Ultrastructural Characteristics of Glutamatergic and GABAergic Terminals in Cat Lamina IX Before and After Spinal Cord Injury

Abstract

The present study was designed to: 1) morpholog ically characterize cat glutamate and GABAergic synaptic term inals in lamina IX in the intact spinal cord at the electron microscopic leve l using postembedding immunochemical techniques and 2), begin an analysis of how the synaptic architecture of glutamate and GABAergic termi nals changes after an ipsilateral spinal cord hemisection. The present study shows that glutamate immunoreactive terminals are characte rized by a wide synaptic cleft, asymmetric synaptic membrane densities and spherical synaptic vesicles. Most of the glutamatergic terminals are presynaptic to small or medium size dendrites. In contrast, GABAergic terminals display typical pleomorphic ·synaptic vesicles , a narrow synaptic cleft and a symmetrical membrane density. Qualitative ana lys is indicated that 13-17 months after hemisection , the length of the s ynaptic active zones in both glutamatergic a nd GABAergic terminals ipsilateral to hemisection is longer tha n those observed in the terminals cont ra lateral to hemisection or in normal control cats. Furthermore, the perimeters of both dendrites and either glutamate or GABA immunoreactive terminals are longer on the hemisected side compared with those observed in the nonhemisected s ide of the spina l co rd . These results are important for complete understand ing of the mechanisms which unde rlie locomotor recovery in mammals following spinal cord injury. (J Spinal Cord Med 1997;20:311 -318)

Phrenic motoneuron discharge patterns following chronic cervical spinal cord injury

“…This suggestion is supported by the observation that during the acute post-injury phase (i.e., 2 days post-C2Hx; before extensive neuroplasticity and/or anatomical remodeling), PhMNs have already adopted a primarily Late-I phenotype (El-Bohy and Goshgarian, 1999). Progressive increases in PhMN excitability over weeks-months post-C2Hx, as suggested by prior work (Goshgarian, 2009; Tai et al, 1997a; Tai et al, 1997b) may offset the reduction in excitatory bulbospinal inputs to these cells, but without ever fully correcting the C2Hx-induced reductions in phrenic output.…”

“…While definitive testing of this possibility will require intracellular recordings (e.g., (Enriquez Denton et al , 2012)), we hypothesize that decreased PhMN excitability does not explain the observed bursting patterns. Mantilla and colleagues suggested in a preliminary report that PhMN soma size decreases after C2Hx (Mantilla and Sieck, 2009), and molecular changes in and around PhMNs after C2Hx are also consistent with increased excitability (Goshgarian, 2009; Sperry and Goshgarian, 1993; Tai et al, 1997a; Tai et al, 1997b). In our opinion, the more likely scenario is that the decreased burst frequency and Late-I phenotype occur due to the dramatic reduction in bulbospinal synaptic inputs to ipsilateral PhMNs after C2Hx.…”

“…Within the cervical spinal cord, neuroplastic changes occurring after C2Hx have been postulated to facilitate PhMN recruitment (Goshgarian, 2009; Tai et al, 1997a; Tai et al, 1997b) and lead to partial functional recovery. For example, increases in cervical spinal glutamatergic (Alilain and Goshgarian, 2008; Mantilla et al, 2012) and/or serotonergic receptor expression (Basura et al , 2001; Fuller et al , 2005; Mantilla et al , 2012) could both serve to increase PhMN excitability.…”

Complexities and uncertainties of neuronal network function

“…In mammalian systems, there is evidence that spinal injury triggers plastic effects in the spinal cord (Edgerton et al 2001;Dietz 2003). This includes changes in the number, size and distribution of synapses (Tai et al 1997), in the properties of neurotransmitter systems (Edgerton et al 2001), and in cellular and synaptic properties (Hochman and McRea 1994;Tillakaratne et al 2002;Li et al 2004). These changes may reflect adaptive plasticity mechanisms (see above) that attempt to compensate for the effects of injury.…”

Pharmacological Approaches to Functional Recovery After Spinal Injury

“…The functional recovery in mice is not due to the regeneration of descending inputs, as it persists after the spinal cord is relesioned [57]. The recovery of locomotor function after spinal lesions is associated with changes in synapse structure, including the number, size, and distribution of synapses [58,59], as well as functional changes in cellular and synaptic properties [3,4,52,60].…”