of loss of afferent efficacy is similar to the rate of loss of afferent axons (52% in one week) in an abdominal sensory nerve in crayfish following nerve section (Govind et al 1992).…”

Degeneration of afferent neurons and long-term stability of the ventilatory central pattern generator in chronically deafferented crabs

“…The observations that LN stimulation following chronic deafferentation does not increase CPG V burst rate supports the argument made in the previous paper (Wilkens and DiCaprio 1994) that the accelerating effects arise from impulses carried by the small afferent neurons only. Stimulation of LN on the 22nd and 60th days after chronic deafferentation fails to speed the CPG v rhythm.…”

“…The proposed inhibitory input of the OOAs onto the CPG~ is supported by the observation that current injection into single oval organ terminals within the thoracic ganglion can reset (trains of stimuli), slow or stop the rhythm (repeat-mode stimuli), and when the rhythm is stopped stimuli inhibit all levator motor neurons and cause the depressor motor neurons to fire tonically (Wilkens and DiCaprio 1994). The level of OOA activity required to inhibit the CPG~ following small afferent degeneration is somewhat lower than that required in acute preparations.…”

“…Sixty days after nerve section when all small afferents have degenerated LN stimulation at 20 Hz induced pausing in each of three ganglia (Fig. 1), while 50 Hz stimulation caused pausing in only 2 or 10 acutely deafferented ganglia (Wilkens and DiCaprio 1994). It is not known if the surviving OOA axons increase their synaptic efficacy onto follower cells in the ganglion, but increase in synaptic efficacy of surviving afferents onto interneuronS following partial deafferentation has been documented in other arthropod cases (Murphey and Lemere 1984;Murphey and Levine 1980;Shepherd and Murphey 1986;Volman 1989).…”

“…Following this the rate of bursting usually increases until by 30-60 min regular bursting became reestablished. Bursting in quiescent CPGvs can often be started by delivering electrical stimuli to the circumesophageal connectives, adding dopamine to the perfusate, reducing the oxygen tension of the perfusate, or stimulating the levator nerve (Simmers and Bush 1983;DiCaprio and Fourtner 1984;Wilkens et al 1989;Rajashekhar and Wilkens 1992;Wilkens and DiCaprio 1994). In marked contrast, the operated-side CPG v which has been without afferent input for several days does not respond negatively to the surgical isolation of the ganglion.…”

“…At 60 days LN stimulation still caused the elimination of motor units from the depressor burst. This is assumed to arise from impulses carried by the OOA axons (Wilkens and DiCaprio 1994), since these axons do not degenerate following scaphognathectomy. The rate of loss of afferent efficacy is similar to the rate of loss of afferent axons (52% in one week) in an abdominal sensory nerve in crayfish following nerve section (Govind et al 1992).…”

Degeneration of afferent neurons and long-term stability of the ventilatory central pattern generator in chronically deafferented crabs

“…The observations that LN stimulation following chronic deafferentation does not increase CPG V burst rate supports the argument made in the previous paper (Wilkens and DiCaprio 1994) that the accelerating effects arise from impulses carried by the small afferent neurons only. Stimulation of LN on the 22nd and 60th days after chronic deafferentation fails to speed the CPG v rhythm.…”

“…The proposed inhibitory input of the OOAs onto the CPG~ is supported by the observation that current injection into single oval organ terminals within the thoracic ganglion can reset (trains of stimuli), slow or stop the rhythm (repeat-mode stimuli), and when the rhythm is stopped stimuli inhibit all levator motor neurons and cause the depressor motor neurons to fire tonically (Wilkens and DiCaprio 1994). The level of OOA activity required to inhibit the CPG~ following small afferent degeneration is somewhat lower than that required in acute preparations.…”

“…Sixty days after nerve section when all small afferents have degenerated LN stimulation at 20 Hz induced pausing in each of three ganglia (Fig. 1), while 50 Hz stimulation caused pausing in only 2 or 10 acutely deafferented ganglia (Wilkens and DiCaprio 1994). It is not known if the surviving OOA axons increase their synaptic efficacy onto follower cells in the ganglion, but increase in synaptic efficacy of surviving afferents onto interneuronS following partial deafferentation has been documented in other arthropod cases (Murphey and Lemere 1984;Murphey and Levine 1980;Shepherd and Murphey 1986;Volman 1989).…”

“…Following this the rate of bursting usually increases until by 30-60 min regular bursting became reestablished. Bursting in quiescent CPGvs can often be started by delivering electrical stimuli to the circumesophageal connectives, adding dopamine to the perfusate, reducing the oxygen tension of the perfusate, or stimulating the levator nerve (Simmers and Bush 1983;DiCaprio and Fourtner 1984;Wilkens et al 1989;Rajashekhar and Wilkens 1992;Wilkens and DiCaprio 1994). In marked contrast, the operated-side CPG v which has been without afferent input for several days does not respond negatively to the surgical isolation of the ganglion.…”

“…At 60 days LN stimulation still caused the elimination of motor units from the depressor burst. This is assumed to arise from impulses carried by the OOA axons (Wilkens and DiCaprio 1994), since these axons do not degenerate following scaphognathectomy. The rate of loss of afferent efficacy is similar to the rate of loss of afferent axons (52% in one week) in an abdominal sensory nerve in crayfish following nerve section (Govind et al 1992).…”