Significance of monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro.

Stimulation of a dorsal root in an isolated spinal cord, elicited a monosynaptic reflex (MSR) in the corresponding ventral root at a latency of 3-5 msec and a dorsal root reflex (DRR) in an adjacent dorsal root 2-3 times the latency of MSR. The magnitude of DRR was 10 times smaller than the MSR. These reflexes could be decreased by the agents which suppress synaptic transmission e.g. either by decreasing the [Ca2+]0 or by increasing [Mg2+]0. In the absence of magnesium ([Mg2+]0) in the perfusing medium, the MSR was 15-20% greater in its magnitude and the segmental polysynaptic reflex (PSR) was distinctly seen at 8-10 msec latency. Segmental PSR disappeared when [Mg2+]0 ions are added to perfusing medium probably indicating the involvement of N-methyl-D-aspartate receptors. Further, in this preparation homosynaptic inhibition and pre- or post-synaptic inhibitions could be elicited. This preparation, thus serves as useful model for the study of central synaptic transmission to study the pharmacological or neurotoxic agents.

Thyrotropin releasing hormone-induced potentiation of spinal monosynaptic reflex in rats in vitro.

Superfusion of thyrotropin-releasing hormone (TRH) in neonatal rat spinal cord in vitro produced dose (0.01-1.00 microM) dependent potentiation of monosynaptic reflex (MSR) which was maximum (44% of control) at 1 microM of TRH. But no ventral root depolarization was observed with TRH (1 microM) although potassium concentration out side ([K+]0) when increased produced a depolarization at the magnitude of 0.2 mV/mM of [K+]0. TRH-induced potentiation of MSR was not altered in spinal cords, obtained from the animals pretreated with 5,7-dihydroxytryptamine or 6-hydroxydopamine. Neither serotonin antagonists (spiperone, ketanserin, cyproheptadine or 3-troponyl-indole-3-carboxylate) nor adrenergic antagonists (phentolamine or haloperidol) could attenuate TRH-induced potentiation. Inhibition of MSR observed in the spinal cord elicited by stimulating the adjacent dorsal root was unaffected by TRH. The results suggest that, TRH potentiates MSR by directly acting on the motoneurons, without involving presynaptic serotonergic or catecholaminergic neuronal systems or the disinhibition of pre- or post-synaptic inhibition in the spinal cord.

Effects and site of action of a single-breath of 100% CO2 on the monosynaptic reflexes in cats.

A single breath of 100% CO2 produces depression of the monosynaptic reflexes, recorded from L7 or S1 ventral root, after stimulation of the Posterior Biceps and Semitendinosus nerve (PBST) in anaesthetised cats. As the depression could not be attributed to the J-reflex(1), the possible site of action of the CO2 induced depression of monosynaptic reflexes was worked out. PBST nerve threshold did not change after CO2 introduction and the depression persisted in paralysed cats under controlled ventilation, thus eliminating the possibility of movement effect of the spinal cord due to tachypnoea. Spinal cord sections at the level of L1 and C1 abolished the depression, whereas the depression persisted in the decerebrate preparation. Thus it is concluded that a single-breath of 100% CO2 depresses the monosynaptic reflexes at the supraspinal level. Blood gas tensions (PO2 and pCO2) measured before and after CO2 introduction showed a shortlasting increase in pCO2 and not much significant change in pO2 compared to the long lasting depression of monosynaptic reflexes.

Limitations in the use of CO2 as a method for studying the J-reflex.

In order to study the J-reflex, monosynaptic reflexes were recorded from L7 or S1 ventral root after stimulation of the posterior biceps, and semi-tendinosus nerve (PBST) from the lower limb in cats anaesthetized with Pentobarbitone sodium. Intratracheal CO2 (60 ml, 100%) depressed the monosynaptic reflexes, and the depression was comparable to the effects of right atrial phenyl diguanide injection. Bilateral vagotomy did not abolish the response showing that the afferent pathway of this depression does not travel via the vagus nerve. Thus it is concluded that CO2 cannot be used to study the J-reflex.